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<item rdf:about="http://jaha.ahajournals.org/content/6/5/e003796.short?rss=1">
<title><![CDATA[Peripheral Artery Disease Prevalence and Incidence Estimated From Both Outpatient and Inpatient Settings Among Medicare Fee-for-Service Beneficiaries in the Atherosclerosis Risk in Communities (ARIC) Study [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e003796.short?rss=1</link>
<description><![CDATA[BackgroundOutpatient ascertainment of peripheral artery disease (PAD) is rarely considered in the measurement of PAD clinical burden; therefore, the clinical burden of PAD likely has been underestimated while contributing to a decreased awareness of PAD in comparison to other circulatory system disorders.Methods and ResultsThe purpose of this study was to estimate the age‐standardized annual period prevalence and incidence of PAD in the outpatient and inpatient settings using data from the Atherosclerosis Risk in Communities (ARIC) study linked with Centers for Medicare and Medicaid Services claims. The majority (>70%) of all PAD encounters occurred in the outpatient setting. The weighted mean age‐standardized prevalence and incidence of outpatient PAD was 11.8% (95% CI 11.5–12.1) and 22.4 per 1000 person‐years (95% CI 20.8–24.0), respectively. Black patients had higher weighted mean age‐standardized prevalence (15.6%; 95% CI 14.6–16.4) compared with white patients (11.4%; 95% CI 11.1–11.7). Black women had the highest weighted mean age‐standardized prevalence (16.9%; 95% CI 16.0–17.8). Black patients also had a higher incidence rate of PAD (31.3 per 1000 person‐years; 95% CI 27.3–35.4) compared with white patients (25.4 per 1000 person‐years; 95% CI 23.5–27.3). PAD prevalence and incidence did not differ by sex alone.ConclusionsThis study provides comprehensive estimates of PAD in the inpatient and outpatient settings where the majority of PAD burden was found. PAD is an important circulatory system disorder similar in prevalence to stroke and coronary heart disease.]]></description>
<dc:creator><![CDATA[Kalbaugh, C. A., Kucharska-Newton, A., Wruck, L., Lund, J. L., Selvin, E., Matsushita, K., Bengtson, L. G. S., Heiss, G., Loehr, L.]]></dc:creator>
<dc:date>2017-05-03T09:37:44-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.003796</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.003796</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Peripheral Vascular Disease]]></dc:subject>
<dc:title><![CDATA[Peripheral Artery Disease Prevalence and Incidence Estimated From Both Outpatient and Inpatient Settings Among Medicare Fee-for-Service Beneficiaries in the Atherosclerosis Risk in Communities (ARIC) Study [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-03</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e003821.short?rss=1">
<title><![CDATA[C-GRApH: A Validated Scoring System for Early Stratification of Neurologic Outcome After Out-of-Hospital Cardiac Arrest Treated With Targeted Temperature Management [Resuscitation Science]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e003821.short?rss=1</link>
<description><![CDATA[BackgroundOut‐of‐hospital cardiac arrest (OHCA) results in significant morbidity and mortality, primarily from neurologic injury. Predicting neurologic outcome early post‐OHCA remains difficult in patients receiving targeted temperature management.Methods and ResultsRetrospective analysis was performed on consecutive OHCA patients receiving targeted temperature management (32–34°C) for 24 hours at a tertiary‐care center from 2008 to 2012 (development cohort, n=122). The primary outcome was favorable neurologic outcome at hospital discharge, defined as cerebral performance category 1 to 2 (poor 3–5). Patient demographics, pre‐OHCA diagnoses, and initial laboratory studies post‐resuscitation were compared between favorable and poor neurologic outcomes with multivariable logistic regression used to develop a simple scoring system (C‐GRApH). The C‐GRApH score ranges 0 to 5 using equally weighted variables: (C): coronary artery disease, known pre‐OHCA; (G): glucose ≥200 mg/dL; (R): rhythm of arrest not ventricular tachycardia/fibrillation; (A): age >45; (pH): arterial pH ≤7.0. A validation cohort (n=344) included subsequent patients from the initial site (n=72) and an external quaternary‐care health system (n=272) from 2012 to 2014. The c‐statistic for predicting neurologic outcome was 0.82 (0.74–0.90, P<0.001) in the development cohort and 0.81 (0.76–0.87, P<0.001) in the validation cohort. When subdivided by C‐GRApH score, similar rates of favorable neurologic outcome were seen in both cohorts, 70% each for low (0–1, n=60), 22% versus 19% for medium (2–3, n=307), and 0% versus 2% for high (4–5, n=99) C‐GRApH scores in the development and validation cohorts, respectively.ConclusionsC‐GRApH stratifies neurologic outcomes following OHCA in patients receiving targeted temperature management (32–34°C) using objective data available at hospital presentation, identifying patient subsets with disproportionally favorable (C‐GRApH ≤1) and poor (C‐GRApH ≥4) prognoses.]]></description>
<dc:creator><![CDATA[Kiehl, E. L., Parker, A. M., Matar, R. M., Gottbrecht, M. F., Johansen, M. C., Adams, M. P., Griffiths, L. A., Dunn, S. P., Bidwell, K. L., Menon, V., Enfield, K. B., Gimple, L. W.]]></dc:creator>
<dc:date>2017-05-20T03:03:20-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.003821</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.003821</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Sudden Cardiac Death, Clinical Studies, Cardiopulmonary Arrest, Quality and Outcomes]]></dc:subject>
<dc:title><![CDATA[C-GRApH: A Validated Scoring System for Early Stratification of Neurologic Outcome After Out-of-Hospital Cardiac Arrest Treated With Targeted Temperature Management [Resuscitation Science]]]></dc:title>
<prism:publicationDate>2017-05-20</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Resuscitation Science</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004264.short?rss=1">
<title><![CDATA[Race-Sex Differences in Statin Use and Low-Density Lipoprotein Cholesterol Control Among People With Diabetes Mellitus in the Reasons for Geographic and Racial Differences in Stroke Study [Health Services and Outcomes Research]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004264.short?rss=1</link>
<description><![CDATA[BackgroundStatin therapy is a cornerstone of cardiovascular disease risk reduction for people with diabetes mellitus. Past reports have shown race‐sex differences in statin use in general populations, but statin patterns by race and sex in those with diabetes mellitus have not been thoroughly studied.Methods and ResultsOur sample of 4288 adults ≥45 years of age with diagnosed diabetes mellitus who had low‐density lipoprotein cholesterol (LDL‐C) >100 mg/dL or were taking statins recruited for the Reasons for Geographic and Racial Differences in Stroke study from 2003 to 2007. Exposures included race‐sex groups (white men [WM], black men [BM], white women [WW], black women [BW]) and factors that may influence healthcare utilization. Proportions and prevalence ratios were calculated for statin use and LDL‐C control. Statin use for WM, BM, WW, and BW was 66.0%, 57.8%, 55.0%, and 53.6%, respectively (P<0.001). After adjustment for healthcare utilization factors, statin use was lower for BM, WW, and BW compared with WM (prevalence ratios [95%CI]: 0.96 [0.89‐1.03], 0.86 [0.80‐0.92], and 0.87 [0.81‐0.93], respectively, P<0.001). LDL‐C control among those taking statins for WM, BM, WW, and BW was 75.3%, 62.7%, 69.0%, and 56.0%, respectively (P<0.001). After adjustment, LDL‐C control was lower for BM, WW, and BW compared with WM (prevalence ratios [95%CI]: 0.85 [0.79‐0.93], 0.89 [0.82‐0.96], and 0.73 [0.67‐0.80], respectively, P<0.001).ConclusionsRace‐sex disparities in statin use and LDL‐C control were only partly explained by factors influencing health services utilization. Healthcare provider awareness of these disparities may help to close the observed race‐sex gaps in statin use and LDL‐C control among people with diabetes mellitus.]]></description>
<dc:creator><![CDATA[Gamboa, C. M., Colantonio, L. D., Brown, T. M., Carson, A. P., Safford, M. M.]]></dc:creator>
<dc:date>2017-05-10T12:11:39-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004264</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004264</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Lipids and Cholesterol, Diabetes, Type 2, Epidemiology, Race and Ethnicity, Health Services]]></dc:subject>
<dc:title><![CDATA[Race-Sex Differences in Statin Use and Low-Density Lipoprotein Cholesterol Control Among People With Diabetes Mellitus in the Reasons for Geographic and Racial Differences in Stroke Study [Health Services and Outcomes Research]]]></dc:title>
<prism:publicationDate>2017-05-10</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Health Services and Outcomes Research</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004276.short?rss=1">
<title><![CDATA[Hospital Performance on Percutaneous Coronary Intervention Process and Outcomes Measures [Health Services and Outcomes Research]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004276.short?rss=1</link>
<description><![CDATA[BackgroundThe Physician Consortium for Performance Improvement recently proposed percutaneous coronary intervention (PCI)‐specific process measures. However, information about hospital performance on these measures and the association of PCI process and outcomes measures are not available.Methods and ResultsWe linked the National Cardiovascular Data Registry (NCDR) CathPCI Registry with Medicare claims data to assess hospital performance on established PCI process measures (aspirin, thienopyridines, and statins on discharge; door‐to‐balloon time; and referral to cardiac rehabilitation), newly proposed PCI process measures (documentation of contrast dose, glomerular filtration rate, and PCI indication; appropriate indication for elective PCI; and use of embolic protection device), and a composite of all process measures. We calculated weighted pair‐wise correlations between each set of process metrics and performed weighted correlation analyses to assess the association between composite measure performance with corresponding 30‐day risk‐standardized mortality and readmission rates. We reported the variance in risk‐standardized 30‐day outcome rates explained by process measures. We analyzed 1 268 860 PCIs from 1331 hospitals. For many process measures, median hospital performance exceeded 90%. We found strong correlations between medication‐specific process measures (P<0.01) and weak correlations between hospital performance on the newly proposed and established process measures. The composite process measure explained only 1.3% and 2.0% of the observed variation in mortality and readmission rates, respectively.ConclusionsHospital performance on many PCI‐specific process measures demonstrated little opportunity for improvement and explained only a small percentage of hospital variation in 30‐day outcomes. Efforts to measure and improve hospital quality for PCI patients should focus on both process and outcome measures.]]></description>
<dc:creator><![CDATA[Chui, P. W., Parzynski, C. S., Nallamothu, B. K., Masoudi, F. A., Krumholz, H. M., Curtis, J. P.]]></dc:creator>
<dc:date>2017-04-26T09:24:12-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004276</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004276</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Percutaneous Coronary Intervention, Health Services, Quality and Outcomes, Acute Coronary Syndromes]]></dc:subject>
<dc:title><![CDATA[Hospital Performance on Percutaneous Coronary Intervention Process and Outcomes Measures [Health Services and Outcomes Research]]]></dc:title>
<prism:publicationDate>2017-04-26</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Health Services and Outcomes Research</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004297.short?rss=1">
<title><![CDATA[Performance of AHEAD Score in an Asian Cohort of Acute Heart Failure With Either Preserved or Reduced Left Ventricular Systolic Function [Heart Failure]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004297.short?rss=1</link>
<description><![CDATA[BackgroundAHEAD (A: atrial fibrillation; H: hemoglobin; E: elderly; A: abnormal renal parameters; D: diabetes mellitus) score has been related to clinical outcomes of acute heart failure. However, the prognostic value of the AHEAD score in acute heart failure patients with either reduced or preserved left ventricular ejection fraction (HFrEF and HFpEF) remain to be elucidated.Methods and ResultsThe study population consisted of 2143 patients (age 77±12 years, 68% men, 38% HFrEF) hospitalized primarily for acute heart failure with a median follow‐up of 23.75 months. The performance of the AHEAD score (atrial fibrillation, hemoglobin <13 mg/dL for men and 12 mg/dL for women, age >70 years, creatinine >130 μmol/L, and diabetes mellitus) was evaluated by Cox's regression analysis for predicting cardiovascular and all‐cause mortality. The mean AHEAD scores were 2.7±1.2 in the total study population, 2.6±1.3 in the HFrEF group, and 2.7±1.1 in the HFpEF group. After accounting for sex, sodium, uric acid, and medications, the AHEAD score remained significantly associated with all‐cause and cardiovascular mortality (hazard ratio and 95% CI: 1.49, 1.38–1.60 and 1.48, 1.33–1.64), respectively. The associations of AHEAD score with mortality remained significant in the subgroups of HFrEF (1.63, 1.47–1.82) and HFpEF (1.34, 1.22–1.48). Moreover, when we calculated a new AHEAD‐U score by considering uric acid (>8.6 mg/dL) in addition to the AHEAD score, the net reclassification was improved by 19.7% and 20.1% for predicting all‐cause and cardiovascular mortality, respectively.ConclusionsThe AHEAD score was useful in predicting long‐term mortality in the Asian acute heart failure cohort with either HFrEF or HFpEF. The new AHEAD‐U score may further improve risk stratification.]]></description>
<dc:creator><![CDATA[Chen, Y.-J., Sung, S.-H., Cheng, H.-M., Huang, W.-M., Wu, C.-L., Huang, C.-J., Hsu, P.-F., Yeh, J.-S., Guo, C.-Y., Yu, W.-C., Chen, C.-H.]]></dc:creator>
<dc:date>2017-05-04T11:56:23-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004297</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004297</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Heart Failure]]></dc:subject>
<dc:title><![CDATA[Performance of AHEAD Score in an Asian Cohort of Acute Heart Failure With Either Preserved or Reduced Left Ventricular Systolic Function [Heart Failure]]]></dc:title>
<prism:publicationDate>2017-05-04</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Heart Failure</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004448.short?rss=1">
<title><![CDATA[Randomized Controlled Trial of High-Volume Energy Drink Versus Caffeine Consumption on ECG and Hemodynamic Parameters [Arrhythmia and Electrophysiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004448.short?rss=1</link>
<description><![CDATA[BackgroundCaffeine in doses <400 mg is typically not considered arrhythmogenic, but little is known about the additional ingredients in energy drinks. We evaluated the ECG and blood pressure (BP) effects of high‐volume energy drink consumption compared with caffeine alone.Methods and ResultsThis was a randomized, double‐blind, controlled, crossover study in 18 young, healthy volunteers. Participants consumed either 946 mL (32 ounces) of energy drink or caffeinated control drink, both of which contained 320 mg of caffeine, separated by a 6‐day washout period. ECG, peripheral BP, and central BP measurements were obtained at baseline and 1, 2, 4, 6, and 24 hours post study drink consumption. The time‐matched, baseline‐adjusted changes were compared. The change in corrected QT interval from baseline in the energy drink arm was significantly higher than the caffeine arm at 2 hours (0.44±18.4 ms versus −10.4±14.8 ms, respectively; P=0.02). The QTc changes were not different at other time points. While both the energy drink and caffeine arms raised systolic BP in a similar fashion initially, the systolic BP was significantly higher at 6 hours when compared with the caffeine arm (4.72±4.67 mm Hg versus 0.83±6.09 mm Hg, respectively; P=0.01). Heart rate, diastolic BP, central systolic BP, and central diastolic BP showed no evidence of a difference between groups at any time point. Post energy drink, augmentation index was lower at 6 hours.ConclusionsThe corrected QT interval and systolic BP were significantly higher post high‐volume energy drink consumption when compared with caffeine alone. Larger clinical trials validating these findings and evaluation of noncaffeine ingredients within energy drinks are warranted.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT02023723.]]></description>
<dc:creator><![CDATA[Fletcher, E. A., Lacey, C. S., Aaron, M., Kolasa, M., Occiano, A., Shah, S. A.]]></dc:creator>
<dc:date>2017-04-26T12:45:11-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004448</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004448</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Arrhythmias, Electrophysiology, Diet and Nutrition, Hypertension]]></dc:subject>
<dc:title><![CDATA[Randomized Controlled Trial of High-Volume Energy Drink Versus Caffeine Consumption on ECG and Hemodynamic Parameters [Arrhythmia and Electrophysiology]]]></dc:title>
<prism:publicationDate>2017-04-26</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Arrhythmia and Electrophysiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004453.short?rss=1">
<title><![CDATA[Activation of the Amino Acid Response Pathway Blunts the Effects of Cardiac Stress [Heart Failure]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004453.short?rss=1</link>
<description><![CDATA[BackgroundThe amino acid response (AAR) is an evolutionarily conserved protective mechanism activated by amino acid deficiency through a key kinase, general control nonderepressible 2. In addition to mobilizing amino acids, the AAR broadly affects gene and protein expression in a variety of pathways and elicits antifibrotic, autophagic, and anti‐inflammatory activities. However, little is known regarding its role in cardiac stress. Our aim was to investigate the effects of halofuginone, a prolyl‐tRNA synthetase inhibitor, on the AAR pathway in cardiac fibroblasts, cardiomyocytes, and in mouse models of cardiac stress and failure.Methods and ResultsConsistent with its ability to inhibit prolyl‐tRNA synthetase, halofuginone elicited a general control nonderepressible 2–dependent activation of the AAR pathway in cardiac fibroblasts as evidenced by activation of known AAR target genes, broad regulation of the transcriptome and proteome, and reversal by l‐proline supplementation. Halofuginone was examined in 3 mouse models of cardiac stress: angiotensin II/phenylephrine, transverse aortic constriction, and acute ischemia reperfusion injury. It activated the AAR pathway in the heart, improved survival, pulmonary congestion, left ventricle remodeling/fibrosis, and left ventricular function, and rescued ischemic myocardium. In human cardiac fibroblasts, halofuginone profoundly reduced collagen deposition in a general control nonderepressible 2–dependent manner and suppressed the extracellular matrix proteome. In human induced pluripotent stem cell–derived cardiomyocytes, halofuginone blocked gene expression associated with endothelin‐1‐mediated activation of pathologic hypertrophy and restored autophagy in a general control nonderepressible 2/eIF2α‐dependent manner.ConclusionsHalofuginone activated the AAR pathway in the heart and attenuated the structural and functional effects of cardiac stress.]]></description>
<dc:creator><![CDATA[Qin, P., Arabacilar, P., Bernard, R. E., Bao, W., Olzinski, A. R., Guo, Y., Lal, H., Eisennagel, S. H., Platchek, M. C., Xie, W., del Rosario, J., Nayal, M., Lu, Q., Roethke, T., Schnackenberg, C. G., Wright, F., Quaile, M. P., Halsey, W. S., Hughes, A. M., Sathe, G. M., Livi, G. P., Kirkpatrick, R. B., Qu, X. A., Rajpal, D. K., Faelth Savitski, M., Bantscheff, M., Joberty, G., Bergamini, G., Force, T. L., Gatto, G. J., Hu, E., Willette, R. N.]]></dc:creator>
<dc:date>2017-05-09T11:56:26-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004453</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004453</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Fibrosis, Heart Failure, Hypertrophy]]></dc:subject>
<dc:title><![CDATA[Activation of the Amino Acid Response Pathway Blunts the Effects of Cardiac Stress [Heart Failure]]]></dc:title>
<prism:publicationDate>2017-05-09</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Heart Failure</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004513.short?rss=1">
<title><![CDATA[Observed Cost and Variations in Short Term Cost-Effectiveness of Therapy for Ischemic Stroke in Interventional Management of Stroke (IMS) III [Health Services and Outcomes Research]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004513.short?rss=1</link>
<description><![CDATA[BackgroundExamination of linked data on patient outcomes and cost of care may help identify areas where stroke care can be improved. We report on the association between variations in stroke severity, patient outcomes, cost, and treatment patterns observed over the acute hospital stay and through the 12‐month follow‐up for subjects receiving endovascular therapy compared to intravenous tissue plasminogen activator alone in the IMS (Interventional Management of Stroke) III Trial.Methods and ResultsProspective data collected for a prespecified economic analysis of the trial were used. Data included hospital billing records for the initial stroke admission and subsequent detailed resource use after the acute hospitalization collected at 3, 6, 9, and 12 months. Cost of follow‐up care varied 6‐fold for patients in the lowest (0–1) and highest (20+) National Institutes of Health Stroke Scale category at 5 days, and by modified Rankin Scale at 3 months. The kind of resources used postdischarge also varied between treatment groups. Incremental short‐term cost‐effectiveness ratios varied greatly when treatments were compared for patient subgroups. Patient subgroups predefined by stroke severity had incremental cost‐effectiveness ratios of $97 303/quality‐adjusted life year (severe stroke) and $3 187 805/quality‐adjusted life year (moderately severe stroke).ConclusionsDetailed economic and resource utilization data from IMS III provide powerful evidence for the large effect that patient outcome has on the economic value of medical and endovascular reperfusion therapies. These data can be used to inform process improvements for stroke care and to estimate the cost‐effectiveness of endovascular therapy in the US health system for stroke intervention trials.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Registration number: NCT00359424.]]></description>
<dc:creator><![CDATA[Simpson, K. N., Simpson, A. N., Mauldin, P. D., Palesch, Y. Y., Yeatts, S. D., Kleindorfer, D., Tomsick, T. A., Foster, L. D., Demchuk, A. M., Khatri, P., Hill, M. D., Jauch, E. C., Jovin, T. G., Yan, B., von Kummer, R., Molina, C. A., Goyal, M., Schonewille, W. J., Mazighi, M., Engelter, S. T., Anderson, C., Spilker, J., Carrozzella, J., Ryckborst, K. J., Janis, L. S., Broderick, J. P.,  the Interventional Management of Stroke (IMS) III Investigators]]></dc:creator>
<dc:date>2017-05-08T08:37:20-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004513</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004513</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cost-Effectiveness, Health Services, Cerebrovascular Procedures, Ischemic Stroke]]></dc:subject>
<dc:title><![CDATA[Observed Cost and Variations in Short Term Cost-Effectiveness of Therapy for Ischemic Stroke in Interventional Management of Stroke (IMS) III [Health Services and Outcomes Research]]]></dc:title>
<prism:publicationDate>2017-05-08</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Health Services and Outcomes Research</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004582.short?rss=1">
<title><![CDATA[Prognostic Value of Urinary Neutrophil Gelatinase-Associated Lipocalin on the First Day of Admission for Adverse Events in Patients With Acute Decompensated Heart Failure [Heart Failure]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004582.short?rss=1</link>
<description><![CDATA[BackgroundUrinary neutrophil gelatinase‐associated lipocalin (U‐NGAL) is an early predictor of acute kidney injury and adverse events in various diseases; however, in acute decompensated heart failure patients, its significance remains poorly understood. This study aimed to investigate the prognostic value of U‐NGAL on the first day of admission for the occurrence of acute kidney injury and long‐term outcomes in acute decompensated heart failure patients.Methods and ResultsWe studied 260 acute decompensated heart failure patients admitted to our department between 2011 and 2014 by measuring U‐NGAL in 24‐hour urine samples collected on the first day of admission. Primary end points were all‐cause death, cardiovascular death, and heart failure admission. Patients were divided into 2 groups according to their median U‐NGAL levels (32.5 μg/gCr). The high‐U‐NGAL group had a significantly higher occurrence of acute kidney injury during hospitalization than the low‐U‐NGAL group (P=0.0012). Kaplan‐Meier analysis revealed that the high‐U‐NGAL group exhibited a worse prognosis than the low‐U‐NGAL group in all‐cause death (hazard ratio 2.07; 95%CI 1.38‐3.12, P=0.0004), cardiovascular death (hazard ratio 2.29; 95%CI 1.28‐4.24, P=0.0052), and heart failure admission (hazard ratio 1.77; 95%CI 1.13‐2.77, P=0.0119). The addition of U‐NGAL to the estimated glomerular filtration rate significantly improved the predictive accuracy of all‐cause mortality (P=0.0083).ConclusionsIn acute decompensated heart failure patients, an elevated U‐NGAL level on the first day of admission was related to the development of clinical acute kidney injury and independently associated with poor prognosis.]]></description>
<dc:creator><![CDATA[Nakada, Y., Kawakami, R., Matsui, M., Ueda, T., Nakano, T., Takitsume, A., Nakagawa, H., Nishida, T., Onoue, K., Soeda, T., Okayama, S., Watanabe, M., Kawata, H., Okura, H., Saito, Y.]]></dc:creator>
<dc:date>2017-05-18T13:01:49-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004582</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004582</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Heart Failure]]></dc:subject>
<dc:title><![CDATA[Prognostic Value of Urinary Neutrophil Gelatinase-Associated Lipocalin on the First Day of Admission for Adverse Events in Patients With Acute Decompensated Heart Failure [Heart Failure]]]></dc:title>
<prism:publicationDate>2017-05-18</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Heart Failure</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004725.short?rss=1">
<title><![CDATA[Lifestyle and Risk of Screening-Detected Abdominal Aortic Aneurysm in Men [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004725.short?rss=1</link>
<description><![CDATA[BackgroundModifiable lifestyle‐related factors associated with risk of abdominal aortic aneurysm (AAA) are rarely investigated with a prospective design. We aimed to study possible associations among such factors and comorbidities with mean abdominal aortic diameter (AAD) and with risk of AAA among men screened for the disease.Methods and ResultsSelf‐reported lifestyle‐related exposures were assessed at baseline (January 1, 1998) among 14 249 men from the population‐based Cohort of Swedish Men, screened for AAA between 65 and 75 years of age (mean 13 years after baseline). Multivariable prediction of mean AAD was estimated with linear regression, and hazard ratios (HRs) of AAA (AAD ≥30 mm) with Cox proportional hazard regression. The AAA prevalence was 1.2% (n=168). Smoking, body mass index, and cardiovascular disease were associated with a larger mean AAD, whereas consumption of alcohol and diabetes mellitus were associated with a smaller mean AAD. The HR of AAA was increased among participants who were current smokers with ≥25 pack‐years smoked compared with never smokers (HR 15.59, 95% CI 8.96–27.15), those with a body mass index ≥25 versus <25 (HR 1.89, 95% CI, 1.22–2.93), and those with cardiovascular disease (HR 1.77, 95% CI, 1.13–2.77), and hypercholesterolemia (HR 1.59, 95% CI 1.08–2.34). Walking or bicycling for >40 minutes/day (versus almost never) was associated with lower AAA hazard (HR 0.59, 95% CI 0.36–0.97) compared with almost never walking or bicycling.ConclusionsThis prospective study confirms that modifiable lifestyle‐related factors are associated with AAD and with AAA disease.]]></description>
<dc:creator><![CDATA[Stackelberg, O., Wolk, A., Eliasson, K., Hellberg, A., Bersztel, A., Larsson, S. C., Orsini, N., Wanhainen, A., B&#x0237;orck, M.]]></dc:creator>
<dc:date>2017-05-10T10:24:11-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004725</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004725</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Exercise, Lifestyle, Obesity, Risk Factors]]></dc:subject>
<dc:title><![CDATA[Lifestyle and Risk of Screening-Detected Abdominal Aortic Aneurysm in Men [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-10</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004809.short?rss=1">
<title><![CDATA[Hepatic Fibrosis Is Universal Following Fontan Operation, and Severity is Associated With Time From Surgery: A Liver Biopsy and Hemodynamic Study [Congenital Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004809.short?rss=1</link>
<description><![CDATA[BackgroundCongestive hepatopathy is a recognized complication of Fontan physiology. Data regarding the incidence of hepatopathy and risk factors are lacking.Methods and ResultsLiver biopsies and cardiac catherizations were performed as part of an evaluation offered to all patients ≥10 years after Fontan. Quantitative determination of hepatic fibrosis was performed using Sirius red staining with automated calculation of collagen deposition per slide (%CD). Biopsies from included subjects were compared to stained specimens from controls without known fibrotic liver disease. Patient characteristics, echocardiographic findings, and hemodynamic measures were evaluated as potential risk factors. The cohort consisted of 67 patients (31 female) at mean age of 17.3±4.5 years and mean time from Fontan of 14.9±4.5 years. Right ventricular morphology was present in 37 subjects. Median %CD by Sirius red staining was 21.6% (range 8.7% to 49.4%) compared to 2.6% (range 2.2% to 3.0%) in controls. There was a significant correlation between time from Fontan and degree of Sirius red staining (r=0.33, P<0.01). Serum liver enzymes and platelet count did not correlate with %CD. The median inferior vena cava pressure was 13 mm Hg (range 6‐24 mm Hg) and did not correlate with %CD. There was no difference in %CD based on ventricular morphology or severity of atrioventricular valve insufficiency.ConclusionsIn this cohort of predominantly asymptomatic children and adolescents electively evaluated after a Fontan operation, all exhibited evidence for hepatic fibrosis as measured by collagen deposition in the liver. Time from Fontan was the only factor significantly associated with collagen deposition. These findings demonstrate that liver fibrosis is an inherent feature of Fontan physiology and that the degree of fibrosis increases over time.]]></description>
<dc:creator><![CDATA[Goldberg, D. J., Surrey, L. F., Glatz, A. C., Dodds, K., O'Byrne, M. L., Lin, H. C., Fogel, M., Rome, J. J., Rand, E. B., Russo, P., Rychik, J.]]></dc:creator>
<dc:date>2017-04-26T08:31:42-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004809</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004809</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Fibrosis, Congenital Heart Disease, Heart Failure]]></dc:subject>
<dc:title><![CDATA[Hepatic Fibrosis Is Universal Following Fontan Operation, and Severity is Associated With Time From Surgery: A Liver Biopsy and Hemodynamic Study [Congenital Heart Disease]]]></dc:title>
<prism:publicationDate>2017-04-26</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Congenital Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004834.short?rss=1">
<title><![CDATA[Post-Myocardial Infarction T-tubules Form Enlarged Branched Structures With Dysregulation of Junctophilin-2 and Bridging Integrator 1 (BIN-1) [Heart Failure]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004834.short?rss=1</link>
<description><![CDATA[BackgroundHeart failure is a common secondary complication following a myocardial infarction (MI), characterized by impaired cardiac contraction and t‐tubule (t‐t) loss. However, post‐MI nano‐scale morphological changes to the remaining t‐ts are poorly understood.Method and ResultsWe utilized a porcine model of MI, using a nonlethal microembolization method to generate controlled microinfarcts. Using serial block face scanning electron microscopy, we report that post‐MI, after mild left‐ventricular dysfunction has developed, t‐ts are not only lost in the peri‐infarct region, but also the remnant t‐ts form enlarged, highly branched disordered structures, containing a dense intricate inner membrane. Biochemical and proteomics analyses showed that the calcium release channel, ryanodine receptor 2 (RyR2), abundance is unchanged, but junctophilin‐2 (JP2), important for maintaining t‐t trajectory, is depressed (−0.5×) in keeping with the t‐ts being disorganized. However, immunolabeling shows that populations of RyR2 and JP2 remain associated with the remodeled t‐ts. The bridging integrator 1 protein (BIN‐1), a regulator of tubulogensis, is upregulated (+5.4×), consistent with an overdeveloped internal membrane system, a feature not present in control t‐ts. Importantly, we have determined that t‐ts, in the remote region, are narrowed and also contain dense membrane folds (BIN‐1 is up‐regulated +3.4×), whereas the t‐ts have a radial organization comparable to control JP2 is upregulated +1.7×.ConclusionsThis study reveals previously unidentified remodeling of the t‐t nano‐architecture in the post‐MI heart that extends to the remote region. Our findings highlight that targeting JP2 may be beneficial for preserving the orientation of the t‐ts, attenuating the development of hypocontractility post‐MI.]]></description>
<dc:creator><![CDATA[Pinali, C., Malik, N., Davenport, J. B., Allan, L. J., Murfitt, L., Iqbal, M. M., Boyett, M. R., Wright, E. J., Walker, R., Zhang, Y., Dobryznski, H., Holt, C. M., Kitmitto, A.]]></dc:creator>
<dc:date>2017-05-04T09:02:02-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004834</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004834</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cell Biology/Structural Biology, Heart Failure, Myocardial Infarction, Remodeling]]></dc:subject>
<dc:title><![CDATA[Post-Myocardial Infarction T-tubules Form Enlarged Branched Structures With Dysregulation of Junctophilin-2 and Bridging Integrator 1 (BIN-1) [Heart Failure]]]></dc:title>
<prism:publicationDate>2017-05-04</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Heart Failure</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004841.short?rss=1">
<title><![CDATA[Effects of the Mean Amplitude of Glycemic Excursions and Vascular Endothelial Dysfunction on Cardiovascular Events in Nondiabetic Patients With Coronary Artery Disease [Preventive Cardiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004841.short?rss=1</link>
<description><![CDATA[BackgroundMean amplitude of glycemic excursion (MAGE) is commonly used to gauge the degree of glucose level fluctuations. MAGE plays a significant role in vascular endothelial dysfunction and cardiovascular events in patients with diabetes mellitus (DM), but its significance is not clear in non‐DM patients. Thus, we examined the impact of MAGE and vascular endothelial dysfunction on clinical outcomes in non‐DM patients with coronary artery disease.Methods and ResultsWe followed non‐DM patients (n=65) for 12 months who underwent percutaneous coronary intervention and assessed the relationship among MAGE, reactive hyperemia index (RHI) measured by reactive hyperemia peripheral arterial tonometry as endothelial function, and cardiovascular events. Cardiovascular events analyzed were cardiovascular death, myocardial infarction, unstable angina, and revascularizations. Compared with patients with MAGE <65 mg/dL (normal glycemic excursions), the group with MAGE ≥65 mg/dL (high glycemic excursions) had significantly higher high‐sensitivity C‐reactive protein (0.10±0.11 mg/dL versus 0.18±0.13 mg/dL, P=0.006) and lower RHI (0.64±0.21 versus 0.51±0.22, P=0.035). The multivariable analysis identified high MAGE and low RHI (≤0.56) as risk factors associated with cardiovascular events (hazard ratio, 5.6; 95% RI, 1.72–18.4 [P=0.004] versus hazard ratio, 4.5; 95% RI, 1.37–14.9 [P=0.013]). When the prognosis was classified by combination with MAGE and RHI, the incidence of cardiovascular events was 46.7% (high MAGE+low RHI), 26.7% (high MAGE+high RHI), 20.0% (low MAGE+low RHI), and 6.6% (low MAGE+high RHI) in descending order (P=0.014). Receiver operating characteristic curve analysis revealed that MAGE, RHI, and MAGE+RHI were each associated with cardiovascular events (area under the curve 0.780, 0.727, and 0.796, respectively).ConclusionsMAGE was associated with cardiovascular events in non‐DM patients with coronary artery disease. Furthermore, the combination with MAGE and RHI was useful for further subdivision of the risk of cardiovascular events.]]></description>
<dc:creator><![CDATA[Akasaka, T., Sueta, D., Tabata, N., Takashio, S., Yamamoto, E., Izumiya, Y., Tsujita, K., Kojima, S., Kaikita, K., Matsui, K., Hokimoto, S.]]></dc:creator>
<dc:date>2017-04-26T10:10:01-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004841</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004841</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Quality and Outcomes]]></dc:subject>
<dc:title><![CDATA[Effects of the Mean Amplitude of Glycemic Excursions and Vascular Endothelial Dysfunction on Cardiovascular Events in Nondiabetic Patients With Coronary Artery Disease [Preventive Cardiology]]]></dc:title>
<prism:publicationDate>2017-04-26</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Preventive Cardiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004880.short?rss=1">
<title><![CDATA[Normalization of Testosterone Levels After Testosterone Replacement Therapy Is Associated With Decreased Incidence of Atrial Fibrillation [Arrhythmia and Electrophysiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004880.short?rss=1</link>
<description><![CDATA[BackgroundAtrial fibrillation (AF) is the most common cardiac dysrhythmia associated with significant morbidity and mortality. Several small studies have reported that low serum total testosterone (TT) levels were associated with a higher incidence of AF. In contrast, it is also reported that anabolic steroid use is associated with an increase in the risk of AF. To date, no study has explored the effect of testosterone normalization on new incidence of AF after testosterone replacement therapy (TRT) in patients with low testosterone.Methods and ResultsUsing data from the Veterans Administrations Corporate Data Warehouse, we identified a national cohort of 76 639 veterans with low TT levels and divided them into 3 groups. Group 1 had TRT resulting in normalization of TT levels (normalized TRT), group 2 had TRT without normalization of TT levels (nonnormalized TRT), and group 3 did not receive TRT (no TRT). Propensity score–weighted stabilized inverse probability of treatment weighting Cox proportional hazard methods were used for analysis of the data from these groups to determine the association between post‐TRT levels of TT and the incidence of AF. Group 1 (40 856 patients, median age 66 years) had significantly lower risk of AF than group 2 (23 939 patients, median age 65 years; hazard ratio 0.90, 95% CI 0.81–0.99, P=0.0255) and group 3 (11 853 patients, median age 67 years; hazard ratio 0.79, 95% CI 0.70–0.89, P=0.0001). There was no statistical difference between groups 2 and 3 (hazard ratio 0.89, 95% CI 0.78– 1.0009, P=0.0675) in incidence of AF.ConclusionsThese novel results suggest that normalization of TT levels after TRT is associated with a significant decrease in the incidence of AF.]]></description>
<dc:creator><![CDATA[Sharma, R., Oni, O. A., Gupta, K., Sharma, M., , Singh, V., Parashara, D., Kamalakar, S., Dawn, B., Chen, G., Ambrose, J. A., Barua, R. S.]]></dc:creator>
<dc:date>2017-05-09T09:29:16-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004880</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004880</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Arrhythmias]]></dc:subject>
<dc:title><![CDATA[Normalization of Testosterone Levels After Testosterone Replacement Therapy Is Associated With Decreased Incidence of Atrial Fibrillation [Arrhythmia and Electrophysiology]]]></dc:title>
<prism:publicationDate>2017-05-09</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Arrhythmia and Electrophysiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004892.short?rss=1">
<title><![CDATA[Patients With Heart Failure Readmitted to the Original Hospital Have Better Outcomes Than Those Readmitted Elsewhere [Health Services and Outcomes Research]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004892.short?rss=1</link>
<description><![CDATA[BackgroundUp to one fifth of readmissions after a heart failure hospitalization occur at a different hospital. This negatively impacts information continuity, but whether site of readmission impacts subsequent outcomes is unclear.Methods and ResultsRetrospective cohort study of all patients discharged with a primary diagnosis of heart failure in Canada between April 2004 and December 2013. We compared patients readmitted within 30 days to the original hospital versus a different hospital. Of the 217 039 heart failure patients (mean age, 76.8 years, 50.1% male), 39 368 (18.1%) were readmitted within 30 days—32 771 (83.2%) to the original hospital and 6597 (16.8%) to a different hospital (increasing over time from 15.6% in 2004 to 18.5% by 2013; P for trend=0.001). Patients readmitted to different hospitals were younger and were more likely to be male, have a rural residence, a more‐recent discharge year, an index hospitalization at a teaching hospital, and to be brought in by ambulance at the time of the readmission. Readmissions to the original hospital were substantially shorter (mean, 10.4 days [95% CI, 10.3–10.6] versus 11.6 days [95% CI, 11.3–12.0]; adjusted means, 11.0 versus 12.0; P<0.0001) and had lower mortality (14.4% versus 15.0%; adjusted odds ratio, 0.89; 95% CI, 0.82–0.96) than readmissions to different hospitals.ConclusionsReadmissions to a different hospital are becoming more frequent over time and are associated with longer stays and higher mortality rates than readmissions to the original hospital. Our findings provide further evidence that care fragmentation may be deleterious for patients with heart failure.]]></description>
<dc:creator><![CDATA[McAlister, F. A., Youngson, E., Kaul, P.]]></dc:creator>
<dc:date>2017-05-10T12:40:37-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004892</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004892</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Heart Failure, Health Services]]></dc:subject>
<dc:title><![CDATA[Patients With Heart Failure Readmitted to the Original Hospital Have Better Outcomes Than Those Readmitted Elsewhere [Health Services and Outcomes Research]]]></dc:title>
<prism:publicationDate>2017-05-10</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Health Services and Outcomes Research</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004896.short?rss=1">
<title><![CDATA[Prognostic Value of Dehydroepiandrosterone Sulfate for Patients With Cardiovascular Disease: A Systematic Review and Meta&ndash;Analysis [Systematic Review and Meta-Analysis]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004896.short?rss=1</link>
<description><![CDATA[BackgroundThe aim of the present study was to estimate the impact of dehydroepiandrosterone sulfate (DHEAS) on the prognosis of patients with cardiovascular disease by performing a systematic review and meta‐analysis.Methods and ResultsThe Embase, PubMed, Web of Science, CNKI, and WanFang databases were searched up to September 5, 2016, to identify eligible studies. The quality of each study was assessed using the Newcastle‐Ottawa Scale. The association between DHEAS, either on admission or at discharge, and cardiovascular disease outcomes were reviewed. The overall risk ratio for the effect of DHEAS on all‐cause mortality and fatal and nonfatal cardiovascular events was pooled using a fixed‐effects or a random‐effects model. The publication bias was evaluated using funnel plots. Twenty‐five studies were included for systematic review. The follow‐up duration ranged from 1 to 19 years. Eighteen studies were included in the meta‐analysis. We found that lower DHEAS levels indicated a significant increased risk for all‐cause mortality (risk ratio, 1.47; 95% CI, 1.38–1.56 [P<0.00001]), fatal cardiovascular event (risk ratio, 1.58; 95% CI, 1.30–1.91 [P<0.00001]), and nonfatal cardiovascular event (risk ratio, 1.42; 95% CI, 1.24–1.62 [P<0.0001]) in patients with cardiovascular disease.ConclusionsPatients with cardiovascular disease who have lower DHEAS levels may have poorer prognosis than those with higher DHEAS levels.]]></description>
<dc:creator><![CDATA[Wu, T.-T., Chen, Y., Zhou, Y., Adi, D., Zheng, Y.-Y., Liu, F., Ma, Y.-T., Xie, X.]]></dc:creator>
<dc:date>2017-05-05T08:41:50-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004896</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004896</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiovascular Disease, Meta Analysis, Mortality/Survival]]></dc:subject>
<dc:title><![CDATA[Prognostic Value of Dehydroepiandrosterone Sulfate for Patients With Cardiovascular Disease: A Systematic Review and Meta&ndash;Analysis [Systematic Review and Meta-Analysis]]]></dc:title>
<prism:publicationDate>2017-05-05</prism:publicationDate>
<prism:section>Systematic Review and Meta&#x2010;Analysis</prism:section>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004966.short?rss=1">
<title><![CDATA[Comparison of Expert Adjudicated Coronary Heart Disease and Cardiovascular Disease Mortality With the National Death Index: Results From the REasons for Geographic And Racial Differences in Stroke (REGARDS) Study [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004966.short?rss=1</link>
<description><![CDATA[BackgroundThe National Death Index (NDI) is widely used to detect coronary heart disease (CHD) and cardiovascular disease (CVD) deaths, but its reliability has not been examined recently.Methods and ResultsWe compared CHD and CVD deaths detected by NDI with expert adjudication of 4010 deaths that occurred between 2003 and 2013 among participants in the REGARDS (REasons for Geographic And Racial Differences in Stroke) cohort of black and white adults in the United States. NDI derived CHD mortality had sensitivity 53.6%, specificity 90.3%, positive predictive value 54.2%, and negative predictive value 90.1%. NDI‐derived CVD mortality had sensitivity 73.4%, specificity 84.5%, positive predictive value 70.6%, and negative predictive value 86.2%. Among NDI‐derived CHD and CVD deaths, older age (odds ratios, 1.06 and 1.04 per 1‐year increase) was associated with a higher probability of disagreement with the adjudicated cause of death, whereas among REGARDS adjudicated CHD and CVD deaths a history of CHD or CVD was associated with a lower probability of disagreement with the NDI‐derived causes of death (odds ratios, 0.59 and 0.67, respectively).ConclusionsThe modest accuracy and differential performance of NDI‐derived cause of death may impact CHD and CVD mortality statistics.]]></description>
<dc:creator><![CDATA[Olubowale, O. T., Safford, M. M., Brown, T. M., Durant, R. W., Howard, V. J., Gamboa, C., Glasser, S. P., Rhodes, J. D., Levitan, E. B.]]></dc:creator>
<dc:date>2017-05-03T12:50:20-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004966</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004966</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiovascular Disease, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Comparison of Expert Adjudicated Coronary Heart Disease and Cardiovascular Disease Mortality With the National Death Index: Results From the REasons for Geographic And Racial Differences in Stroke (REGARDS) Study [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-03</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004971.short?rss=1">
<title><![CDATA[Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel [Hypertension]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004971.short?rss=1</link>
<description><![CDATA[BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms.Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats.ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity.]]></description>
<dc:creator><![CDATA[Yu, W., Liao, Y., Huang, Y., Chen, S. Y., Sun, Y., Sun, C., Wu, Y., Tang, C., Du, J., Jin, H.]]></dc:creator>
<dc:date>2017-05-16T13:44:22-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004971</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004971</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Vascular Biology, High Blood Pressure, Hypertension]]></dc:subject>
<dc:title><![CDATA[Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel [Hypertension]]]></dc:title>
<prism:publicationDate>2017-05-16</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Hypertension</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e004987.short?rss=1">
<title><![CDATA[Changes in Cardiovascular Disease Risk Factors With Immediate Versus Deferred Antiretroviral Therapy Initiation Among HIV-Positive Participants in the START (Strategic Timing of Antiretroviral Treatment) Trial [Preventive Cardiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e004987.short?rss=1</link>
<description><![CDATA[IntroductionHIV infection and certain antiretroviral therapy (ART) medications increase atherosclerotic cardiovascular disease risk, mediated, in part, through traditional cardiovascular disease risk factors.Methods and ResultsWe studied cardiovascular disease risk factor changes in the START (Strategic Timing of Antiretroviral Treatment) trial, a randomized study of immediate versus deferred ART initiation among HIV‐positive persons with CD4+ cell counts >500 cells/mm3. Mean change from baseline in risk factors and the incidence of comorbid conditions were compared between groups. The characteristics among 4685 HIV‐positive START trial participants include a median age of 36 years, a CD4 cell count of 651 cells/mm3, an HIV viral load of 12 759 copies/mL, a current smoking status of 32%, a median systolic/diastolic blood pressure of 120/76 mm Hg, and median levels of total cholesterol of 168 mg/dL, low‐density lipoprotein cholesterol of 102 mg/dL, and high‐density lipoprotein cholesterol of 41 mg/dL. Mean follow‐up was 3.0 years. The immediate and deferred ART groups spent 94% and 28% of follow‐up time taking ART, respectively. Compared with patients in the deferral group, patients in the immediate ART group had increased total cholesterol and low‐density lipoprotein cholesterol and higher use of lipid‐lowering therapy (1.2%; 95% CI, 0.1–2.2). Concurrent increases in high‐density lipoprotein cholesterol with immediate ART resulted in a 0.1 lower total cholesterol to high‐density lipoprotein cholesterol ratio (95% CI, 0.1–0.2). Immediate ART resulted in 2.3% less BP‐lowering therapy use (95% CI, 0.9–3.6), but there were no differences in new‐onset hypertension or diabetes mellitus.ConclusionsAmong HIV‐positive persons with preserved immunity, immediate ART led to increases in total cholesterol and low‐density lipoprotein cholesterol but also concurrent increases in high‐density lipoprotein cholesterol and decreased use of blood pressure medications. These opposing effects suggest that, in the short term, the net effect of early ART on traditional cardiovascular disease risk factors may be clinically insignificant."Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT00867048.]]></description>
<dc:creator><![CDATA[Baker, J. V., Sharma, S., Achhra, A. C., Bernardino, J. I., Bogner, J. R., Duprez, D., Emery, S., Gazzard, B., Gordin, J., Grandits, G., Phillips, A. N., Schwarze, S., Soliman, E. Z., Spector, S. A., Tambussi, G., Lundgren, J.,  the INSIGHT (International Network for Strategic Initiatives in Global HIV Trials) START (Strategic Timing of Antiretroviral Treatment) Study Group]]></dc:creator>
<dc:date>2017-05-22T06:38:07-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.004987</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.004987</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Lipids and Cholesterol, Cardiovascular Disease, Risk Factors]]></dc:subject>
<dc:title><![CDATA[Changes in Cardiovascular Disease Risk Factors With Immediate Versus Deferred Antiretroviral Therapy Initiation Among HIV-Positive Participants in the START (Strategic Timing of Antiretroviral Treatment) Trial [Preventive Cardiology]]]></dc:title>
<prism:publicationDate>2017-05-22</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Preventive Cardiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005027.short?rss=1">
<title><![CDATA[Ranolazine in Symptomatic Diabetic Patients Without Obstructive Coronary Artery Disease: Impact on Microvascular and Diastolic Function [Imaging]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005027.short?rss=1</link>
<description><![CDATA[BackgroundTreatments for patients with myocardial ischemia in the absence of angiographic obstructive coronary artery disease are limited. In these patients, particularly those with diabetes mellitus, diffuse coronary atherosclerosis and microvascular dysfunction is a common phenotype and may be accompanied by diastolic dysfunction. Our primary aim was to determine whether ranolazine would quantitatively improve exercise‐stimulated myocardial blood flow and cardiac function in symptomatic diabetic patients without obstructive coronary artery disease.Methods and ResultsWe conducted a double‐blinded crossover trial with 1:1 random allocation to the order of ranolazine and placebo. At baseline and after each 4‐week treatment arm, left ventricular myocardial blood flow and coronary flow reserve (CFR; primary end point) were measured at rest and after supine bicycle exercise using 13N‐ammonia myocardial perfusion positron emission tomography. Resting echocardiography was also performed. Multilevel mixed‐effects linear regression was used to determine treatment effects. Thirty‐five patients met criteria for inclusion. Ranolazine did not significantly alter rest or postexercise left ventricular myocardial blood flow or CFR. However, patients with lower baseline CFR were more likely to experience improvement in CFR with ranolazine (r=−0.401, P=0.02) than with placebo (r=−0.188, P=0.28). In addition, ranolazine was associated with an improvement in E/septal e′ (P=0.001) and E/lateral e′ (P=0.01).ConclusionsIn symptomatic diabetic patients without obstructive coronary artery disease, ranolazine did not change exercise‐stimulated myocardial blood flow or CFR but did modestly improve diastolic function. Patients with more severe baseline impairment in CFR may derive more benefit from ranolazine.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT01754259.]]></description>
<dc:creator><![CDATA[Shah, N. R., Cheezum, M. K., Veeranna, V., Horgan, S. J., Taqueti, V. R., Murthy, V. L., Foster, C., Hainer, J., Daniels, K. M., Rivero, J., Shah, A. M., Stone, P. H., Morrow, D. A., Steigner, M. L., Dorbala, S., Blankstein, R., Di Carli, M. F.]]></dc:creator>
<dc:date>2017-05-04T13:09:12-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005027</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005027</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Coronary Circulation, Diabetes, Type 2, Nuclear Cardiology and PET]]></dc:subject>
<dc:title><![CDATA[Ranolazine in Symptomatic Diabetic Patients Without Obstructive Coronary Artery Disease: Impact on Microvascular and Diastolic Function [Imaging]]]></dc:title>
<prism:publicationDate>2017-05-04</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Imaging</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005031.short?rss=1">
<title><![CDATA[Survival in Women Versus Men Following Implantation of Pacemakers, Defibrillators, and Cardiac Resynchronization Therapy Devices in a Large, Nationwide Cohort [Arrhythmia and Electrophysiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005031.short?rss=1</link>
<description><![CDATA[BackgroundWhether outcomes differ between sexes following treatment with pacemakers (PM), implantable cardioverter defibrillators, and cardiac resynchronization therapy (CRT) devices is unclear.Methods and ResultsConsecutive US patients with newly implanted PM, implantable cardioverter defibrillators, and CRT devices from a large remote monitoring database between 2008 and 2011 were included in this observational cohort study. Sex‐specific all‐cause survival postimplant was compared within each device type using a multivariable Cox proportional hazards model, stratified on age and adjusted for remote monitoring utilization and ZIP‐based socioeconomic variables. A total of 269 471 patients were assessed over a median 2.9 [interquartile range, 2.2, 3.6] years. Unadjusted mortality rates (MR; deaths/100 000 patient‐years) were similar between women versus men receiving PMs (n=115 076, 55% male; MR 4193 versus MR 4256, respectively; adjusted hazard ratio, 0.87; 95% CI, 0.84–0.90; P<0.001) and implantable cardioverter defibrillators (n=85 014, 74% male; MR 4417 versus MR 4479, respectively; adjusted hazard ratio, 0.98; 95% CI, 0.93–1.02; P=0.244). In contrast, survival was superior in women receiving CRT defibrillators (n=61 475, 72% male; MR 5270 versus male MR 7175; adjusted hazard ratio, 0.73; 95% CI, 0.70–0.76; P<0.001) and also CRT pacemakers (n=7906, 57% male; MR 5383 versus male MR 7625, adjusted hazard ratio, 0.69; 95% CI, 0.61–0.78; P<0.001). This relative difference increased with time. These results were unaffected by age or remote monitoring utilization.ConclusionsWomen accounted for less than 30% of high‐voltage implants and fewer than half of low‐voltage implants in a large, nation‐wide cohort. Survival for women and men receiving implantable cardioverter defibrillators and PMs was similar, but dramatically greater for women receiving both defibrillator‐ and PM‐based CRT.]]></description>
<dc:creator><![CDATA[Varma, N., Mittal, S., Prillinger, J. B., Snell, J., Dalal, N., Piccini, J. P.]]></dc:creator>
<dc:date>2017-05-10T06:40:43-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005031</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005031</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Catheter Ablation and Implantable Cardioverter-Defibrillator, Electrophysiology, Heart Failure, Mortality/Survival]]></dc:subject>
<dc:title><![CDATA[Survival in Women Versus Men Following Implantation of Pacemakers, Defibrillators, and Cardiac Resynchronization Therapy Devices in a Large, Nationwide Cohort [Arrhythmia and Electrophysiology]]]></dc:title>
<prism:publicationDate>2017-05-10</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Arrhythmia and Electrophysiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005045.short?rss=1">
<title><![CDATA[American College of Cardiology/American Heart Association (ACC/AHA) Class I Guidelines for the Treatment of Cholesterol to Reduce Atherosclerotic Cardiovascular Risk: Implications for US Hispanics/Latinos Based on Findings From the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005045.short?rss=1</link>
<description><![CDATA[BackgroundThe prevalence estimates of statin eligibility among Hispanic/Latinos living in the United States under the new 2013 American College of Cardiology/American Heart Association (ACC/AHA) cholesterol treatment guidelines are not known.Methods and ResultsWe estimated prevalence of statin eligibility under 2013 ACC/AHA and 3rd National Cholesterol Education Program Adult Treatment Panel (NCEP/ATP III) guidelines among Hispanic Community Health Study/Study of Latinos (n=16 415; mean age 41 years, 40% males) by using sampling weights calibrated to the 2010 US census. We examined the characteristics of Hispanic/Latinos treated and not treated with statins under both guidelines. We also redetermined the statin‐therapy eligibility by using black risk estimates for Dominicans, Cubans, Puerto Ricans, and Central Americans. Compared with NCEP/ATP III guidelines, statin eligibility increased from 15.9% (95% CI 15.0–16.7%) to 26.9% (95% CI 25.7–28.0%) under the 2013 ACC/AHA guidelines. This was mainly driven by the ≥7.5% atherosclerotic cardiovascular disease risk criteria (prevalence 13.9% [95% CI 13.0–14.7%]). Of the participants eligible for statin eligibility under NCEP/ATP III and ACC/AHA guidelines, only 28.2% (95% CI 26.3–30.0%) and 20.6% (95% CI 19.4–21.9%) were taking statins, respectively. Statin‐eligible participants who were not taking statins had a higher prevalence of cardiovascular risk factors compared with statin‐eligible participants who were taking statins. There was no significant increase in statin eligibility when atherosclerotic cardiovascular disease risk was calculated by using black estimates instead of recommended white estimates (increase by 1.4%, P=0.12) for Hispanic/Latinos.ConclusionsThe eligibility of statin therapy increased consistently across all Hispanic/Latinos subgroups under the 2013 ACC/AHA guidelines and therefore will potentially increase the number of undertreated Hispanic/Latinos in the United States.]]></description>
<dc:creator><![CDATA[Qureshi, W. T., Kaplan, R. C., Swett, K., Burke, G., Daviglus, M., Jung, M., Talavera, G. A., Chirinos, D. A., Reina, S. A., Davis, S., Rodriguez, C. J.]]></dc:creator>
<dc:date>2017-05-11T07:58:37-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005045</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005045</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiovascular Disease, Epidemiology]]></dc:subject>
<dc:title><![CDATA[American College of Cardiology/American Heart Association (ACC/AHA) Class I Guidelines for the Treatment of Cholesterol to Reduce Atherosclerotic Cardiovascular Risk: Implications for US Hispanics/Latinos Based on Findings From the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-11</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005090.short?rss=1">
<title><![CDATA[Age-Specific Vascular Risk Factor Profiles According to Stroke Subtype [Stroke]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005090.short?rss=1</link>
<description><![CDATA[BackgroundIschemic and hemorrhagic stroke are increasingly recognized as heterogeneous diseases with distinct subtypes and etiologies. Information on variation in distribution of vascular risk factors according to age in stroke subtypes is limited. We investigated the prevalence of vascular risk factors in stroke subtypes in relation to age.Methods and ResultsWe studied a prospective multicenter university hospital–based cohort of 4033 patients. For patients with ischemic stroke caused by large artery atherosclerosis, small vessel disease, or cardioembolism and for patients with spontaneous intracerebral hemorrhage or aneurysmal subarachnoid hemorrhage, we calculated prevalences of vascular risk factors in 4 age groups: <55, 55 to 65, 65 to 75, and ≥75 years, and mean differences with 95% CIs in relation to the reference age group. Patients aged <55 years were significantly more often of non‐white origin (in particular in spontaneous intracerebral hemorrhage and aneurysmal subarachnoid hemorrhage patients) and most often smoked (most prominent for aneurysmal subarachnoid hemorrhage patients). Patients aged <55 years with ischemic stroke caused by large artery atherosclerosis or small vessel disease more often had hypertension, hyperlipidemia, and diabetes mellitus than patients with ischemic stroke of cardiac origin. Overall, the frequency of hypertension, hyperlipidemia, and diabetes mellitus increased with age among all stroke subtypes, whereas smoking decreased with age. Regardless of age, accumulation of potentially modifiable risk factors was most pronounced in patients with ischemic stroke caused by large artery atherosclerosis or small vessel disease.ConclusionsThe prevalence of common cardiovascular risk factors shows different age‐specific patterns among various stroke subtypes. Recognition of these patterns may guide tailored stroke prevention efforts aimed at specific risk groups.]]></description>
<dc:creator><![CDATA[Hauer, A. J., Ruigrok, Y. M., Algra, A., van Di&#x0237;k, E. J., Koudstaal, P. J., Lui&#x0237;ckx, G.&ndash;J., Nederkoorn, P. J., van Oostenbrugge, R. J., Visser, M. C., Wermer, M. J., Kappelle, L. J., Kli&#x0237;n, C. J. M.,  the Dutch Parelsnoer Institute-Cerebrovascular Accident Study Group]]></dc:creator>
<dc:date>2017-05-08T09:56:41-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005090</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005090</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Risk Factors, Intracranial Hemorrhage, Ischemic Stroke]]></dc:subject>
<dc:title><![CDATA[Age-Specific Vascular Risk Factor Profiles According to Stroke Subtype [Stroke]]]></dc:title>
<prism:publicationDate>2017-05-08</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Stroke</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005108.short?rss=1">
<title><![CDATA[New Role for Interleukin-13 Receptor {alpha}1 in Myocardial Homeostasis and Heart Failure [Heart Failure]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005108.short?rss=1</link>
<description><![CDATA[BackgroundThe immune system plays a pivotal role in myocardial homeostasis and response to injury. Interleukins‐4 and ‐13 are anti‐inflammatory type‐2 cytokines, signaling via the common interleukin‐13 receptor α1 chain and the type‐2 interleukin‐4 receptor. The role of interleukin‐13 receptor α1 in the heart is unknown.Methods and ResultsWe analyzed myocardial samples from human donors (n=136) and patients with end‐stage heart failure (n=177). We found that the interleukin‐13 receptor α1 is present in the myocardium and, together with the complementary type‐2 interleukin‐4 receptor chain Il4ra, is significantly downregulated in the hearts of patients with heart failure. Next, we showed that Il13ra1‐deficient mice develop severe myocardial dysfunction and dyssynchrony compared to wild‐type mice (left ventricular ejection fraction 29.7±9.9 versus 45.0±8.0; P=0.004, left ventricular end‐diastolic diameter 4.2±0.2 versus 3.92±0.3; P=0.03). A bioinformatic analysis of mouse hearts indicated that interleukin‐13 receptor α1 regulates critical pathways in the heart other than the immune system, such as extracellular matrix (normalized enrichment score=1.90; false discovery rate q=0.005) and glucose metabolism (normalized enrichment score=−2.36; false discovery rate q=0). Deficiency of Il13ra1 was associated with reduced collagen deposition under normal and pressure‐overload conditions.ConclusionsThe results of our studies in humans and mice indicate, for the first time, a role of interleukin‐13 receptor α1 in myocardial homeostasis and heart failure and suggests a new therapeutic target to treat heart disease.]]></description>
<dc:creator><![CDATA[Amit, U., Kain, D., Wagner, A., Sahu, A., Nevo-Caspi, Y., Gonen, N., Molotski, N., Konfino, T., Landa, N., Naftali-Shani, N., Blum, G., Merquiol, E., Karo-Atar, D., Kanfi, Y., Paret, G., Munitz, A., Cohen, H. Y., Ruppin, E., Hannenhalli, S., Leor, J.]]></dc:creator>
<dc:date>2017-05-20T13:51:11-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005108</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005108</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Growth Factors/Cytokines]]></dc:subject>
<dc:title><![CDATA[New Role for Interleukin-13 Receptor {alpha}1 in Myocardial Homeostasis and Heart Failure [Heart Failure]]]></dc:title>
<prism:publicationDate>2017-05-20</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Heart Failure</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005110.short?rss=1">
<title><![CDATA[Associations of Acid Suppressive Therapy With Cardiac Mortality in Heart Failure Patients [Heart Failure]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005110.short?rss=1</link>
<description><![CDATA[BackgroundIt has been recently reported that histamine H2 receptor antagonists (H2RAs) are associated with impairment of ventricular remodeling and incident heart failure. In addition, favorable pleiotropic effects and adverse effects of proton pump inhibitors (PPIs) on cardiovascular disease have also been reported. We examined the associations of acid suppressive therapy using H2RAs or PPIs with cardiac mortality in patients with heart failure.Methods and ResultsIn total, 1191 consecutive heart failure patients were divided into 3 groups: a non–acid suppressive therapy group (n=363), an H2RA group (n=164), and a PPI group (n=664). In the follow‐up period (mean 995 days), 169 cardiac deaths occurred. In the Kaplan–Meier analysis, cardiac mortality was significantly lower in the PPI group than in the H2RA and non–acid suppressive therapy groups (11.0% versus 21.3% and 16.8%, respectively; log‐rank P=0.004). In the multivariable Cox proportional hazards analysis, use of PPIs, but not H2RAs, was found to be an independent predictor of cardiac mortality (PPIs: hazard ratio 0.488, P=0.002; H2RAs: hazard ratio 0.855, P=0.579). The propensity‐matched 1:1 cohort was assessed based on propensity score (H2RAs, n=164; PPIs, n=164). Cardiac mortality was significantly lower in the PPI group than in the H2RA group in the postmatched cohort (log‐rank P=0.025). In the Cox proportional hazards analysis, the use of PPIs was a predictor of cardiac mortality in the postmatched cohort (hazard ratio 0.528, P=0.028).ConclusionsPPIs may be associated with better outcome in patients with heart failure.]]></description>
<dc:creator><![CDATA[Yoshihisa, A., Takiguchi, M., Kanno, Y., Sato, A., Yokokawa, T., Miura, S., Abe, S., Misaka, T., Sato, T., Suzuki, S., Oikawa, M., Kobayashi, A., Yamaki, T., Kunii, H., Nakazato, K., Suzuki, H., Saitoh, S.-i., Takeishi, Y.]]></dc:creator>
<dc:date>2017-05-16T11:33:44-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005110</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005110</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Heart Failure]]></dc:subject>
<dc:title><![CDATA[Associations of Acid Suppressive Therapy With Cardiac Mortality in Heart Failure Patients [Heart Failure]]]></dc:title>
<prism:publicationDate>2017-05-16</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Heart Failure</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005126.short?rss=1">
<title><![CDATA[Gastric Bypass Surgery Produces a Durable Reduction in Cardiovascular Disease Risk Factors and Reduces the Long-Term Risks of Congestive Heart Failure [Preventive Cardiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005126.short?rss=1</link>
<description><![CDATA[BackgroundObesity and its association with reduced life expectancy are well established, with cardiovascular disease as one of the major causes of fatality. Metabolic surgery is a powerful intervention for severe obesity, resulting in improvement in comorbid diseases and in cardiovascular risk factors. This study investigates the relationship between metabolic surgery and long‐term cardiovascular events.Methods and ResultsA cohort of Roux‐en‐Y gastric bypass surgery (RYGB) patients was tightly matched by age, body mass index, sex, Framingham Risk Score, smoking history, use of antihypertension medication, diabetes mellitus status, and calendar year with a concurrent cohort of nonoperated control patients. The primary study end points of major cardiovascular events (myocardial infarction, stroke, and congestive heart failure) were evaluated using Cox regression. Secondary end points of longitudinal cardiovascular risk factors were evaluated using repeated‐measures regression. The RYGB and matched controls (N=1724 in each cohort) were followed for up to 12 years after surgery (overall median of 6.3 years). Kaplan–Meier analysis revealed a statistically significant reduction in incident major composite cardiovascular events (P=0.017) and congestive heart failure (0.0077) for the RYGB cohort. Adjusted Cox regression models confirmed the reductions in severe composite cardiovascular events in the RYGB cohort (hazard ratio=0.58, 95% CI=0.42–0.82). Improvements of cardiovascular risk factors (eg, 10‐year cardiovascular risk score, total cholesterol, high‐density lipoprotein, systolic blood pressure, and diabetes mellitus) were observed within the RYGB cohort after surgery.ConclusionsGastric bypass is associated with a reduced risk of major cardiovascular events and the development of congestive heart failure.]]></description>
<dc:creator><![CDATA[Benotti, P. N., Wood, G. C., Carey, D. J., Mehra, V. C., Mirshahi, T., Lent, M. R., Petrick, A. T., Still, C., Gerhard, G. S., Hirsch, A. G.]]></dc:creator>
<dc:date>2017-05-23T05:43:30-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005126</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005126</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiomyopathy, Heart Failure, Metabolic Syndrome, Remodeling, Cerebrovascular Disease/Stroke]]></dc:subject>
<dc:title><![CDATA[Gastric Bypass Surgery Produces a Durable Reduction in Cardiovascular Disease Risk Factors and Reduces the Long-Term Risks of Congestive Heart Failure [Preventive Cardiology]]]></dc:title>
<prism:publicationDate>2017-05-23</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Preventive Cardiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005133.short?rss=1">
<title><![CDATA[Traditional Cardiovascular Risk Factors and Their Relation to Future Surgery for Valvular Heart Disease or Ascending Aortic Disease: A Case-Referent Study [Valvular Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005133.short?rss=1</link>
<description><![CDATA[BackgroundRisk factors for developing heart valve and ascending aortic disease are based mainly on retrospective data. To elucidate these factors in a prospective manner, we have performed a nested case–referent study using data from large, population‐based surveys.Methods and ResultsA total of 777 patients operated for heart valve disease or disease of the ascending aorta had previously participated in population‐based health surveys in Northern Sweden. Median time (interquartile range) from survey to surgery was 10.5 (9.0) years. Primary indications for surgery were aortic stenosis (41%), aortic regurgitation (12%), mitral regurgitation (23%), and dilatation/dissection of the ascending aorta (17%). For each case, referents were allocated, matched for age, sex, and geographical area. In multivariable models, surgery for aortic stenosis was predicted by hypertension, high cholesterol levels, diabetes mellitus, and active smoking. Surgery for aortic regurgitation was associated with a low cholesterol level, whereas a high cholesterol level predicted surgery for mitral regurgitation. Hypertension, blood pressure, and previous smoking predicted surgery for disease of the ascending aorta whereas diabetes mellitus was associated with reduced risk. After exclusion of cases with coronary atherosclerosis, only the inverse associations between cholesterol and aortic regurgitation and between diabetes mellitus and disease of the ascending aorta remained.ConclusionsThis is the first truly prospective study of traditional cardiovascular risk factors and their association with valvular heart disease and disease of the ascending aorta. We confirm the strong association between traditional risk factors and aortic stenosis, but only in patients with concomitant coronary artery disease. In isolated valvular heart disease, the impact of traditional risk factors is varying.]]></description>
<dc:creator><![CDATA[L&#x0237;ungberg, J., Johansson, B., Engstrom, K. G., Albertsson, E., Holmer, P., Norberg, M., Bergdahl, I. A., Soderberg, S.]]></dc:creator>
<dc:date>2017-05-05T07:52:07-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005133</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005133</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Risk Factors, Valvular Heart Disease]]></dc:subject>
<dc:title><![CDATA[Traditional Cardiovascular Risk Factors and Their Relation to Future Surgery for Valvular Heart Disease or Ascending Aortic Disease: A Case-Referent Study [Valvular Heart Disease]]]></dc:title>
<prism:publicationDate>2017-05-05</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Valvular Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005155.short?rss=1">
<title><![CDATA[Temporal Trends in Incidence, Prevalence, and Mortality of Atrial Fibrillation in Primary Care [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005155.short?rss=1</link>
<description><![CDATA[BackgroundIncidence and prevalence of atrial fibrillation (AF) are expected to increase dramatically; however, we currently lack comprehensive data on temporal trends in unselected clinical populations.Methods and ResultsAnalysis of the UK Clinical Practice Research Datalink (CPRD) from 1998 to 2010 of patients with incident AF, excluding major valvular disease, linked to hospital admission data and national statistics. Fifty‐seven thousand eight hundred eighteen adults were identified with mean age 74.2 (SD, 11.7) years and 48.3% women. Overall age‐adjusted incidence of AF per 1000 person years was 1.11 (95% CI, 1.09–1.13) in 1998–2001, 1.33 (1.31–1.34) in 2002–2006, and 1.33 (1.31–1.35) in 2007–2010. Ongoing increases in incidence were noted for patients aged ≥75 years, with similar temporal patterns in women and men. Associated comorbidities varied over time, with a constant prevalence of previous stroke, increases in hypertension and diabetes mellitus, and decreases in ischemic heart disease. Among patients aged 55 to 74 years, there was a significant reduction in mortality over time (P<0.001), but mortality rates in patients aged ≥75 years remained static at 14% to 15% per year (P=0.84). Projections of AF prevalence demonstrated a constant yearly rise, increasing from 700 000 patients in 2010 to between 1.3 and 1.8 million patients with AF in the United Kingdom by 2060.ConclusionsIn a large general practice population, incident AF increased and then plateaued overall, with a continued increase in patients aged ≥75 years. The large projected increase in AF prevalence associated with temporal changes in AF‐related comorbidities suggests the need for comprehensive implementation of AF prevention and management strategies.]]></description>
<dc:creator><![CDATA[Lane, D. A., Sk&#x0237;oth, F., Lip, G. Y. H., Larsen, T. B., Kotecha, D.]]></dc:creator>
<dc:date>2017-04-28T08:56:33-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005155</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005155</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Catheter Ablation and Implantable Cardioverter-Defibrillator, Mortality/Survival, Quality and Outcomes]]></dc:subject>
<dc:title><![CDATA[Temporal Trends in Incidence, Prevalence, and Mortality of Atrial Fibrillation in Primary Care [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-04-28</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005198.short?rss=1">
<title><![CDATA[Netrin-1 Preserves Blood-Brain Barrier Integrity Through Deleted in Colorectal Cancer/Focal Adhesion Kinase/RhoA Signaling Pathway Following Subarachnoid Hemorrhage in Rats [Imaging]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005198.short?rss=1</link>
<description><![CDATA[BackgroundNetrin‐1 (NTN‐1) has been established to be a novel intrinsic regulator of blood‐brain barrier (BBB) maintenance. This study was carried out to investigate the potential roles of exogenous NTN‐1 in preserving BBB integrity after experimental subarachnoid hemorrhage (SAH) as well as the underlying mechanisms of its protective effects.Methods and ResultsA total of 309 male Sprague‐Dawley rats were subjected to an endovascular perforation model of SAH. Recombinant NTN‐1 was administered intravenously 1 hour after SAH induction. NTN‐1 small interfering RNA or Deleted in Colorectal Cancer small interfering RNA was administered intracerebroventricular at 48 hours before SAH. Focal adhesion kinase inhibitor was administered by intraperitoneal injection at 1 hour prior to SAH. Neurological scores, brain water content, BBB permeability, RhoA activity, Western blot, and immunofluorescence staining were evaluated. The expression of endogenous NTN‐1 and its receptor Deleted in Colorectal Cancer were increased after SAH. Administration of exogenous NTN‐1 significantly reduced brain water content and BBB permeability and ameliorated neurological deficits at 24 and 72 hours after SAH. Exogenous NTN‐1 treatment significantly promoted phosphorylated focal adhesion kinase activation and inhibited RhoA activity, as well as upregulated the expression of ZO‐1 and Occludin. Conversely, depletion of endogenous NTN‐1 aggravated BBB breakdown and neurological impairments at 24 hours after SAH. The protective effects of NTN‐1 at 24 hours after SAH were also abolished by pretreatment with Deleted in Colorectal Cancer small interfering RNA and focal adhesion kinase inhibitor.ConclusionsNTN‐1 treatment preserved BBB integrity and improved neurological functions through a Deleted in Colorectal Cancer/focal adhesion kinase/RhoA signaling pathway after SAH. Thus, NTN‐1 may serve as a promising treatment to alleviate early brain injury following SAH.]]></description>
<dc:creator><![CDATA[Xie, Z., Enkhjargal, B., Reis, C., Huang, L., Wan, W., Tang, J., Cheng, Y., Zhang, J. H.]]></dc:creator>
<dc:date>2017-05-19T11:54:33-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005198</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005198</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Animal Models of Human Disease, Basic Science Research, Ischemia]]></dc:subject>
<dc:title><![CDATA[Netrin-1 Preserves Blood-Brain Barrier Integrity Through Deleted in Colorectal Cancer/Focal Adhesion Kinase/RhoA Signaling Pathway Following Subarachnoid Hemorrhage in Rats [Imaging]]]></dc:title>
<prism:publicationDate>2017-05-19</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Imaging</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005205.short?rss=1">
<title><![CDATA[Initiation Patterns of Statins in the 2 Years After Release of the 2013 American College of Cardiology/American Heart Association (ACC/AHA) Cholesterol Management Guideline in a Large US Health Plan [Health Services and Outcomes Research]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005205.short?rss=1</link>
<description><![CDATA[BackgroundThe purpose of this study was to characterize changes in statin utilization patterns in patients newly initiated on therapy in the 2 years following the release of the 2013 American College of Cardiology/American Heart Association (ACC/AHA) cholesterol management guideline in a large US health plan population.Methods and ResultsThis retrospective, observational study used administrative medical and pharmacy claims data to identify patients newly initiated on statin therapy over 4 quarters prior to and 8 quarters following the release of the guideline (average N/quarter=3596). Patients were divided into the 4 statin benefit groups (SBGs) based on risk factors and laboratory lipid levels as defined in the guideline: SBG1 (with atherosclerotic cardiovascular disease [ASCVD]; N=1046/quarter), SBG2 (without ASCVD, with low‐density lipoprotein cholesterol ≥190 mg/dL; N=454/quarter), SBG3 (without ASCVD, aged 40–75 years, with diabetes mellitus, low‐density lipoprotein cholesterol 70–189 mg/dL; N=1391/quarter), SBG4 (no ASCVD or diabetes mellitus, age 40–75 years, low‐density lipoprotein cholesterol 70–189 mg/dL, estimated 10‐year ASCVD risk of ≥7.5%; N=705/quarter). Demographic variables, statin utilization patterns, lipid levels, and comorbidities were analyzed for pre‐ and postguideline periods. Postguideline, gradually increased high‐intensity statin initiation occurred in SBG1, SBG2, and in SBG3 patients with 10‐year ASCVD risk ≥7.5%. Moderate‐ to high‐intensity statin initiation gradually increased among SBG4 patients. Recommended‐intensity statin choice changed to a greater degree among patients treated by specialty care physicians. Regarding sex, target‐intensity statin initiation was lower in women in all groups before and after guideline release.ConclusionsPrescriber implementation of the guideline recommendations has gradually increased, with the most marked change in the increased initiation of high‐intensity statins in patients with ASCVD and in those treated by a specialist.]]></description>
<dc:creator><![CDATA[Olufade, T., Zhou, S., Anzalone, D., Kern, D. M., Tunceli, O., Cziraky, M. J., Willey, V. J.]]></dc:creator>
<dc:date>2017-05-04T07:17:54-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005205</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005205</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiovascular Disease, Epidemiology, Risk Factors, Health Services]]></dc:subject>
<dc:title><![CDATA[Initiation Patterns of Statins in the 2 Years After Release of the 2013 American College of Cardiology/American Heart Association (ACC/AHA) Cholesterol Management Guideline in a Large US Health Plan [Health Services and Outcomes Research]]]></dc:title>
<prism:publicationDate>2017-05-04</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Health Services and Outcomes Research</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005227.short?rss=1">
<title><![CDATA[Relations of Liver Fat With Prevalent and Incident Atrial Fibrillation in the Framingham Heart Study [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005227.short?rss=1</link>
<description><![CDATA[BackgroundObesity is an important risk factor for nonalcoholic fatty liver disease and atrial fibrillation (AF). Less is known about the relations between nonalcoholic fatty liver disease and AF. We sought to evaluate the association between fatty liver and prevalent and incident AF in the community.Methods and ResultsWe examined Framingham Heart Study participants who underwent a study‐directed computed tomography scan, had hepatic steatosis (HS) evaluated, and did not report heavy alcohol use between 2002 and 2005. We evaluated cross‐sectional associations between liver fat and prevalent AF with logistic regression models. We assessed the relations between liver fat and incident AF during 12‐year follow‐up with Cox proportional hazards models. Of 2122 participants (53% women; mean age, 59.0±9.6 years), 20% had HS. AF prevalence (n=62) among individuals with HS was 4% compared to 3% among those without HS. There was no significant association between HS (measured as continuous or dichotomous variables) and prevalent AF in age‐ and sex‐adjusted or multivariable‐adjusted models. Incidence of AF (n=153) among participants with and without HS was 8.7 cases and 7.8 cases per 1000 person‐years, respectively. In age‐ and sex‐adjusted and multivariable‐adjusted models, there were no significant associations between continuous or dichotomous measures of HS and incident AF.ConclusionsIn our community‐based, longitudinal cohort study, liver fat by computed tomography scan was not significantly associated with increased prevalence or incidence of AF over 12 years of follow‐up.]]></description>
<dc:creator><![CDATA[Long, M. T., Yin, X., Larson, M. G., Ellinor, P. T., Lubitz, S. A., McManus, D. D., Magnani, J. W., Staerk, L., Ko, D., Helm, R. H., Hoffmann, U., Chung, R. T., Benjamin, E. J.]]></dc:creator>
<dc:date>2017-05-02T07:08:23-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005227</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005227</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Arrhythmias, Inflammation, Epidemiology, Obesity]]></dc:subject>
<dc:title><![CDATA[Relations of Liver Fat With Prevalent and Incident Atrial Fibrillation in the Framingham Heart Study [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-02</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005231.short?rss=1">
<title><![CDATA[Risk for Incident Heart Failure: A Sub&&jnodot;nodot;ect&ndash;Level Meta&ndash;Analysis From the Heart &&num;x201C;OMics&&num;x201D; in AGEing (HOMAGE) Study [Systematic Review and Meta-Analysis]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005231.short?rss=1</link>
<description><![CDATA[BackgroundTo address the need for personalized prevention, we conducted a subject‐level meta‐analysis within the framework of the Heart “OMics” in AGEing (HOMAGE) study to develop a risk prediction model for heart failure (HF) based on routinely available clinical measurements.Methods and ResultsThree studies with elderly persons (Health Aging and Body Composition [Health ABC], Valutazione della PREvalenza di DIsfunzione Cardiaca asinTOmatica e di scompenso cardiaco [PREDICTOR], and Prospective Study of Pravastatin in the Elderly at Risk [PROSPER]) were included to develop the HF risk function, while a fourth study (Anglo‐Scandinavian Cardiac Outcomes Trial [ASCOT]) was used as a validation cohort. Time‐to‐event analysis was conducted using the Cox proportional hazard model. Incident HF was defined as HF hospitalization. The Cox regression model was evaluated for its discriminatory performance (area under the receiver operating characteristic curve) and calibration (Grønnesby‐Borgan χ2 statistic). During a follow‐up of 3.5 years, 470 of 10 236 elderly persons (mean age, 74.5 years; 51.3% women) developed HF. Higher age, BMI, systolic blood pressure, heart rate, serum creatinine, smoking, diabetes mellitus, history of coronary artery disease, and use of antihypertensive medication were associated with increased HF risk. The area under the receiver operating characteristic curve of the model was 0.71, with a good calibration (χ2 7.9, P=0.54). A web‐based calculator was developed to allow easy calculations of the HF risk.ConclusionsSimple measurements allow reliable estimation of the short‐term HF risk in populations and patients. The risk model may aid in risk stratification and future HF prevention strategies.]]></description>
<dc:creator><![CDATA[Jacobs, L., Efremov, L., Ferreira, J. P., Thi&#x0237;s, L., Yang, W.&ndash;Y., Zhang, Z.&ndash;Y., Latini, R., Masson, S., Agabiti, N., Sever, P., Delles, C., Sattar, N., Butler, J., Cleland, J. G. F., Kuznetsova, T., Staessen, J. A., Zannad, F.,  the Heart &#x201C;OMics&#x201D; in AGEing (HOMAGE) investigators]]></dc:creator>
<dc:date>2017-05-02T07:08:23-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005231</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005231</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Risk Factors, Heart Failure]]></dc:subject>
<dc:title><![CDATA[Risk for Incident Heart Failure: A Sub&&jnodot;nodot;ect&ndash;Level Meta&ndash;Analysis From the Heart &&num;x201C;OMics&&num;x201D; in AGEing (HOMAGE) Study [Systematic Review and Meta-Analysis]]]></dc:title>
<prism:publicationDate>2017-05-02</prism:publicationDate>
<prism:section>Systematic Review and Meta&#x2010;Analysis</prism:section>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005278.short?rss=1">
<title><![CDATA[Different Determinants of Ventilatory Inefficiency at Different Stages of Reduced Ejection Fraction Chronic Heart Failure Natural History [Heart Failure]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005278.short?rss=1</link>
<description><![CDATA[BackgroundIt is not known whether determinants of ventilation (VE)/volume of exhaled carbon dioxide (VCO2) slope during incremental exercise may differ at different stages of reduced ejection fraction chronic heart failure natural history.Methods and ResultsVE/VCO2 slope was fitted up to lowest VE/VCO2 ratio, that is, a proxy of the VE/perfusion ratio devoid of nonmetabolic stimuli to ventilatory drive. VE/VCO2 slope tertiles were generated from our database (<27.5 [tertile 1], ≥27.5 to <32.0 [tertile 2], and ≥32.0 [tertile 3]), and 147 chronic heart failure patients with repeated tests yielding VE/VCO2 slopes in 2 different tertiles were selected. Determinants of VE/VCO2 slope changes across tertile pairs 1 versus 2, 2 versus 3, and 1 versus 3 were assessed by exploring changes in VE and VCO2 at lowest VE/VCO2 and those in VE/work rate (W) and VCO2/W slope. Resting and peak cardiac output (CO) were calculated as VO2/estimated arteriovenous O2 difference and the CO/W slope analyzed. Notwithstanding a progressively lower W with increasing tertile, VE at lowest VE/VCO2 and VE/W slope were significantly higher in tertiles 2 and 3 versus tertile 1. Conversely, VCO2 at lowest VE/VCO2 and CO/W slope significantly decreased across tertiles, whereas VCO2/W slope did not. Difference (Δ) in VE/W slope between tertiles accounted for 71% of ΔVE/VCO2 slope variance, with ΔVCO2/W slope explaining an additional 26% (model r=0.99; r2=0.97; P<0.0001). Similar results were obtained substituting ΔVCO2/W slope with ΔCO/W slope.ConclusionsVentilatory overactivation is the predominant cause of VE/VCO2 slope increase at initial stages of chronic heart failure, whereas hemodynamic impairment plays an additional role at more‐advanced pathophysiological stages.]]></description>
<dc:creator><![CDATA[Mezzani, A., Giordano, A., Komici, K., Corra, U.]]></dc:creator>
<dc:date>2017-05-09T03:00:33-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005278</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005278</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Pathophysiology, Heart Failure, Exercise Testing]]></dc:subject>
<dc:title><![CDATA[Different Determinants of Ventilatory Inefficiency at Different Stages of Reduced Ejection Fraction Chronic Heart Failure Natural History [Heart Failure]]]></dc:title>
<prism:publicationDate>2017-05-09</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Heart Failure</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005310.short?rss=1">
<title><![CDATA[T-Wave Morphology Restitution Predicts Sudden Cardiac Death in Patients With Chronic Heart Failure [Health Services and Outcomes Research]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005310.short?rss=1</link>
<description><![CDATA[BackgroundPatients with chronic heart failure are at high risk of sudden cardiac death (SCD). Increased dispersion of repolarization restitution has been associated with SCD, and we hypothesize that this should be reflected in the morphology of the T‐wave and its variations with heart rate. The aim of this study is to propose an electrocardiogram (ECG)‐based index characterizing T‐wave morphology restitution (TMR), and to assess its association with SCD risk in a population of chronic heart failure patients.Methods and ResultsHolter ECGs from 651 ambulatory patients with chronic heart failure from the MUSIC (MUerte Súbita en Insuficiencia Cardiaca) study were available for the analysis. TMR was quantified by measuring the morphological variation of the T‐wave per RR increment using time‐warping metrics, and its predictive power was compared to that of clinical variables such as the left ventricular ejection fraction and other ECG‐derived indices, such as T‐wave alternans and heart rate variability. TMR was significantly higher in SCD victims than in the rest of patients (median 0.046 versus 0.039, P<0.001). When TMR was dichotomized at TMR=0.040, the SCD rate was significantly higher in the TMR≥0.040 group (P<0.001). Cox analysis revealed that TMR≥0.040 was strongly associated with SCD, with a hazard ratio of 3.27 (P<0.001), independently of clinical and ECG‐derived variables. No association was found between TMR and pump failure death.ConclusionsThis study shows that TMR is specifically associated with SCD in a population of chronic heart failure patients, and it is a better predictor than clinical and ECG‐derived variables.]]></description>
<dc:creator><![CDATA[Ramirez, J., Orini, M., Minchole, A., Monasterio, V., Cygankiewicz, I., Bayes de Luna, A., Martinez, J. P., Pueyo, E., Laguna, P.]]></dc:creator>
<dc:date>2017-05-19T08:28:58-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005310</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005310</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Arrhythmias, Sudden Cardiac Death, Biomarkers, Heart Failure, Mortality/Survival]]></dc:subject>
<dc:title><![CDATA[T-Wave Morphology Restitution Predicts Sudden Cardiac Death in Patients With Chronic Heart Failure [Health Services and Outcomes Research]]]></dc:title>
<prism:publicationDate>2017-05-19</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Health Services and Outcomes Research</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005316.short?rss=1">
<title><![CDATA[Antidepressants, Depression, and Venous Thromboembolism Risk: Large Prospective Study of UK Women [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005316.short?rss=1</link>
<description><![CDATA[BackgroundSome investigators have reported an excess risk of venous thromboembolism (VTE) associated with depression and with use of antidepressant drugs. We explored these associations in a large prospective study of UK women.Methods and ResultsThe Million Women Study recruited 1.3 million women through the National Health Service Breast Screening Programme in England and Scotland. Three years after recruitment, women were sent a second questionnaire that enquired about depression and regular use of medications in the previous 4 weeks. The present analysis included those who responded and did not have prior VTE, cancer, or recent surgery. Follow‐up for VTE was through linkage to routinely collected National Health Service statistics. Cox regression analyses yielded adjusted hazard ratios and 95% CIs. A total of 734 092 women (mean age 59.9 years) were included in the analysis; 6.9% reported use of antidepressants, 2.7% reported use of other psychotropic drugs, and 1.8% reported being treated for depression or anxiety but not use of psychotropic drugs. During follow‐up for an average of 7.3 years, 3922 women were hospitalized for and/or died from VTE. Women who reported antidepressant use had a significantly higher risk of VTE than women who reported neither depression nor use of psychotropic drugs (hazard ratio, 1.39; 95% CI, 1.23–1.56). VTE risk was not significantly increased in women who reported being treated for depression or anxiety but no use of antidepressants or other psychotropic drugs (hazard ratio, 1.19; 95% CI, 0.95–1.49).ConclusionsUse of antidepressants is common in UK women and is associated with an increased risk of VTE.]]></description>
<dc:creator><![CDATA[Parkin, L., Balkwill, A., Sweetland, S., Reeves, G. K., Green, J., Beral, V.,  the Million Women Study Collaborators]]></dc:creator>
<dc:date>2017-05-17T05:47:19-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005316</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005316</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Risk Factors, Embolism, Thrombosis]]></dc:subject>
<dc:title><![CDATA[Antidepressants, Depression, and Venous Thromboembolism Risk: Large Prospective Study of UK Women [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005336.short?rss=1">
<title><![CDATA[Risk Factors for Heart Failure in Patients With Chronic Kidney Disease: The CRIC (Chronic Renal Insufficiency Cohort) Study [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005336.short?rss=1</link>
<description><![CDATA[BackgroundHeart failure is common in patients with chronic kidney disease. We studied risk factors for incident heart failure among 3557 participants in the CRIC (Chronic Renal Insufficiency Cohort) Study.Methods and ResultsKidney function was assessed by estimated glomerular filtration rate (eGFR) using serum creatinine, cystatin C, or both, and 24‐hour urine albumin excretion. During an average of 6.3 years of follow‐up, 452 participants developed incident heart failure. After adjustment for age, sex, race, and clinical site, hazard ratio (95% CI) for heart failure associated with 1 SD lower creatinine‐based eGFR was 1.67 (1.49, 1.89), 1 SD lower cystatin C‐based‐eGFR was 2.43 (2.10, 2.80), and 1 SD higher log‐albuminuria was 1.65 (1.53, 1.78), all P<0.001. When all 3 kidney function measures were simultaneously included in the model, lower cystatin C‐based eGFR and higher log‐albuminuria remained significantly and directly associated with incidence of heart failure. After adjusting for eGFR, albuminuria, and other traditional cardiovascular risk factors, anemia (1.37, 95% CI 1.09, 1.72, P=0.006), insulin resistance (1.16, 95% CI 1.04, 1.28, P=0.006), hemoglobin A1c (1.27, 95% CI 1.14, 1.41, P<0.001), interleukin‐6 (1.15, 95% CI 1.05, 1.25, P=0.002), and tumor necrosis factor‐α (1.10, 95% CI 1.00, 1.21, P=0.05) were all significantly and directly associated with incidence of heart failure.ConclusionsOur study indicates that cystatin C‐based eGFR and albuminuria are better predictors for risk of heart failure compared to creatinine‐based eGFR. Furthermore, anemia, insulin resistance, inflammation, and poor glycemic control are independent risk factors for the development of heart failure among patients with chronic kidney disease.]]></description>
<dc:creator><![CDATA[He, J., Shlipak, M., Anderson, A., Roy, J. A., Feldman, H. I., Kallem, R. R., Kanthety, R., Kusek, J. W., Ojo, A., Rahman, M., Ricardo, A. C., Soliman, E. Z., Wolf, M., Zhang, X., Raj, D., Hamm, L.,  for the CRIC (Chronic Renal Insufficiency Cohort) Investigators]]></dc:creator>
<dc:date>2017-05-17T07:44:48-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005336</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005336</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Risk Factors, Heart Failure]]></dc:subject>
<dc:title><![CDATA[Risk Factors for Heart Failure in Patients With Chronic Kidney Disease: The CRIC (Chronic Renal Insufficiency Cohort) Study [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005341.short?rss=1">
<title><![CDATA[An Initial Evaluation of the Impact of Pokemon GO on Physical Activity [Health Services and Outcomes Research]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005341.short?rss=1</link>
<description><![CDATA[BackgroundPokémon GO is a location‐based augmented reality game. Using GPS and the camera on a smartphone, the game requires players to travel in real world to capture animated creatures, called Pokémon. We examined the impact of Pokémon GO on physical activity (PA).Methods and ResultsA pre‐post observational study of 167 Pokémon GO players who were self‐enrolled through recruitment flyers or online social media was performed. Participants were instructed to provide screenshots of their step counts recorded by the iPhone Health app between June 15 and July 31, 2016, which was 3 weeks before and 3 weeks after the Pokémon GO release date. Of 167 participants, the median age was 25 years (interquartile range, 21–29 years). The daily average steps of participants at baseline was 5678 (SD, 2833; median, 5718 [interquartile range, 3675–7279]). After initiation of Pokémon GO, daily activity rose to 7654 steps (SD, 3616; median, 7232 [interquartile range, 5041–9744], pre‐post change: 1976; 95% CI, 1494–2458, or a 34.8% relative increase [P<0.001]). On average, 10 000 “XP” points (a measure of game progression) was associated with 2134 additional steps per day (95% CI, 1673–2595), suggesting a potential dose‐response relationship. The number of participants achieving a goal of 10 000+ steps per day increased from 15.3% before to 27.5% after (odds ratio, 2.06; 95% CI, 1.70–2.50). Increased PA was also observed in subgroups, with the largest increases seen in participants who spent more time playing Pokémon GO, those who were overweight/obese, or those with a lower baseline PA level.ConclusionsPokémon GO participation was associated with a significant increase in PA among young adults. Incorporating PA into gameplay may provide an alternative way to promote PA in persons who are attracted to the game.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT02888314.]]></description>
<dc:creator><![CDATA[Xian, Y., Xu, H., , Liang, L., Hernandez, A. F., Wang, T. Y., Peterson, E. D.]]></dc:creator>
<dc:date>2017-05-16T06:49:15-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005341</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005341</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Exercise, Lifestyle, Primary Prevention, Quality and Outcomes]]></dc:subject>
<dc:title><![CDATA[An Initial Evaluation of the Impact of Pokemon GO on Physical Activity [Health Services and Outcomes Research]]]></dc:title>
<prism:publicationDate>2017-05-16</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Health Services and Outcomes Research</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005354.short?rss=1">
<title><![CDATA[Change in Physical Activity and Sitting Time After Myocardial Infarction and Mortality Among Postmenopausal Women in the Women's Health Initiative-Observational Study [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005354.short?rss=1</link>
<description><![CDATA[BackgroundHow physical activity (PA) and sitting time may change after first myocardial infarction (MI) and the association with mortality in postmenopausal women is unknown.Methods and ResultsParticipants included postmenopausal women in the Women's Health Initiative‐Observational Study, aged 50 to 79 years who experienced a clinical MI during the study. This analysis included 856 women who had adequate data on PA exposure and 533 women for sitting time exposures. Sitting time was self‐reported at baseline, year 3, and year 6. Self‐reported PA was reported at baseline through year 8. Change in PA and sitting time were calculated as the difference between the cumulative average immediately following MI and the cumulative average immediately preceding MI. The 4 categories of change were: maintained low, decreased, increased, and maintained high. The cut points were ≥7.5 metabolic equivalent of task hours/week versus <7.5 metabolic equivalent of task hours/week for PA and ≥8 h/day versus <8 h/day for sitting time. Cox proportional hazard models estimated hazard ratios and 95% CIs for all‐cause, coronary heart disease, and cardiovascular disease mortality. Compared with women who maintained low PA (referent), the risk of all‐cause mortality was: 0.54 (0.34–0.86) for increased PA and 0.52 (0.36–0.73) for maintained high PA. Women who had pre‐MI levels of sitting time <8 h/day, every 1 h/day increase in sitting time was associated with a 9% increased risk (hazard ratio=1.09, 95% CI: 1.01, 1.19) of all‐cause mortality.ConclusionsMeeting the recommended PA guidelines pre‐ and post‐MI may have a protective role against mortality in postmenopausal women.]]></description>
<dc:creator><![CDATA[Gorczyca, A. M., Eaton, C. B., LaMonte, M. J., Manson, J. E., Johnston, J. D., Bidulescu, A., Waring, M. E., Manini, T., Martin, L. W., Stefanick, M. L., He, K., Chomistek, A. K.]]></dc:creator>
<dc:date>2017-05-15T06:51:05-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005354</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005354</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Aging, Cardiovascular Disease, Epidemiology, Exercise, Women]]></dc:subject>
<dc:title><![CDATA[Change in Physical Activity and Sitting Time After Myocardial Infarction and Mortality Among Postmenopausal Women in the Women's Health Initiative-Observational Study [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-15</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005396.short?rss=1">
<title><![CDATA[Long-Term Outcomes of Patients With Mediastinal Radiation-Associated Severe Aortic Stenosis and Subsequent Surgical Aortic Valve Replacement: A Matched Cohort Study [Valvular Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005396.short?rss=1</link>
<description><![CDATA[BackgroundCardiac disease after mediastinal radiotherapy for thoracic malignancy (chest radiotherapy [XRT]) often manifests as progressive aortic stenosis. In patients with XRT‐induced severe aortic stenosis undergoing surgical aortic valve replacement (SAVR), we sought to: (1) study long‐term survival and compare these patients with a matched cohort undergoing SAVR during the same time frame; and (2) identify potential predictors of long‐term mortality.Methods and ResultsWe studied patients with symptomatic severe aortic stenosis undergoing SAVR at our institution, of which there were 172 mediastinal XRT patients (63±13 years, 62% women) matched in a 1:1 fashion (based on age, sex, time of surgery, and aortic valve area) with 172 non‐XRT patients (comparison group). Baseline clinical and postoperative data were obtained. Society of Thoracic Surgeons score was calculated and mortality was recorded. In the XRT group, the median Society of Thoracic Surgeons score was 4% (interquartile range 2–13), while mean left ventricular ejection fraction, left ventricular stroke volume index, and mean aortic valve gradient were 54±11%, 38±14 mL/m2, and 39±11 mm Hg, respectively. In the entire cohort, 27% and 34% of patients underwent concomitant coronary artery bypass grafting and aortic surgery at the time of SAVR, respectively. Thirty‐day/in‐hospital deaths occurred in 4 (2%) patients in the XRT group and 0 patients in the comparison group. At 6±3 years of follow‐up, on matched group analysis, there were 95 (28%) deaths (83 [48%] in the XRT group versus 12 [7%] in the comparison group (log‐rank 89, P<0.001). On multivariable Cox survival analysis, in the whole cohort, higher Society of Thoracic Surgeons score (hazard ratio, 1.14; 95% CI, 1.03–1.26) and mediastinal XRT (hazard ratio, 8.12; 95% CI, 4.26–15.64) were associated with increased longer‐term mortality (both P<0.01).ConclusionsIn patients with severe aortic stenosis undergoing SAVR, patients with prior mediastinal XRT have significantly worse longer‐term survival versus a matched cohort.]]></description>
<dc:creator><![CDATA[Donnellan, E., Masri, A., Johnston, D. R., Pettersson, G. B., Rodriguez, L. L., Popovic, Z. B., Roselli, E. E., Smedira, N. G., Svensson, L. G., Griffin, B. P., Desai, M. Y.]]></dc:creator>
<dc:date>2017-05-05T03:00:27-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005396</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005396</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Valvular Heart Disease]]></dc:subject>
<dc:title><![CDATA[Long-Term Outcomes of Patients With Mediastinal Radiation-Associated Severe Aortic Stenosis and Subsequent Surgical Aortic Valve Replacement: A Matched Cohort Study [Valvular Heart Disease]]]></dc:title>
<prism:publicationDate>2017-05-05</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Valvular Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005465.short?rss=1">
<title><![CDATA[Cigarette Smoking-Associated Alterations in Serotonin/Adrenalin Signaling Pathways of Platelets [Coronary Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005465.short?rss=1</link>
<description><![CDATA[BackgroundCigarette smoking plays a major role in cardiovascular diseases. The acute effects of cigarette smoking produce central nervous system–mediated activation of the sympathetic nervous system. The overactive sympathetic nervous system stimulates the secretion of serotonin (5‐HT) and catecholamine into blood at supraphysiological levels. The correlation between these pathological conditions induced by smoking and the increased risk of thrombosis has not been thoroughly investigated. The goal of our study was to explore cigarette smoking–associated changes in platelet biology mediated by elevated 5‐HT and catecholamine levels in blood plasma.Methods and ResultsUsing blood samples collected from healthy nonsmokers and smokers (15 minutes after smoking), we determined that cigarette smoking increased the plasma 5‐HT/catecholamine concentration by several fold and the percent aggregation of platelets 2‐fold. Liquid chromatography–tandem mass spectrometry analysis of proteins eluted from platelet plasma membranes of smokers and nonsmokers demonstrated that GTPase‐activating proteins and proteins participating in the actin cytoskeletal network were differentially and significantly elevated in smokers' platelet membranes compared with those of nonsmokers. Interestingly, Matrix‐assisted laser desorption/ionization–mass spectrometry analyses of the glycans eluted from platelet plasma membranes of the smokers demonstrated that the level and structures of glycans are different from the nonsmokers' platelet surface glycans. Pharmacological blockade of 5‐HT or catecholamine receptors counteracted the 5‐HT/catecholamine‐mediated aggregation and altered the level and composition of glycan on platelet surfaces.ConclusionsBased on our findings, we propose that smoking‐associated 5‐HT/catecholamine signaling accelerates the trafficking dynamics of platelets, and this remodels the surface proteins and glycans and predisposes platelets to hyperactive levels. Smokers' platelets also had correspondingly higher resting concentrations of intracellular calcium and transglutaminase activity. These findings suggest a link among smoking, platelet 5‐HT, catecholamine signaling, and their downstream effectors—including phospholipase C and inositol‐1,4,5‐triphosphate pathways—resulting in an increased tonic level of platelet activation in smokers.]]></description>
<dc:creator><![CDATA[Lowery, C. L., Elliott, C., Cooper, A., Hadden, C., Sonon, R. N., Azadi, P., Williams, D. K., Marsh, J. D., Woulfe, D. S., Kilic, F.]]></dc:creator>
<dc:date>2017-05-18T09:55:14-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.116.005465</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.116.005465</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cell Signaling/Signal Transduction, Mechanisms, Platelets, Proteomics, Translational Studies]]></dc:subject>
<dc:title><![CDATA[Cigarette Smoking-Associated Alterations in Serotonin/Adrenalin Signaling Pathways of Platelets [Coronary Heart Disease]]]></dc:title>
<prism:publicationDate>2017-05-18</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Coronary Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005466.short?rss=1">
<title><![CDATA[Long-Term Effects of Unprovoked Venous Thromboembolism on Mortality and Ma&#x0237;or Cardiovascular Events [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005466.short?rss=1</link>
<description><![CDATA[BackgroundPatients with unprovoked venous thromboembolism (VTE) are at an increased risk of mortality, but whether their cardiovascular risks also increase remains to be determined. We aimed to investigate the factors associated with overall mortality and major adverse cardiovascular events in patients with unprovoked VTE.Methods and ResultsWe identified 2154 patients newly diagnosed with unprovoked VTE from Taiwan's National Health Insurance Database between 2000 and 2013, excluding those with reversible etiologies, underlying cancer, or autoimmune diseases. These patients with VTE were compared with an age‐, sex‐, and cardiovascular risk‐matched cohort of 4308 controls. The risk of mortality and major adverse cardiovascular events in patients with VTE was 2.23 (CI, 1.93–2.57; P<0.0001) and 1.86 (CI, 1.65–2.09; P<0.0001) times, respectively, higher than that of the conditions in controls. These events mostly occurred during the first year after the diagnosis of unprovoked VTE. Among patients with VTE, advanced age, male sex, and comorbid diabetes mellitus indicated a higher incidence of mortality and major adverse cardiovascular events. Conversely, comorbid hyperlipidemia attenuated these risks.ConclusionsThis nation‐wide cohort study revealed that patients with unprovoked VTE, particularly older males with diabetes mellitus, had an elevated risk of both mortality and cardiovascular events. Risk of mortality and major adverse cardiovascular events were highest within the first year after diagnosis and persisted during the 10 years of follow‐up.]]></description>
<dc:creator><![CDATA[Chang, W.-T., Chang, C.-L., Ho, C.-H., Hong, C.-S., Wang, J.-J., Chen, Z.-C.]]></dc:creator>
<dc:date>2017-05-03T13:37:15-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005466</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005466</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Embolism, Thrombosis]]></dc:subject>
<dc:title><![CDATA[Long-Term Effects of Unprovoked Venous Thromboembolism on Mortality and Ma&#x0237;or Cardiovascular Events [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-03</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005479.short?rss=1">
<title><![CDATA[Impact of the Metabolic Syndrome on Mortality is Modified by Objective Short Sleep Duration [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005479.short?rss=1</link>
<description><![CDATA[BackgroundTo examine whether objective sleep duration is an effect modifier of the impact of metabolic syndrome (MetS) on all‐cause and cardiovascular disease/cerebrovascular mortality.Methods and ResultsWe addressed this question in the Penn State Adult Cohort, a random, general population sample of 1344 men and women (48.8±14.2 years) who were studied in the sleep laboratory and followed up for 16.6±4.2 years. MetS was defined by the presence of 3 or more of obesity (≥30 kg/m2), elevated total cholesterol (≥200 mg/dL), triglycerides (≥150 mg/dL), fasting glucose (≥100 mg/dL), and blood pressure (≥130/85 mm Hg). Polysomnographic sleep duration was classified into clinically meaningful categories. Among the 1344 participants, 22.0% of them died during the follow‐up. We tested the interaction between MetS and polysomnographic sleep duration on mortality using Cox proportional hazard models controlling for multiple potential confounders (P<0.05). The hazard ratios (95% CI) of all‐cause and cardiovascular disease/cerebrovascular mortality associated with MetS were 1.29 (0.89–1.87) and 1.49 (0.75–2.97) for individuals who slept ≥6 hours and 1.99 (1.53–2.59) and 2.10 (1.39–3.16) for individuals who slept <6 hours. Interestingly, this effect modification was primarily driven by the elevated blood pressure and glucose dysregulation components of MetS.ConclusionsThe risk of mortality associated with MetS is increased in those with short sleep duration. Short sleep in individuals with MetS may be linked to greater central autonomic and metabolic dysfunction. Future clinical trials should examine whether lengthening sleep improves the prognosis of individuals with MetS.]]></description>
<dc:creator><![CDATA[Fernandez-Mendoza, J., He, F., LaGrotte, C., Vgontzas, A. N., Liao, D., Bixler, E. O.]]></dc:creator>
<dc:date>2017-05-17T12:42:55-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005479</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005479</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Lifestyle, Risk Factors, Metabolic Syndrome, Mortality/Survival]]></dc:subject>
<dc:title><![CDATA[Impact of the Metabolic Syndrome on Mortality is Modified by Objective Short Sleep Duration [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005482.short?rss=1">
<title><![CDATA[Synergistic Effect of Dofetilide and Mexiletine on Prevention of Atrial Fibrillation [Arrhythmia and Electrophysiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005482.short?rss=1</link>
<description><![CDATA[BackgroundAlthough atrial fibrillation (AF) is the most common abnormal heart rhythm and its prevalence continues to rise, there is a marked paucity of effective and safe antiarrhythmic drugs for AF. This study was done to test whether combined use of dofetilide and mexiletine exhibits not only a synergistic effect on AF suppression but also a safer profile in drug‐induced ventricular proarrhythmias.Methods and ResultsThe effects of dofetilide plus mexiletine on atrial effective refractory period (ERP), AF inducibility, QT, and QT‐related ventricular arrhythmias were studied using the isolated arterially perfused rabbit atrial and ventricular wedge preparations. Dofetilide or mexiletine alone mildly to moderately prolonged atrial ERP, but their combined use produced a markedly rate‐dependent increase in atrial ERP. Dofetilide (3 nmol/L) plus mexiletine (10 μmol/L) increased the ERP by 28.2% from 72.2±5.7 to 92.8±5.9 ms (n=9, P<0.01) at a pacing rate of 0.5 Hz and by 94.5% from 91.7±5.2 to 178.3±12.0 ms (n=9, P<0.01) at 3.3 Hz. Dofetilide plus mexiletine strongly suppressed AF inducibility. On the other hand, dofetilide at 10 nmol/L produced marked QT and Tp‐e prolongation, steeper QT‐BCL and Tp‐e‐BCL slopes, and induced early afterdepolarizations and torsade de pointes in the ventricular wedges. Mexiletine at 10 μmol/L reduced dofetilide‐induced QT and Tp‐e prolongation, QT‐BCL and Tp‐e‐BCL slopes, and abolished early afterdepolarizations and torsade de pointes.ConclusionsIn rabbits, combined use of dofetilide and mexiletine not only synergistically increases atrial ERP and effectively suppresses AF inducibility, but also markedly reduces QT liability and torsade de pointes risk posed by dofetilide alone.]]></description>
<dc:creator><![CDATA[Liu, G., Xue, X., Gao, C., Huang, J., Qi, D., Zhang, Y., Dong, J.-Z., Ma, C.-S., Yan, G.-X.]]></dc:creator>
<dc:date>2017-05-18T07:31:18-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005482</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005482</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Arrhythmias, Basic Science Research]]></dc:subject>
<dc:title><![CDATA[Synergistic Effect of Dofetilide and Mexiletine on Prevention of Atrial Fibrillation [Arrhythmia and Electrophysiology]]]></dc:title>
<prism:publicationDate>2017-05-18</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Arrhythmia and Electrophysiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005491.short?rss=1">
<title><![CDATA[Association Between Self-Reported Potentially Modifiable Cardiac Risk Factors and Perceived Need to Improve Physical Health: A Population-Based Study [Preventive Cardiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005491.short?rss=1</link>
<description><![CDATA[BackgroundAn individual's perceived need to improve their physical health (PNIPH) is an essential precursor to adopting healthy behaviors. Nine potentially modifiable risk factors (PMRFs) for myocardial infarction collectively account for ≥90% of the population attributable risk. Though widely recognized, their impact on individuals’ health perceptions is unclear.Methods and ResultsResidents from 6 provinces were administered a module on changes to improve health as part of the 2011–2012 Canadian Community Health Survey, yielding relevant data for 8 of the 9 PMRFs sought. The potential effects of PMRFs individually and cumulatively on PNIPH were examined using modified Poisson regression. In total, 45 443 respondents were included, representing 11 006 123 individuals and corresponding to 96.8% of the adult population of the sampled provinces. The sum of PMRFs was positively associated with PNIPH (adjusted prevalence ratio, 1.08; 95% CI, 1.07–1.09 per additional PMRF) with 82.3% of individuals with ≥5 PMRFs reporting this perception. Smoking, obesity, and low physical activity were most strongly associated with PNIPH, whereas hypertension and diabetes mellitus exhibited no association with this outcome after adjusting for potential confounders. Barriers to adopting healthy behaviors were reported by 55.9% of individuals endorsing PNIPH.ConclusionsThe cumulative burden of PMRFs is positively associated with PNIPH; however, individual PMRFs differentially contribute to this perception. Among those at highest cardiac risk, ≈1 in 5 denied PNIPH. A better understanding of factors underlying health perceptions and behaviors is needed to capitalize on cardiovascular preventive efforts.]]></description>
<dc:creator><![CDATA[Ramirez, F. D., Chen, Y., Di Santo, P., Simard, T., Motazedian, P., Hibbert, B.]]></dc:creator>
<dc:date>2017-05-03T12:40:34-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005491</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005491</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiovascular Disease, Epidemiology, Lifestyle, Risk Factors]]></dc:subject>
<dc:title><![CDATA[Association Between Self-Reported Potentially Modifiable Cardiac Risk Factors and Perceived Need to Improve Physical Health: A Population-Based Study [Preventive Cardiology]]]></dc:title>
<prism:publicationDate>2017-05-03</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Preventive Cardiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005505.short?rss=1">
<title><![CDATA[Heart Rate Recovery and Risk of Cardiovascular Events and All&ndash;Cause Mortality: A Meta&ndash;Analysis of Prospective Cohort Studies [Systematic Review and Meta-Analysis]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005505.short?rss=1</link>
<description><![CDATA[BackgroundHeart rate recovery (HRR) is a noninvasive assessment of autonomic dysfunction and has been implicated with risk of cardiovascular events and all‐cause mortality. However, evidence has not been systematically assessed. We performed a meta‐analysis of prospective cohort studies to quantify these associations in the general population.Methods and ResultsA literature search using 3 databases up to August 2016 was conducted for studies that reported hazard ratios with 95% CIs for the association between baseline HRR and outcomes of interest. The overall hazard ratios were calculated using a random‐effects model. There were 9 eligible studies in total, with 5 for cardiovascular events enrolling 1061 cases from 34 267 participants, and 9 for all‐cause mortality enrolling 2082 cases from 41 600 participants. The pooled hazard ratios associated with attenuated HRR versus fast HRR that served as the referent were 1.69 (95% CI 1.05–2.71) for cardiovascular events and 1.68 (95% CI 1.51–1.88) for all‐cause mortality. For every 10 beats per minute decrements in HRR, the hazard ratios were 1.13 (95% CI 1.05–1.21) and 1.09 (95% CI 1.01–1.19), respectively. Further analyses suggested that the associations observed between attenuated HRR and risk of fatal cardiovascular events and all‐cause mortality were independent of traditional metabolic factors for cardiovascular disease (all P<0.05).ConclusionsAttenuated HRR is associated with increased risk of cardiovascular events and all‐cause mortality, which supports the recommendation of recording HRR for risk assessment in clinical practice as a routine.]]></description>
<dc:creator><![CDATA[Qiu, S., Cai, X., Sun, Z., Li, L., Zuegel, M., Steinacker, J. M., Schumann, U.]]></dc:creator>
<dc:date>2017-05-09T03:00:33-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005505</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005505</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Electrophysiology, Cardiovascular Disease, Epidemiology, Exercise]]></dc:subject>
<dc:title><![CDATA[Heart Rate Recovery and Risk of Cardiovascular Events and All&ndash;Cause Mortality: A Meta&ndash;Analysis of Prospective Cohort Studies [Systematic Review and Meta-Analysis]]]></dc:title>
<prism:publicationDate>2017-05-09</prism:publicationDate>
<prism:section>Systematic Review and Meta&#x2010;Analysis</prism:section>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005520.short?rss=1">
<title><![CDATA[Bilirubin Decreases Macrophage Cholesterol Efflux and ATP-Binding Cassette Transporter A1 Protein Expression [Coronary Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005520.short?rss=1</link>
<description><![CDATA[BackgroundMild but chronically elevated circulating unconjugated bilirubin is associated with reduced total and low‐density lipoprotein cholesterol concentration, which is associated with reduced cardiovascular disease risk. We aimed to investigate whether unconjugated bilirubin influences macrophage cholesterol efflux, as a potential mechanism for the altered circulating lipoprotein concentrations observed in hyperbilirubinemic individuals.Methods and ResultsCholesterol efflux from THP‐1 macrophages was assessed using plasma obtained from normo‐ and hyperbilirubinemic (Gilbert syndrome) humans (n=60 per group) or (heterozygote/homozygote Gunn) rats (n=20 per group) as an acceptor. Hyperbilirubinemic plasma from patients with Gilbert syndrome and Gunn rats induced significantly reduced cholesterol efflux compared with normobilirubinemic plasma. Unconjugated bilirubin (3–17.1 μmol/L) exogenously added to plasma‐ or apolipoprotein A1–supplemented media also decreased macrophage cholesterol efflux in a concentration‐ and time‐dependent manner. We also showed reduced protein expression of the ATP‐binding cassette transporter A1 (ABCA1), a transmembrane cholesterol transporter involved in apolipoprotein A1–mediated cholesterol efflux, in THP‐1 macrophages treated with unconjugated bilirubin and in peripheral blood mononuclear cells obtained from hyperbilirubinemic individuals. Furthermore, we demonstrated that bilirubin accelerates the degradation rate of the ABCA1 protein in THP‐1 macrophages.ConclusionsCholesterol efflux from THP‐1 macrophages is decreased in the presence of plasma obtained from humans and rats with mild hyperbilirubinemia. A direct effect of unconjugated bilirubin on cholesterol efflux was demonstrated and is associated with decreased ABCA1 protein expression. These data improve our knowledge concerning bilirubin's impact on cholesterol transport and represent an important advancement in our understanding of bilirubin's role in cardiovascular disease.]]></description>
<dc:creator><![CDATA[Wang, D., Tosevska, A., Heiss, E. H., Ladurner, A., Molzer, C., Wallner, M., Bulmer, A., Wagner, K.&ndash;H., Dirsch, V. M., Atanasov, A. G.]]></dc:creator>
<dc:date>2017-04-28T08:56:33-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005520</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005520</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Lipids and Cholesterol, Cardiovascular Disease, Atherosclerosis]]></dc:subject>
<dc:title><![CDATA[Bilirubin Decreases Macrophage Cholesterol Efflux and ATP-Binding Cassette Transporter A1 Protein Expression [Coronary Heart Disease]]]></dc:title>
<prism:publicationDate>2017-04-28</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Coronary Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005522.short?rss=1">
<title><![CDATA[Remote Ischemic Perconditioning to Reduce Reperfusion In&&jnodot;nodot;ury During Acute ST&ndash;Segment&ndash;Elevation Myocardial Infarction: A Systematic Review and Meta&ndash;Analysis [Systematic Review and Meta-Analysis]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005522.short?rss=1</link>
<description><![CDATA[BackgroundRemote ischemic conditioning (RIC) is a noninvasive therapeutic strategy that uses brief cycles of blood pressure cuff inflation and deflation to protect the myocardium against ischemia–reperfusion injury. The objective of this systematic review was to determine the impact of RIC on myocardial salvage index, infarct size, and major adverse cardiovascular events when initiated before catheterization.Methods and ResultsElectronic searches of Medline, Embase, and Cochrane Central Register of Controlled Trials were conducted and reference lists were hand searched. Randomized controlled trials comparing percutaneous coronary intervention (PCI) with and without RIC for patients with ST‐segment–elevation myocardial infarction were included. Two reviewers independently screened abstracts, assessed quality of the studies, and extracted data. Data were pooled using random‐effects models and reported as mean differences and relative risk with 95% confidence intervals. Eleven articles (9 randomized controlled trials) were included with a total of 1220 patients (RIC+PCI=643, PCI=577). Studies with no events were excluded from meta‐analysis. The myocardial salvage index was higher in the RIC+PCI group compared with the PCI group (mean difference: 0.08; 95% confidence interval, 0.02–0.14). Infarct size was reduced in the RIC+PCI group compared with the PCI group (mean difference: −2.46; 95% confidence interval, −4.66 to −0.26). Major adverse cardiovascular events were lower in the RIC+PCI group (9.5%) compared with the PCI group (17.0%; relative risk: 0.57; 95% confidence interval, 0.40–0.82).ConclusionsRIC appears to be a promising adjunctive treatment to PCI for the prevention of reperfusion injury in patients with ST‐segment–elevation myocardial infarction; however, additional high‐quality research is required before a change in practice can be considered.]]></description>
<dc:creator><![CDATA[McLeod, S. L., Iansavichene, A., Cheskes, S.]]></dc:creator>
<dc:date>2017-05-17T11:42:29-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005522</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005522</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Myocardial Infarction, Percutaneous Coronary Intervention, Revascularization, Treatment, Meta Analysis]]></dc:subject>
<dc:title><![CDATA[Remote Ischemic Perconditioning to Reduce Reperfusion In&&jnodot;nodot;ury During Acute ST&ndash;Segment&ndash;Elevation Myocardial Infarction: A Systematic Review and Meta&ndash;Analysis [Systematic Review and Meta-Analysis]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Systematic Review and Meta&#x2010;Analysis</prism:section>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005526.short?rss=1">
<title><![CDATA[Impact of Antihypertensive Treatment on Maternal and Perinatal Outcomes in Pregnancy Complicated by Chronic Hypertension: A Systematic Review and Meta&ndash;Analysis [Systematic Review and Meta-Analysis]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005526.short?rss=1</link>
<description><![CDATA[BackgroundChronic hypertension complicates around 3% of all pregnancies. There is evidence that treating severe hypertension reduces maternal morbidity. This study aimed to systematically review randomized controlled trials of antihypertensive agents treating chronic hypertension in pregnancy to determine the effect of this intervention.Methods and ResultsMedline (via OVID), Embase (via OVID) and the Cochrane Trials Register were searched from their earliest entries until November 30, 2016. All randomized controlled trials evaluating antihypertensive treatments for chronic hypertension in pregnancy were included. Data were extracted and analyzed in Stata (version 14.1). Fifteen randomized controlled trials (1166 women) were identified for meta‐analysis. A clinically important reduction in the incidence of severe hypertension was seen with antihypertensive treatment versus no antihypertensive treatment/placebo (5 studies, 446 women; risk ratio 0.33, 95%CI 0.19‐0.56; I2 0.0%). There was no difference in the incidence of superimposed pre‐eclampsia (7 studies, 727 women; risk ratio 0.74, 95%CI 0.49‐1.11; I2 28.1%), stillbirth/neonatal death (4 studies, 667 women; risk ratio 0.37, 95%CI 0.11‐1.26; I2 0.0%), birth weight (7 studies, 802 women; weighted mean difference −60 g, 95%CI −200 to 80 g; I2 0.0%), or small for gestational age (4 studies, 369 women; risk ratio 1.01, 95%CI 0.53‐1.94; I2 0.0%) with antihypertensive treatment versus no treatment/placebo.ConclusionsAntihypertensive treatment reduces the risk of severe hypertension in pregnant women with chronic hypertension. A considerable paucity of data exists to guide choice of antihypertensive agent. Adequately powered head‐to‐head randomized controlled trials of commonly used antihypertensive agents are required to inform prescribing.]]></description>
<dc:creator><![CDATA[Webster, L. M., Conti-Ramsden, F., Seed, P. T., Webb, A. J., Nelson-Piercy, C., Chappell, L. C.]]></dc:creator>
<dc:date>2017-05-17T05:03:02-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005526</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005526</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Pregnancy, Hypertension, Treatment, Meta Analysis]]></dc:subject>
<dc:title><![CDATA[Impact of Antihypertensive Treatment on Maternal and Perinatal Outcomes in Pregnancy Complicated by Chronic Hypertension: A Systematic Review and Meta&ndash;Analysis [Systematic Review and Meta-Analysis]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Systematic Review and Meta&#x2010;Analysis</prism:section>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005568.short?rss=1">
<title><![CDATA[Therapeutic Strategies and Drug Development for Vascular Cognitive Impairment [Contemporary Review]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005568.short?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Smith, E. E., Cieslak, A., Barber, P., Chen, J., Chen, Y.-W., Donnini, I., Edwards, J. D., Frayne, R., Field, T. S., Hegedus, J., Hanganu, V., Ismail, Z., Kanji, J., Nakajima, M., Noor, R., Peca, S., Sahlas, D., Sharma, M., Sposato, L. A., Swartz, R. H., Zerna, C., Black, S. E., Hachinski, V.]]></dc:creator>
<dc:date>2017-05-05T10:55:59-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005568</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005568</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Secondary Prevention, Cerebrovascular Disease/Stroke, Cognitive Impairment, Neuroprotectants]]></dc:subject>
<dc:title><![CDATA[Therapeutic Strategies and Drug Development for Vascular Cognitive Impairment [Contemporary Review]]]></dc:title>
<prism:publicationDate>2017-05-05</prism:publicationDate>
<prism:section>Contemporary Review</prism:section>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005574.short?rss=1">
<title><![CDATA[Quantitative Value of Aldosterone-Renin Ratio for Detection of Aldosterone-Producing Adenoma: The Aldosterone-Renin Ratio for Primary Aldosteronism (AQUARR) Study [Cardiovascular Surgery]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005574.short?rss=1</link>
<description><![CDATA[BackgroundCurrent guidelines recommend use of the aldosterone‐renin ratio (ARR) for the case detection of primary aldosteronism followed by confirmatory tests to exclude false‐positive results from further diagnostic workup. We investigated the hypothesis that this could be unnecessary in patients with a high ARR value if the quantitative information carried by the ARR is taken into due consideration.Methods and ResultsWe interrogated 2 large data sets of prospectively collected patients studied with the same predefined protocol, which included the captopril challenge test. We used an unambiguous diagnosis of aldosterone‐producing adenoma as reference index. We also assessed whether the post‐captopril ARR and plasma aldosterone concentration fall furnished a diagnostic gain over baseline ARR values. We found that the false‐positive rate fell exponentially, and, conversely, the specificity increased with rising ARR values. At receiver operating characteristics curves and diagnostic odds ratio analysis, the high baseline ARR values implied very high positive likelihood ratio and diagnostic odds ratio values. The baseline and post‐captopril ARR showed similar diagnostic accuracy (area under the receiver operating characteristics curve) in both the exploratory and validation cohorts, indicating lack of diagnostic gain with this confirmatory test (between‐area under the curve difference, 0.005; 95% CI, −0.031 to 0.040; P=0.7 for comparison, and 0.05; 95% CI, −0.061 to 0.064; P=0.051 for comparison, respectively).ConclusionsThese results indicate that the ARR conveys key quantitative information that, if properly used, can simplify the diagnostic workup, resulting in saving of money and resources. This can offer the chance of diagnosis and ensuing adrenalectomy to a larger number of hypertensive patients, ultimately resulting in better control of blood pressure.]]></description>
<dc:creator><![CDATA[Maiolino, G., Rossitto, G., Bisogni, V., Cesari, M., Seccia, T. M., Plebani, M., Rossi, G. P.,  the PAPY Study Investigators]]></dc:creator>
<dc:date>2017-05-21T04:33:09-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005574</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005574</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Hypertension]]></dc:subject>
<dc:title><![CDATA[Quantitative Value of Aldosterone-Renin Ratio for Detection of Aldosterone-Producing Adenoma: The Aldosterone-Renin Ratio for Primary Aldosteronism (AQUARR) Study [Cardiovascular Surgery]]]></dc:title>
<prism:publicationDate>2017-05-21</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Cardiovascular Surgery</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005608.short?rss=1">
<title><![CDATA[Midlife and Late-Life Vascular Risk Factors and White Matter Microstructural Integrity: The Atherosclerosis Risk in Communities Neurocognitive Study [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005608.short?rss=1</link>
<description><![CDATA[BackgroundDiffusion tensor imaging measures of white matter (WM) microstructural integrity appear to provide earlier indication of WM injury than WM hyperintensities; however, risk factors for poor WM microstructural integrity have not been established. Our study quantifies the association between vascular risk factors in midlife and late life with measures of late‐life WM microstructural integrity.Methods and ResultsWe used data from 1851 participants in ARIC (Atherosclerosis Risk in Communities Study) who completed 3‐T magnetic resonance imaging, including diffusion tensor imaging, as part of the ARIC Neurocognitive Study (ARIC‐NCS). We quantified the association among lipids, glucose, and blood pressure from the baseline ARIC visit (1987–1989, ages 44–65, midlife) and visit 5 of ARIC (2011–2013, ages 67–90, late life, concurrent with ARIC‐NCS) with regional and overall WM mean diffusivity and fractional anisotropy obtained at ARIC visit 5 for ARIC participants. We also considered whether these associations were independent of or modified by WM hyperintensity volumes. We found that elevated blood pressure in midlife and late life and elevated glucose in midlife, but not late life, were associated with worse late‐life WM microstructural integrity. These associations were independent of the degree of WM hyperintensity, and the association between glucose and WM microstructural integrity appeared stronger for those with the least WM hyperintensity. There was little support for an adverse association between lipids and WM microstructural integrity.ConclusionsHypertension in both midlife and late life and elevated glucose in midlife are related to worse WM microstructural integrity in late life.]]></description>
<dc:creator><![CDATA[Power, M. C., Tingle, J. V., Reid, R. I., Huang, J., Sharrett, A. R., Coresh, J., Griswold, M., Kantarci, K., Jack, C. R., Knopman, D., Gottesman, R. F., Mosley, T. H.]]></dc:creator>
<dc:date>2017-05-18T11:56:52-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005608</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005608</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Lipids and Cholesterol, Diabetes, Type 2, Epidemiology, Risk Factors, High Blood Pressure]]></dc:subject>
<dc:title><![CDATA[Midlife and Late-Life Vascular Risk Factors and White Matter Microstructural Integrity: The Atherosclerosis Risk in Communities Neurocognitive Study [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-18</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005633.short?rss=1">
<title><![CDATA[Long&ndash;Term Cardiovascular Risk After Radiotherapy in Women With Breast Cancer [Systematic Review and Meta-Analysis]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005633.short?rss=1</link>
<description><![CDATA[BackgroundRadiotherapy for breast cancer often involves some incidental exposure of the heart to ionizing radiation. The effect of this exposure on the subsequent risk of heart disease is uncertain. We performed a meta‐analysis to investigate the link between radiotherapy and long‐term cardiovascular morbidity and mortality in patients with breast cancer.Methods and ResultsWe performed a literature search using MEDLINE (January 1966 to January 2015) and EMBASE (January 1980 to January 2015) with no restrictions. Studies that reported relative risk (RR) estimates with 95%CIs for the associations of interest were included. Pooled effect estimates were obtained by using random‐effects meta‐analysis. Thirty‐nine studies involving 1 191 371 participants were identified. Patients who received left‐sided radiotherapy, as compared with those receiving right‐sided radiotherapy, experienced increased risks of developing coronary heart disease (RR 1.29, 95%CI 1.13‐1.48), cardiac death (RR 1.22, 95%CI 1.08‐1.37) and death from any cause (RR 1.05, 95%CI 1.01‐1.10). In a comparison of patients with radiotherapy and without radiotherapy, the RRs were 1.30 (95%CI 1.13‐1.49) for coronary heart disease and 1.38 (95%CI 1.18‐1.62) for cardiac mortality. Radiotherapy for breast cancer was associated with an absolute risk increase of 76.4 (95%CI 36.8‐130.5) cases of coronary heart disease and 125.5 (95%CI 98.8‐157.9) cases of cardiac death per 100 000 person‐years. The risk started to increase within the first decade for coronary heart disease and from the second decade for cardiac mortality.ConclusionsExposure of the heart to ionizing radiation during radiotherapy for breast cancer increases the subsequent risk of coronary heart disease and cardiac mortality.]]></description>
<dc:creator><![CDATA[Cheng, Y.-J., Nie, X.-Y., Ji, C.-C., Lin, X.-X., Liu, L.-J., Chen, X.-M., Yao, H., Wu, S.-H.]]></dc:creator>
<dc:date>2017-05-21T03:03:07-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005633</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005633</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiovascular Disease, Epidemiology, Primary Prevention, Risk Factors, Women]]></dc:subject>
<dc:title><![CDATA[Long&ndash;Term Cardiovascular Risk After Radiotherapy in Women With Breast Cancer [Systematic Review and Meta-Analysis]]]></dc:title>
<prism:publicationDate>2017-05-21</prism:publicationDate>
<prism:section>Systematic Review and Meta&#x2010;Analysis</prism:section>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005648.short?rss=1">
<title><![CDATA[Calcification and Oxidative Modifications Are Associated With Progressive Bioprosthetic Heart Valve Dysfunction [Valvular Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005648.short?rss=1</link>
<description><![CDATA[BackgroundBioprosthetic heart valves (BHVs), fabricated from glutaraldehyde‐pretreated bovine pericardium or porcine aortic valves, are widely used for the surgical or interventional treatment of heart valve disease. Reoperation becomes increasingly necessary over time because of BHV dysfunction.Methods and ResultsForty‐seven explanted BHV aortic valve replacements were retrieved at reoperation for clinically severe BHV dysfunction over the period 2010–2016. Clinical explant analyses of BHV leaflets for calcium (atomic absorption spectroscopy) and oxidized amino acids, per mass spectroscopy, were primary end points. Comorbidities for earlier BHV explant included diabetes mellitus and coronary artery bypass grafting. Mean calcium levels in BHV leaflets were significantly increased compared with unimplanted BHV (P<0.001); however, time to reoperation did not differ comparing calcified and noncalcified BHV. BHV dityrosine, an oxidized amino acid cross‐link, was significantly increased in the explants (227.55±33.27 μmol/mol [dityrosine/tyrosine]) but was undetectable in unimplanted leaflets (P<0.001). BHV regional analyses revealed that dityrosine, ranging from 57.5 to 227.8 μmol/mol (dityrosine/tyrosine), was detectable only in the midleaflet samples, indicating the site‐specific nature of dityrosine formation. 3‐Chlorotyrosine, an oxidized amino acid formed by myeloperoxidase‐catalyzed chlorinating oxidants, correlated with BHV calcium content in leaflet explant analyses from coronary artery bypass graft patients (r=0.62, P=0.01) but was not significantly correlated with calcification in non–coronary artery bypass graft explanted BHV.ConclusionsBoth increased BHV leaflet calcium levels and elevated oxidized amino acids were associated with bioprosthesis dysfunction necessitating reoperation; however, BHV calcium levels were not a determinant of implant duration, indicating a potentially important role for oxidized amino acid formation in BHV dysfunction.]]></description>
<dc:creator><![CDATA[Lee, S., Levy, R. J., Christian, A. J., Hazen, S. L., Frick, N. E., Lai, E. K., Grau, J. B., Bavaria, J. E., Ferrari, G.]]></dc:creator>
<dc:date>2017-05-08T11:11:31-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005648</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005648</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Valvular Heart Disease, Aortic Valve Replacement/Transcatheter Aortic Valve Implantation, Cardiovascular Surgery]]></dc:subject>
<dc:title><![CDATA[Calcification and Oxidative Modifications Are Associated With Progressive Bioprosthetic Heart Valve Dysfunction [Valvular Heart Disease]]]></dc:title>
<prism:publicationDate>2017-05-08</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Valvular Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005661.short?rss=1">
<title><![CDATA[Graded Association Between Kidney Function and Impaired Orthostatic Blood Pressure Stabilization in Older Adults [Hypertension]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005661.short?rss=1</link>
<description><![CDATA[BackgroundImpaired orthostatic blood pressure (BP) stabilization is highly prevalent in older adults and is a predictor of end‐organ injury, falls, and mortality. We sought to characterize the relationship between postural BP responses and the kidney.Methods and ResultsWe performed a cross‐sectional analysis of 4204 participants from The Irish Longitudinal Study on Ageing, a national cohort of community‐dwelling adults aged ≥50 years. Beat‐to‐beat systolic and diastolic BP were measured during a 2‐minute active stand test. The primary predictor was cystatin C estimated glomerular filtration rate (eGFR) categorized as follows (mL/min per 1.73 m2): ≥90 (reference, n=1414); 75 to 89 (n=1379); 60 to 74 (n=942); 45 to 59 (n=337); <45 (n=132). We examined the association between eGFR categories and (1) sustained orthostatic hypotension, defined as a BP drop exceeding consensus thresholds (systolic BP drop ≥20 mm Hg±diastolic BP drop ≥10 mm Hg) at each 10‐second interval from 60 to 110 seconds inclusive; (2) pattern of BP stabilization, characterized as the difference from baseline in mean systolic BP/diastolic BP at 10‐second intervals. The mean age of subjects was 61.6 years; 47% of subjects were male, and the median eGFR was 82 mL/min per 1.73 m2. After multivariable adjustment, participants with eGFR <60 mL/min per 1.73 m2 were approximately twice as likely to have sustained orthostatic hypotension (P=0.008 for trend across eGFR categories). We observed a graded association between eGFR categories and impaired orthostatic BP stabilization, particularly within the first minute of standing.ConclusionsWe report a novel, graded relationship between diminished eGFR and impaired orthostatic BP stabilization. Mapping the postural BP response merits further study in kidney disease as a potential means of identifying those at risk of hypotension‐related events.]]></description>
<dc:creator><![CDATA[Canney, M., O'Connell, M. D. L., Sexton, D. J., O'Leary, N., Kenny, R. A., Little, M. A., O'Seaghdha, C. M.]]></dc:creator>
<dc:date>2017-04-25T16:27:12-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005661</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005661</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Autonomic Nervous System, Nephrology and Kidney, Epidemiology, Blood Pressure]]></dc:subject>
<dc:title><![CDATA[Graded Association Between Kidney Function and Impaired Orthostatic Blood Pressure Stabilization in Older Adults [Hypertension]]]></dc:title>
<prism:publicationDate>2017-04-25</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Hypertension</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005686.short?rss=1">
<title><![CDATA[Effects of Sodium&ndash;Glucose Cotransporter 2 Inhibitors on 24&ndash;Hour Ambulatory Blood Pressure: A Systematic Review and Meta&ndash;Analysis [Systematic Review and Meta-Analysis]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005686.short?rss=1</link>
<description><![CDATA[BackgroundSodium‐glucose cotransporter 2 (SGLT2) inhibitors are a novel class of antihyperglycemic agents that improve glycemic control by increasing glycosuria. Additional benefits beyond glucose lowering include significant improvements in seated clinic blood pressure (BP), partly attributed to their diuretic‐like actions. Less known are the effects of this class on 24‐hour ambulatory BP, which is a better predictor of cardiovascular risk than seated clinic BP.Methods and ResultsWe performed a meta‐analysis of randomized, double‐blind, placebo‐controlled trials to investigate the effects of SGLT2 inhibitors on 24‐hour ambulatory BP. We searched all studies published before August 17, 2016, which reported 24‐hour ambulatory BP data. Mean differences in 24‐hour BP, daytime BP, and nighttime BP were calculated by a random‐effects model. SGLT2 inhibitors significantly reduce 24‐hour ambulatory systolic and diastolic BP by −3.76 mm Hg (95% CI, −4.23 to −2.34; I2=0.99) and −1.83 mm Hg (95% CI, −2.35 to −1.31; I2=0.76), respectively. Significant reductions in daytime and nighttime systolic and diastolic BP were also found. No association between baseline BP or change in body weight were observed.ConclusionsThis meta‐analysis shows that the reduction in 24‐hour ambulatory BP observed with SGLT2 inhibitors is a class effect. The diurnal effect of SGLT2 inhibitors on 24‐hour ambulatory BP may contribute to their favorable effects on cardiovascular outcomes.]]></description>
<dc:creator><![CDATA[Baker, W. L., Buckley, L. F., Kelly, M. S., Bucheit, J. D., Parod, E. D., Brown, R., Carbone, S., Abbate, A., Dixon, D. L.]]></dc:creator>
<dc:date>2017-05-18T05:03:14-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005686</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005686</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Diabetes, Type 2, High Blood Pressure, Hypertension, Meta Analysis]]></dc:subject>
<dc:title><![CDATA[Effects of Sodium&ndash;Glucose Cotransporter 2 Inhibitors on 24&ndash;Hour Ambulatory Blood Pressure: A Systematic Review and Meta&ndash;Analysis [Systematic Review and Meta-Analysis]]]></dc:title>
<prism:publicationDate>2017-05-18</prism:publicationDate>
<prism:section>Systematic Review and Meta&#x2010;Analysis</prism:section>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005735.short?rss=1">
<title><![CDATA[Outcome of Alcohol Septal Ablation in Mildly Symptomatic Patients With Hypertrophic Obstructive Cardiomyopathy: A Long-Term Follow-Up Study Based on the Euro-Alcohol Septal Ablation Registry [Arrhythmia and Electrophysiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005735.short?rss=1</link>
<description><![CDATA[BackgroundThe long‐term efficacy and safety of alcohol septal ablation (ASA) in patients with highly symptomatic hypertrophic obstructive cardiomyopathy has been demonstrated. The aim of this study was to evaluate the long‐term outcomes of mildly symptomatic patients with hypertrophic obstructive cardiomyopathy treated with ASA.Methods and ResultsWe retrospectively evaluated consecutive patients enrolled in the Euro‐ASA registry (1427 patients) and identified 161 patients (53±13 years; 27% women) who were mildly symptomatic (New York Heart Association [NYHA] class II) pre‐ASA. The median (interquartile range) follow‐up was 4.8 (1.7–8.5) years. The clinical outcome was assessed and compared with the age‐ and sex‐matched general population. The 30‐day mortality after ASA was 0.6% and the annual all‐cause mortality rate was 1.7%, which was similar to the age‐ and sex‐matched general population (P=0.62). A total of 141 (88%) patients had resting left ventricular outflow tract gradient at the last clinical checkup ≤30 mm Hg. Obstruction was reduced from 63±32 to 15±19 mm Hg (P<0.01), and the mean NYHA class decreased from 2.0±0 to 1.3±0.1 (P<0.01); 69%, 29%, and 2% of patients were in NYHA class I, II, and III at the last clinical checkup, respectively.ConclusionsMildly symptomatic hypertrophic obstructive cardiomyopathy patients treated with ASA had sustained symptomatic and hemodynamic relief with a low risk of developing severe heart failure. Their survival is comparable to the general population.]]></description>
<dc:creator><![CDATA[Veselka, J., Faber, L., Liebregts, M., Cooper, R., Januska, J., Krejci, J., Bartel, T., Dabrowski, M., Hansen, P. R., Almaas, V. M., Seggewiss, H., Horstkotte, D., Adlova, R., Bundgaard, H., ten Berg, J., Stables, R. H., Jensen, M. K.]]></dc:creator>
<dc:date>2017-05-16T08:51:14-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005735</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005735</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiomyopathy, Percutaneous Coronary Intervention, Mortality/Survival]]></dc:subject>
<dc:title><![CDATA[Outcome of Alcohol Septal Ablation in Mildly Symptomatic Patients With Hypertrophic Obstructive Cardiomyopathy: A Long-Term Follow-Up Study Based on the Euro-Alcohol Septal Ablation Registry [Arrhythmia and Electrophysiology]]]></dc:title>
<prism:publicationDate>2017-05-16</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Arrhythmia and Electrophysiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005764.short?rss=1">
<title><![CDATA[Circulating Levels of Proprotein Convertase Subtilisin/Kexin Type 9 and Arterial Stiffness in a Large Population Sample: Data From the Brisighella Heart Study [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005764.short?rss=1</link>
<description><![CDATA[BackgroundProprotein convertase subtilisin/kexin type 9 (PCSK9) circulating levels are significantly associated with an increased risk of cardiovascular events. This study aimed to evaluate the relationship between circulating levels of PCSK9 and arterial stiffness, an early instrumental biomarker of cardiovascular disease risk, in a large sample of overall healthy participants.Methods and ResultsFrom the historical cohort of the Brisighella Heart Study, after exclusion of active smokers, participants in secondary prevention for cardiovascular disease, and patients in treatment with statins or vasodilating agents, we selected 227 premenopausal women and 193 age‐matched men and 460 postmenopausal women and 416 age‐matched men. In these participants, we evaluated the correlation between PCSK9 plasma circulating levels and pulse wave velocity. Postmenopausal women showed higher PCSK9 levels (309.9±84.1 ng/mL) compared with the other groups (P<0.001). Older men had significant higher levels than younger men (283.2±75.6 versus 260.9±80.4 ng/mL; P=0.008). In the whole sample, pulse wave velocity was predicted mainly by age (B=0.116, 95% CI 0.96–0.127, P<0.001), PCSK9 (B=0.014, 95% CI 0.011–0.016, P<0.001), and serum uric acid (B=0.313, 95% CI 0.024–0.391, P=0.026). Physical activity, low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, and estimated glomerular filtration rate were not associated with pulse wave velocity (P>0.05).By considering the subgroups described, age and PCSK9 levels were mainly associated with pulse wave velocity, which also correlated with serum uric acid in postmenopausal women.ConclusionsIn the Brisighella Heart Study cohort, circulating PCSK9 is significantly related to arterial stiffness, independent of sex and menopausal status in women.]]></description>
<dc:creator><![CDATA[Ruscica, M., Ferri, N., Fogacci, F., Rosticci, M., Botta, M., Marchiano, S., Magni, P., D'Addato, S., Giovannini, M., Borghi, C., Cicero, A. F. G.,  the Brisighella Heart Study Group]]></dc:creator>
<dc:date>2017-05-03T10:52:27-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005764</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005764</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Primary Prevention, Risk Factors, Women]]></dc:subject>
<dc:title><![CDATA[Circulating Levels of Proprotein Convertase Subtilisin/Kexin Type 9 and Arterial Stiffness in a Large Population Sample: Data From the Brisighella Heart Study [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-03</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005771.short?rss=1">
<title><![CDATA[Intracoronary Administration of Allogeneic Adipose Tissue-Derived Mesenchymal Stem Cells Improves Myocardial Perfusion But Not Left Ventricle Function, in a Translational Model of Acute Myocardial Infarction [Coronary Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005771.short?rss=1</link>
<description><![CDATA[BackgroundAutologous adipose tissue–derived mesenchymal stem cells (ATMSCs) therapy is a promising strategy to improve post–myocardial infarction outcomes. In a porcine model of acute myocardial infarction, we studied the long‐term effects and the mechanisms involved in allogeneic ATMSCs administration on myocardial performance.Methods and ResultsThirty‐eight pigs underwent 50 minutes of coronary occlusion; the study was completed in 33 pigs. After reperfusion, allogeneic ATMSCs or culture medium (vehicle) were intracoronarily administered. Follow‐ups were performed at short (2 days after acute myocardial infarction vehicle‐treated, n=10; ATMSCs‐treated, n=9) or long term (60 days after acute myocardial infarction vehicle‐treated, n=7; ATMSCs‐treated, n=7). At short term, infarcted myocardium analysis showed reduced apoptosis in the ATMSCs‐treated animals (48.6±6% versus 55.9±5.7% in vehicle; P=0.017); enhancement of the reparative process with up‐regulated vascular endothelial growth factor, granulocyte macrophage colony‐stimulating factor, and stromal‐derived factor‐1α gene expression; and increased M2 macrophages (67.2±10% versus 54.7±10.2% in vehicle; P=0.016). In long‐term groups, increase in myocardial perfusion at the anterior infarct border was observed both on day‐7 and day‐60 cardiac magnetic resonance studies in ATMSCs‐treated animals, compared to vehicle (87.9±28.7 versus 57.4±17.7 mL/min per gram at 7 days; P=0.034 and 99±22.6 versus 43.3±14.7 22.6 mL/min per gram at 60 days; P=0.0001, respectively). At day 60, higher vascular density was detected at the border zone in the ATMSCs‐treated animals (118±18 versus 92.4±24.3 vessels/mm2 in vehicle; P=0.045). Cardiac magnetic resonance–measured left ventricular ejection fraction of left ventricular volumes was not different between groups at any time point.ConclusionsIn this porcine acute myocardial infarction model, allogeneic ATMSCs‐based therapy was associated with increased cardioprotective and reparative mechanisms and with better cardiac magnetic resonance–measured perfusion. No effect on left ventricular volumes or ejection fraction was observed.]]></description>
<dc:creator><![CDATA[Bobi, J., Solanes, N., Fernandez-Jimenez, R., Galan-Arriola, C., Dantas, A. P., Fernandez-Friera, L., Galvez-Monton, C., Rigol-Monzo, E., Aguero, J., Ramirez, J., Roque, M., Bayes-Genis, A., Sanchez-Gonzalez, J., Garcia-Alvarez, A., Sabate, M., Roura, S., Ibanez, B., Rigol, M.]]></dc:creator>
<dc:date>2017-05-03T03:00:22-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005771</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005771</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cell Therapy, Stem Cells, Translational Studies, Myocardial Infarction]]></dc:subject>
<dc:title><![CDATA[Intracoronary Administration of Allogeneic Adipose Tissue-Derived Mesenchymal Stem Cells Improves Myocardial Perfusion But Not Left Ventricle Function, in a Translational Model of Acute Myocardial Infarction [Coronary Heart Disease]]]></dc:title>
<prism:publicationDate>2017-05-03</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Coronary Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005772.short?rss=1">
<title><![CDATA[Force-Sensing Catheters During Pediatric Radiofrequency Ablation: The FEDERATION Study [Pediatric Cardiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005772.short?rss=1</link>
<description><![CDATA[BackgroundBased on data from studies of atrial fibrillation ablations, optimal parameters for the TactiCath (TC; St. Jude Medical, Inc) force‐sensing ablation catheter are a contact force of 20 g and a force‐time integral of 400 g·s for the creation of transmural lesions. We aimed to evaluate TC in pediatric and congenital heart disease patients undergoing ablation.Methods and ResultsComprehensive chart and case reviews were performed from June 2015 to March 2016. Of the 102 patients undergoing electrophysiology study plus ablation, 58 (57%) underwent ablation initially with a force‐sensing catheter. Patients had an average age of 14 (2.4–23) years and weight of 58 (18–195) kg with 15 patients having abnormal cardiac anatomy. Electrophysiology diagnoses for the +TC group included 30 accessory pathway–mediated tachycardia, 24 atrioventricular nodal reentrant tachycardia, and 7 other. Baseline generator settings included a power of 20 W, temperature of 40°, and 6 cc/min flow during lesion creation with 11 patients (19%) having alterations to parameters. Seventeen patients (30%) converted to an alternate ablation source. A total of 516 lesions were performed using the TC with a median contact force of 6 g, force‐time integral of 149 g·s, and lesion size index of 3.3. Median‐term follow‐up demonstrated 5 (10%) recurrences with no acute or median‐term complications.ConclusionsTactiCath can be effectively employed in the treatment of pediatric patients with congenital heart disease with lower forces than previously described in the atrial fibrillation literature. Patients with atrioventricular nodal reentrant tachycardia or atrioventricular reciprocating tachycardia may not require transmural lesions and the TC may provide surrogate markers for success during slow pathway ablation.]]></description>
<dc:creator><![CDATA[Dalal, A. S., Nguyen, H. H., Bowman, T., Van Hare, G. F., Avari Silva, J. N.]]></dc:creator>
<dc:date>2017-05-17T13:24:40-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005772</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005772</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Arrhythmias, Catheter Ablation and Implantable Cardioverter-Defibrillator, Electrophysiology]]></dc:subject>
<dc:title><![CDATA[Force-Sensing Catheters During Pediatric Radiofrequency Ablation: The FEDERATION Study [Pediatric Cardiology]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Pediatric Cardiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005773.short?rss=1">
<title><![CDATA[Merits of Invasive Strategy in Diabetic Patients With Non-ST Elevation Acute Coronary Syndrome [Editorials]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005773.short?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Jneid, H.]]></dc:creator>
<dc:date>2017-05-20T13:51:11-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005773</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005773</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Percutaneous Coronary Intervention, Revascularization, Treatment, Mortality/Survival, Quality and Outcomes]]></dc:subject>
<dc:title><![CDATA[Merits of Invasive Strategy in Diabetic Patients With Non-ST Elevation Acute Coronary Syndrome [Editorials]]]></dc:title>
<prism:publicationDate>2017-05-20</prism:publicationDate>
<prism:section>Editorial</prism:section>
<prism:subsection1>Editorials</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005795.short?rss=1">
<title><![CDATA[Risk of Ischemic Stroke Associated With Calcium Supplements With or Without Vitamin D: A Nested Case-Control Study [Stroke]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005795.short?rss=1</link>
<description><![CDATA[BackgroundThere is controversy surrounding the risk of ischemic stroke associated with the use of calcium supplements either in monotherapy or in combination with vitamin D.Methods and ResultsA nested case‐control study was performed with patients aged 40 to 89 years old, among whom a total of 2690 patients had a first episode of nonfatal ischemic stroke and for which 19 538 controls were randomly selected from the source population and frequency‐matched with cases for age, sex, and calendar year. Logistic regression provided the odds ratios while adjusting for confounding factors. A sensitivity analysis was performed by restricting to patients who were new users of calcium supplements as either monotherapy or with vitamin D. Calcium supplementation with vitamin D was not associated with an increased risk of ischemic stroke (odds ratio 0.85; 95% confidence interval, 0.67–1.08) in the population as a whole or under any of the conditions examined (dose, duration, background cardiovascular risk, sex, or age). Calcium supplement monotherapy was not associated with an increased risk in the population as a whole (odds ratio 1.18; 95% confidence interval, 0.86–1.61), although a significant increased risk at high doses (≥1000 mg/day: odds ratio 2.09; 95% confidence interval, 1.25–3.49; <1000 mg: odds ratio 0.76; 95% confidence interval, 0.45–1.26) compared with nonuse was observed. The sensitivity analysis did not affect the inferences, with similar results observed among new users as to the overall study population.ConclusionsThis study suggests that calcium supplements given as monotherapy at high doses may increase the risk of ischemic stroke, whereas their combination with vitamin D seems to offset this hazard.]]></description>
<dc:creator><![CDATA[de Aba&#x0237;o, F. J., Rodriguez-Martin, S., Rodriguez-Miguel, A., Gil, M. J.]]></dc:creator>
<dc:date>2017-05-18T03:03:03-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005795</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005795</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cerebrovascular Disease/Stroke, Ischemic Stroke]]></dc:subject>
<dc:title><![CDATA[Risk of Ischemic Stroke Associated With Calcium Supplements With or Without Vitamin D: A Nested Case-Control Study [Stroke]]]></dc:title>
<prism:publicationDate>2017-05-18</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Stroke</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005868.short?rss=1">
<title><![CDATA[Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST-Segment Elevation Myocardial Infarction [Coronary Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005868.short?rss=1</link>
<description><![CDATA[BackgroundPlaque erosion causes 30% of ST‐segment elevation myocardial infarctions, but the underlying cause is unknown. Inflammatory infiltrates are less abundant in erosion compared with rupture in autopsy studies. We hypothesized that erosion and rupture are associated with significant differences in intracoronary cytokines in vivo.Methods and ResultsForty ST‐segment elevation myocardial infarction patients with <6 hours of chest pain were classified as ruptured fibrous cap (RFC) or intact fibrous cap (IFC) using optical coherence tomography. Plasma samples from the infarct‐related artery and a peripheral artery were analyzed for expression of 102 cytokines using arrays; results were confirmed with ELISA. Thrombectomy samples were analyzed for differential mRNA expression using quantitative real‐time polymerase chain reaction. Twenty‐three lesions were classified as RFC (58%), 15 as IFC (38%), and 2 were undefined (4%). In addition, 12% (12 of 102) of cytokines were differentially expressed in both coronary and peripheral plasma. I‐TAC was preferentially expressed in RFC (significance analysis of microarrays adjusted P<0.001; ELISA IFC 10.2 versus RFC 10.8 log2 pg/mL; P=0.042). IFC was associated with preferential expression of epidermal growth factor (significance analysis of microarrays adjusted P<0.001; ELISA IFC 7.42 versus RFC 6.63 log2 pg/mL, P=0.036) and thrombospondin 1 (significance analysis of microarrays adjusted P=0.03; ELISA IFC 10.4 versus RFC 8.65 log2 ng/mL, P=0.0041). Thrombectomy mRNA showed elevated I‐TAC in RFC (P=0.0007) epidermal growth factor expression in IFC (P=0.0264) but no differences in expression of thrombospondin 1.ConclusionsThese results demonstrate differential intracoronary cytokine expression in RFC and IFC. Elevated thrombospondin 1 and epidermal growth factor may play an etiological role in erosion.]]></description>
<dc:creator><![CDATA[Chandran, S., Watkins, J., Abdul-Aziz, A., Shafat, M., Calvert, P. A., Bowles, K. M., Flather, M. D., Rushworth, S. A., Ryding, A. D.]]></dc:creator>
<dc:date>2017-05-03T08:55:47-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005868</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005868</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Biomarkers, Inflammation, Myocardial Infarction, Optical Coherence Tomography (OCT), Percutaneous Coronary Intervention]]></dc:subject>
<dc:title><![CDATA[Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST-Segment Elevation Myocardial Infarction [Coronary Heart Disease]]]></dc:title>
<prism:publicationDate>2017-05-03</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Coronary Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005879.short?rss=1">
<title><![CDATA[Pulse Wave Velocity Predicts Response to Renal Denervation in Isolated Systolic Hypertension [Hypertension]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005879.short?rss=1</link>
<description><![CDATA[BackgroundRenal sympathetic denervation seems to be less effective as a treatment for hypertension in patients with isolated systolic hypertension, a condition associated with elevated central arterial stiffness. Because isolated systolic hypertension can also be caused by wave reflection or increased cardiac output, a more differentiated approach might improve patient preselection for renal sympathetic denervation. We sought to evaluate the additional predictive value of invasive pulse wave velocity for response to renal sympathetic denervation in patients with combined versus isolated systolic hypertension.Methods and ResultsPatients scheduled for renal sympathetic denervation underwent additional invasive measurement of pulse wave velocity and pulse pressure before denervation. Blood pressure was assessed via ambulatory measurement at baseline and after 3 months. In total 109 patients (40 patients with isolated systolic hypertension) were included in our analysis. After 3 months, blood pressure reduction was more pronounced among patients with combined hypertension compared with patients with isolated systolic hypertension (systolic 24‐hour average 9.3±10.5 versus 5.0±11.5 mm Hg, P=0.046). However, when stratifying patients with isolated systolic hypertension by invasive pulse wave velocity, patients in the lowest tertile of pulse wave velocity had comparable blood pressure reduction (12.1±12.6 mm Hg, P=0.006) despite lower baseline blood pressure than patients with combined hypertension (systolic 24‐hour average 154.8±12.5 mm Hg in combined hypertension versus 141.2±8.1, 148.4±10.9, and 150.5±12.7 mm Hg, respectively, by tertiles of pulse wave velocity, P=0.002).ConclusionsExtended assessment of arterial stiffness can help improve patient preselection for renal sympathetic denervation and identify a subgroup of isolated systolic hypertension patients who benefit from sympathetic modulation.]]></description>
<dc:creator><![CDATA[Fengler, K., Rommel, K.-P., Hoellriegel, R., Blazek, S., Besler, C., Desch, S., Schuler, G., Linke, A., Lurz, P.]]></dc:creator>
<dc:date>2017-05-17T09:43:36-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005879</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005879</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[High Blood Pressure, Treatment]]></dc:subject>
<dc:title><![CDATA[Pulse Wave Velocity Predicts Response to Renal Denervation in Isolated Systolic Hypertension [Hypertension]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Hypertension</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005894.short?rss=1">
<title><![CDATA[Randomized Trial Comparing the Effects of Ticagrelor Versus Clopidogrel on Myocardial Perfusion in Patients With Coronary Artery Disease [Coronary Heart Disease]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005894.short?rss=1</link>
<description><![CDATA[BackgroundTicagrelor is a P2Y12 receptor inhibitor used in acute coronary syndromes to reduce platelet activity and to decrease thrombus formation. Ticagrelor is associated with a reduction in mortality incremental to that observed with clopidogrel, potentially related to its non–antiplatelet effects. Evidence from animal models indicates that ticagrelor potentiates adenosine‐induced myocardial blood flow (MBF) increases. We investigated MBF at rest and during adenosine‐induced hyperemia in patients with stable coronary artery disease treated with ticagrelor versus clopidogrel.Methods and ResultsThis randomized double‐blinded crossover study included 22 patients who received therapeutic interventions of ticagrelor 90 mg orally twice a day for 10 days and clopidogrel 75 mg orally once a day for 10 days, with a washout period of at least 10 days between the treatments. Global and regional MBF and myocardial flow reserve were measured using rubidium 82 positron emission tomography/computed tomography at baseline and during intermediate‐ and high‐dose adenosine. Global MBF was significantly greater with ticagrelor versus clopidogrel (1.28±0.55 versus 1.13±0.47 mL/min per gram, P=0.002) at intermediate‐dose adenosine and not different at baseline (0.65±0.19 versus 0.60±0.15 mL/min per gram, P=0.084) and at high‐dose adenosine (1.64±0.40 versus 1.61±0.19 mL/min per gram, P=0.53). In regions with impaired myocardial flow reserve (<2.5), MBF was greater with ticagrelor compared with clopidogrel during intermediate and high doses of adenosine (P<0.0001), whereas the differences were not significant at baseline.ConclusionsTicagrelor potentiates global and regional adenosine‐induced MBF increases in patients with stable coronary artery disease. This effect may contribute to the incremental mortality benefit compared with clopidogrel.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT01894789.]]></description>
<dc:creator><![CDATA[Pelletier-Galarneau, M., Hunter, C. R. R. N., Ascah, K. J., Beanlands, R. S. B., Dwivedi, G., deKemp, R. A., Chow, B. J. W., Ruddy, T. D.]]></dc:creator>
<dc:date>2017-05-02T07:08:23-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005894</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005894</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Coronary Circulation, Clinical Studies, Nuclear Cardiology and PET, Coronary Artery Disease]]></dc:subject>
<dc:title><![CDATA[Randomized Trial Comparing the Effects of Ticagrelor Versus Clopidogrel on Myocardial Perfusion in Patients With Coronary Artery Disease [Coronary Heart Disease]]]></dc:title>
<prism:publicationDate>2017-05-02</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Coronary Heart Disease</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005908.short?rss=1">
<title><![CDATA[Weekday and Survival After Cardiac Surgery&#x2014;A Swedish Nationwide Cohort Study in 106 473 Patients [Cardiovascular Surgery]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005908.short?rss=1</link>
<description><![CDATA[BackgroundThe purpose of this study was to investigate the association between weekday of surgery and survival following cardiac surgery.Methods and ResultsIn a nationwide cohort study, we included all patients who underwent cardiac surgery in 1999–2013 from the SWEDEHEART (Swedish Web‐system for Enhancement and Development of Evidence‐based care in Heart disease Evaluated According to Recommended Therapies) register. All‐cause mortality until March 2014 was obtained from national registers. The association between weekday of surgery and mortality was estimated using Cox regression, and reported as hazard ratios with 95% CI. We used the restricted mean survival time difference to estimate loss of life related to weekday of surgery. Among 106 473 patients, 25 221 (24%), 24 471 (23%), 22 977 (22%), 20 189 (19%), 9251 (8.7%), and 4364 (4.1%) underwent surgery during a Monday, Tuesday, Wednesday, Thursday, Friday, and a Saturday/Sunday, respectively. More patients were operated on urgently during Friday to Sunday, and unadjusted analyses showed higher early and late mortality in those patients. The adjusted hazard ratios (95% CI) were 1.00 (0.89–1.13), 1.00 (0.88–1.12), 1.02 (0.90–1.16), 1.17 (1.01–1.37), and 1.05 (0.86–1.29) in patients who underwent surgery during a Tuesday, Wednesday, Thursday, Friday, and Saturday/Sunday compared to a Monday, after 1 year of follow‐up conditional on 30‐day survival. In elective surgery (n=46 146), the 1‐year restricted mean survival time difference (95% CI) was −0.5 (−1.8–0.8), −0.5 (−1.9–0.8), −1.0 (−2.6–0.5), 0.02 (−2.2–2.3), and −1.2 (−6.3–3.9) days in patients who underwent surgery during a Tuesday, Wednesday, Thursday, Friday, and a Saturday/Sunday, respectively, compared to a Monday.ConclusionsWe found no evidence of a clinically relevant weekday effect in patents who underwent cardiac surgery in Sweden during a 15‐year period. These data suggest that the early risk and long‐term prognosis following cardiac surgery was not affected by the weekday of surgery.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT02276950.]]></description>
<dc:creator><![CDATA[Dalen, M., Edgren, G., Ivert, T., Holzmann, M. J., Sartipy, U.]]></dc:creator>
<dc:date>2017-05-16T10:05:35-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005908</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005908</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Cardiovascular Surgery, Mortality/Survival, Quality and Outcomes]]></dc:subject>
<dc:title><![CDATA[Weekday and Survival After Cardiac Surgery&#x2014;A Swedish Nationwide Cohort Study in 106 473 Patients [Cardiovascular Surgery]]]></dc:title>
<prism:publicationDate>2017-05-16</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Cardiovascular Surgery</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e005945.short?rss=1">
<title><![CDATA[Alogliptin, a Dipeptidyl Peptidase-4 Inhibitor, Alleviates Atrial Remodeling and Improves Mitochondrial Function and Biogenesis in Diabetic Rabbits [Arrhythmia and Electrophysiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e005945.short?rss=1</link>
<description><![CDATA[BackgroundThere is increasing evidence implicating atrial mitochondrial dysfunction in the pathogenesis of atrial fibrillation. In this study, we explored whether alogliptin, a dipeptidyl peptidase‐4 inhibitor, can prevent mitochondrial dysfunction and atrial remodeling in a diabetic rabbit model.Methods and ResultsA total of 90 rabbits were randomized into 3 groups as follows: control group (n=30), alloxan‐induced diabetes mellitus group (n=30), and alogliptin‐treated (12.5 mg/kg per day for 8 weeks) diabetes mellitus group (n=30). Echocardiographic and hemodynamic assessments were performed in vivo. The serum concentrations of glucagon‐like peptide‐1, insulin, and inflammatory and oxidative stress markers were measured. Electrophysiological properties of Langendorff‐perfused rabbit hearts were assessed. Mitochondrial morphology, respiratory function, membrane potential, and reactive oxygen species generation rate were assessed. The protein expression of transforming growth factor β1, nuclear factor κB p65, and mitochondrial biogenesis–related proteins were measured by Western blot analysis. Diabetic rabbits exhibited left ventricular hypertrophy and left atrial dilation without obvious hemodynamic abnormalities, and all of these changes were attenuated by alogliptin. Compared with the control group, higher atrial fibrillation inducibility in the diabetes mellitus group was observed, and markedly reduced by alogliptin. Alogliptin decreased mitochondrial reactive oxygen species production rate, prevented mitochondrial membrane depolarization, and alleviated mitochondrial swelling in diabetic rabbits. It also improved mitochondrial biogenesis by peroxisome proliferator–activated receptor‐γ coactivator 1α/nuclear respiratory factor‐1/mitochondrial transcription factor A signaling regulated by adiponectin/AMP‐activated protein kinase.ConclusionsDipeptidyl peptidase‐4 inhibitors can prevent atrial fibrillation by reversing electrophysiological abnormalities, improving mitochondrial function, and promoting mitochondrial biogenesis.]]></description>
<dc:creator><![CDATA[Zhang, X., Zhang, Z., Zhao, Y., Jiang, N., Qiu, J., Yang, Y., Li, J., Liang, X., Wang, X., Tse, G., Li, G., Liu, T.]]></dc:creator>
<dc:date>2017-05-15T11:24:40-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.005945</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.005945</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Arrhythmias, Electrophysiology]]></dc:subject>
<dc:title><![CDATA[Alogliptin, a Dipeptidyl Peptidase-4 Inhibitor, Alleviates Atrial Remodeling and Improves Mitochondrial Function and Biogenesis in Diabetic Rabbits [Arrhythmia and Electrophysiology]]]></dc:title>
<prism:publicationDate>2017-05-15</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Arrhythmia and Electrophysiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e006021.short?rss=1">
<title><![CDATA[Million Hearts: Description of the National Surveillance and Modeling Methodology Used to Monitor the Number of Cardiovascular Events Prevented During 2012-2016 [Epidemiology]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e006021.short?rss=1</link>
<description><![CDATA[BackgroundThis study describes the national surveillance and modeling methodology developed to monitor achievement of the Million Hearts initiative's aim of preventing 1 million acute myocardial infarctions, strokes, and other related cardiovascular events during 2012–2016.Methods and ResultsWe calculate sex‐ and age‐specific cardiovascular event rates (combination of emergency department, hospitalization, and death events) among US adults aged ≥18 from 2006 to 2011 and, based on log‐linear models fitted to the rates, calculate their annual percent change. We describe 2 baseline strategies to be used to compare observed versus expected event totals during 2012–2016: (1) stable baselines assume no rate changes, with modeled 2011 rates held constant through 2016; and (2) trend baselines assume 2006–2011 rate trends will continue, with the annual percent changes applied to the modeled 2011 rates to calculate expected 2012–2016 rates. Events prevented estimates during 2012–2013 were calculated using available data: 115 210 (95% CI, 60 858, 169 562) events were prevented using stable baselines and an excess of 43 934 (95% CI, −14 264, 102 132) events occurred using trend baselines. Women aged ≥75 had the most events prevented (stable, 76 242 [42 067, 110 417]; trend, 39 049 [1901, 76 197]). Men aged 45 to 64 had the greatest number of excess events (stable, 22 912 [95% CI, 855, 44 969]; trend, 38 810 [95% CI, 15 567, 62 053]).ConclusionsAround 115 000 events were prevented during the initiative's first 2 years compared with what would have occurred had 2011 rates remained stable. Recent flattening or reversals in some event rate trends were observed supporting intensifying national action to prevent cardiovascular events.]]></description>
<dc:creator><![CDATA[Ritchey, M. D., Loustalot, F., Wall, H. K., Steiner, C. A., Gillespie, C., George, M. G., Wright, J. S.]]></dc:creator>
<dc:date>2017-05-02T13:00:21-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.006021</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.006021</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Myocardial Infarction, Mortality/Survival, Quality and Outcomes, Cerebrovascular Disease/Stroke]]></dc:subject>
<dc:title><![CDATA[Million Hearts: Description of the National Surveillance and Modeling Methodology Used to Monitor the Number of Cardiovascular Events Prevented During 2012-2016 [Epidemiology]]]></dc:title>
<prism:publicationDate>2017-05-02</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Epidemiology</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e006124.short?rss=1">
<title><![CDATA[Cardiopulmonary Resuscitation Training Disparities in the United States [Resuscitation Science]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e006124.short?rss=1</link>
<description><![CDATA[BackgroundBystander cardiopulmonary resuscitation (CPR) is associated with increased survival from cardiac arrest, yet bystander CPR rates are low in many communities. The overall prevalence of CPR training in the United States and associated individual‐level disparities are unknown. We sought to measure the national prevalence of CPR training and hypothesized that older age and lower socioeconomic status would be independently associated with a lower likelihood of CPR training.Methods and ResultsWe administered a cross‐sectional telephone survey to a nationally representative adult sample. We assessed the demographics of individuals trained in CPR within 2 years (currently trained) and those who had been trained in CPR at some point in time (ever trained). The association of CPR training and demographic variables were tested using survey weighted logistic regression. Between September 2015 and November 2015, 9022 individuals completed the survey; 18% reported being currently trained in CPR, and 65% reported training at some point previously. For each year of increased age, the likelihood of being currently CPR trained or ever trained decreased (currently trained: odds ratio, 0.98; 95% CI, 0.97–0.99; P<0.01; ever trained: OR, 0.99; 95% CI, 0.98–0.99; P=0.04). Furthermore, there was a greater then 4‐fold difference in odds of being currently CPR trained from the 30–39 to 70–79 year old age groups (95% CI, 0.10–0.23). Factors associated with a lower likelihood of CPR training were lesser educational attainment and lower household income (P<0.01 for each of these variables).ConclusionsA minority of respondents reported current training in CPR. Older age, lesser education, and lower income were associated with reduced likelihood of CPR training. These findings illustrate important gaps in US CPR education and suggest the need to develop tailored CPR training efforts to address this variability.]]></description>
<dc:creator><![CDATA[Blewer, A. L., Ibrahim, S. A., Leary, M., Dutwin, D., McNally, B., Anderson, M. L., Morrison, L. J., Aufderheide, T. P., Daya, M., Idris, A. H., Callaway, C. W., Kudenchuk, P. J., Vilke, G. M., Abella, B. S.]]></dc:creator>
<dc:date>2017-05-17T13:43:00-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.006124</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.006124</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiopulmonary Resuscitation and Emergency Cardiac Care]]></dc:subject>
<dc:title><![CDATA[Cardiopulmonary Resuscitation Training Disparities in the United States [Resuscitation Science]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Resuscitation Science</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e006167.short?rss=1">
<title><![CDATA[Systolic Blood Pressure Within 24 Hours After Thrombectomy for Acute Ischemic Stroke Correlates With Outcome [Stroke]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e006167.short?rss=1</link>
<description><![CDATA[BackgroundCurrent guidelines suggest treating blood pressure above 180/105 mm Hg during the first 24 hours in patients with acute ischemic stroke undergoing any form of recanalization therapy. Currently, no studies exist to guide blood pressure management in patients with stroke treated specifically with mechanical thrombectomy. We aimed to determine the association between blood pressure parameters within the first 24 hours after mechanical thrombectomy and patient outcomes.Methods and ResultsWe retrospectively studied a consecutive sample of adult patients who underwent mechanical thrombectomy for acute ischemic stroke of the anterior cerebral circulation at 3 institutions from March 2015 to October 2016. We collected the values of maximum, minimum, and average values of systolic blood pressure, diastolic blood pressure, and mean arterial pressures in the first 24 hours after mechanical thrombectomy. Primary and secondary outcomes were patients’ functional status at 90 days measured on the modified Rankin scale and the incidence and severity of intracranial hemorrhages within 48 hours. Associations were explored using an ordered multivariable logistic regression analyses. A total of 228 patients were included (mean age 65.8±14.3; 104 males, 45.6%). Maximum systolic blood pressure independently correlated with a worse 90‐day modified Rankin scale and hemorrhagic complications within 48 hours (adjusted odds ratio=1.02 [1.01–1.03], P=0.004; 1.02 [1.01–1.04], P=0.002; respectively) in multivariable analyses, after adjusting for several possible confounders.ConclusionsHigher peak values of systolic blood pressure independently correlated with worse 90‐day modified Rankin scale and a higher rate of hemorrhagic complications. Further prospective studies are warranted to identify whether systolic blood pressure is a therapeutic target to improve outcomes.]]></description>
<dc:creator><![CDATA[Mistry, E. A., Mistry, A. M., Nakawah, M. O., Khattar, N. K., Fortuny, E. M., Cruz, A. S., Froehler, M. T., Chitale, R. V., James, R. F., Fusco, M. R., Volpi, J. J.]]></dc:creator>
<dc:date>2017-05-18T04:03:00-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.006167</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.006167</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[High Blood Pressure, Revascularization, Complications, Quality and Outcomes, Ischemic Stroke]]></dc:subject>
<dc:title><![CDATA[Systolic Blood Pressure Within 24 Hours After Thrombectomy for Acute Ischemic Stroke Correlates With Outcome [Stroke]]]></dc:title>
<prism:publicationDate>2017-05-18</prism:publicationDate>
<prism:section>Original Research</prism:section>
<prism:subsection1>Stroke</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e006291.short?rss=1">
<title><![CDATA[Myocardial Metabolism Under Control of a Cytokine Receptor [Editorials]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e006291.short?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ramos, G., Frantz, S.]]></dc:creator>
<dc:date>2017-05-20T13:51:11-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.006291</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.006291</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Basic Science Research, Inflammation, Metabolism, Myocardial Biology]]></dc:subject>
<dc:title><![CDATA[Myocardial Metabolism Under Control of a Cytokine Receptor [Editorials]]]></dc:title>
<prism:publicationDate>2017-05-20</prism:publicationDate>
<prism:section>Editorial</prism:section>
<prism:subsection1>Editorials</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e006292.short?rss=1">
<title><![CDATA[How Symptomatic Should a Hypertrophic Obstructive Cardiomyopathy Patient Be to Consider Alcohol Septal Ablation? [Editorials]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e006292.short?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Jones, B. M., Krishnaswamy, A., Smedira, N. G., Desai, M. Y., Tuzcu, E. M., Kapadia, S. R.]]></dc:creator>
<dc:date>2017-05-16T08:51:14-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.006292</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.006292</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Cardiomyopathy, Hypertrophy, Catheter-Based Coronary and Valvular Interventions, Percutaneous Coronary Intervention]]></dc:subject>
<dc:title><![CDATA[How Symptomatic Should a Hypertrophic Obstructive Cardiomyopathy Patient Be to Consider Alcohol Septal Ablation? [Editorials]]]></dc:title>
<prism:publicationDate>2017-05-16</prism:publicationDate>
<prism:section>Editorial</prism:section>
<prism:subsection1>Editorials</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
<item rdf:about="http://jaha.ahajournals.org/content/6/5/e006293.short?rss=1">
<title><![CDATA[Venous Thromboembolism Risk With Antidepressants: Driven by Disease or Drugs? [Editorials]]]></title>
<link>http://jaha.ahajournals.org/content/6/5/e006293.short?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Branchford, B. R.]]></dc:creator>
<dc:date>2017-05-17T05:47:19-07:00</dc:date>
<dc:identifier>info:doi/10.1161/JAHA.117.006293</dc:identifier>
<dc:identifier>hwp:master-id:ahaoa;JAHA.117.006293</dc:identifier>
<dc:publisher>American Heart Association</dc:publisher>
<dc:subject><![CDATA[Clinical Studies, Epidemiology, Mental Health, Thrombosis]]></dc:subject>
<dc:title><![CDATA[Venous Thromboembolism Risk With Antidepressants: Driven by Disease or Drugs? [Editorials]]]></dc:title>
<prism:publicationDate>2017-05-17</prism:publicationDate>
<prism:section>Editorial</prism:section>
<prism:subsection1>Editorials</prism:subsection1>
<prism:volume>6</prism:volume>
<prism:number>5</prism:number>
</item>
</rdf:RDF>