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2010-04-06T10:52:00.007-08:00

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Mini Heart Attacks Lessen Damage From Major Ones

2008-12-05T10:59:00.003-09:00

Mini Heart Attacks Lessen Damage From Major Ones

ScienceDaily (Dec. 3, 2008) — Researchers have discovered one potential mechanism by which briefly cutting off, then restoring, blood flow to arteries prior to a heart attack lessens the damage caused, according to a study published today in the journal Cardiovascular Research. The new mechanism points to how future drugs could provide protection ahead of heart attacks and strokes for those at highest risk.

In the nearer term, the work may help to prevent damage caused as U.S. heart surgeons temporarily cut off blood flow 450,000 times each year to perform coronary artery bypass graft surgeries. Lastly, the discoveries hold clues to the value of the Mediterranean diet beyond red wine.

In severely diseased coronary arteries, fatty deposits in blood vessel walls become more likely to rupture, which releases proteins into the blood that cause blood clots and cut off blood flow. When a vessel becomes completely blocked (ischemia) the downstream tissue begins to die for lack of oxygen and nutrients. Worse yet, when blood flow is restored (reperfusion), the returning blood throws off cellular chemistry, creating as a side-product a burst of highly reactive "free radicals" that tear apart cell components and cause cells to self-destruct. Later in the process, the immune system attacks the cardiac tissue damaged by ischemia and reperfusion, causing inflammation which can lead to heart failure.

In 1986 then medical student Chuck Murry at Duke University first described a technique called ischemic preconditioning (IPC), which quickly cuts off then restores blood flow to the heart. He found that IPC somehow protected heart tissue against the damage caused by subsequent, prolonged blood vessel blockages. An emerging theory holds that this natural early warning system of IPC has evolved to protect against heart attack. Labs worldwide are seeking to re-create or strengthen this natural protection against ischemia/reperfusion (IR) injury. In the current study, researchers for the first time determined that IPC caused more of a key molecule, nitro-linoleic acid (LNO2), to be made in ischemic cells.

"LNO2 appears to be important in the mechanism by which IPC triggers the body's natural defense mechanisms against heart attack before the major attack comes," said Paul S. Brookes, Ph.D., associate professor of Anesthesiology and of Pharmacology and Physiology at the University of Rochester Medical Center. "Obviously, this natural response, when it follows a major heart attack, is often too little too late. Our hope is that boosting the effect in patients at high risk, perhaps by administering LNO2 beforehand, will reduce heart attack damage in the future. Even sooner, we may be able dramatically reduce reperfusion injury suffered in surgical settings."

Study Details

Going into the study, the mechanisms underlying IPC protection were controversial, but a consensus had emerged recently that mitochondria were involved. The cell's powerhouse, mitochondria use oxygen to convert nutrients into cellular energy supply.

As they do so, they create a gradient of protons across their membranes. When the gradient becomes too large, it triggers the mitochondria to use oxygen to generate free radicals. The problem gets much worse when blood returns to a vessel after a blockage, bringing with it a surge of oxygen and nutrients.

It has long been thought that a group of proteins in the mitochondrial membrane act as a "safety valve" by dissipating too large proton gradients when necessary, which slows free radical generation. The current study identified a novel mechanism involving LNO2, by which IPC turns on this safety valve.

Given their results, the authors propose the following protective mechanism: temporary ischemia causes the generation of nitrated lipids inside the mitochondria via currently unknown mechanisms involving metabolites of the gas nitric oxide (NO). These lipids, including LNO2, then become attached to two proteins – adenine nucleotide translocase and uncoupling protein 2 – changing their shape such that they allow a proton leak across the mitochondrial membrane. The leak lowers the proton gradient just enough to lessen free radical production.

While the current study only looked at the immediate effects of LNO2 treatment, the literature suggests that LNO2 also limits the misplaced immune response seen after reperfusion, suggesting a dual treatment effect. Past studies found that LNO2 inhibits Nfkappa B, a protein known to switch on genes that drive inflammation. LNO2 also activates peroxisome proliferator activated receptor gamma and heme oxygenase 1, both of which block inflammation.

The major finding of the study is that LNO2 is formed naturally in mitochondria during IPC in an isolated rat heart, and that adding extra LNO2 protects heart muscle cells from IR injury. The team measured the ability of isolated rat heart cells to survive ischemia using a dye that the live cells keep out, but that dead cells take in. That enabled researchers to count how many cells survived with and without LNO2 added.

In normal cells following ischemia 70 percent died, but for those receiving extra LNO2 (0.5 micromolar), only 30 percent died. The amount of the LNO2 added was not much more than naturally occurs, suggesting its effect is "extremely potent," researchers said. The LNO2-related proton leak also occurs at the protein level within seconds, a vital quality of any future therapy, considering that IR injury greatly increases with each second it is allowed to proceed.

Brookes is part of the Mitochondrial Research & Innovation Group (MRIG) at the Medical Center, which last year reported in the Journal of Molecular and Cellular Cardiology on the design and testing of a series of patented nitric oxide donors that break down and release NO only within the mitochondria, and protect the heart from ischemia. The team believes these NO donors may work in part by increasing LNO2 supply. In the acute setting, such drugs may offer an advantage over standard nitric oxide donors like nitroglycerin, which increase blood flow in diseased arteries by causing them to dilate throughout the body. Standard NO donors also depress cardiac function by decreasing the pressure of blood returning from the body back into the heart. Early tests in a mouse model have confirmed that the new MRIG NO donor drugs are cardioprotective in-vivo, and do not cause system-wide vessel dilation side effects.

Bruce Freeman, Ph.D., chair of the Department of Pharmacology & Chemical Biology at the University of Pittsburgh School of Medicine, also led the study. Other contributors included postdoctoral fellow Sergiy Nadtochiy, Ph.D. in Rochester, and Paul Baker, Ph.D. research assistant professor in Pittsburgh.

"Our interest in this area stems from the fact that many different stimuli appear to funnel down into the mitochondria where they may trigger LNO2 production, any of which may suggest a new way to prevent damage," Freeman said. "Along with IPC, olive oil has been shown to produce LNO2 in the stomach, offering an explanation for the value of the Mediterranean diet."

http://www.sciencedaily.com/releases/2008/12/081202080819.htm

Music and the Heart

2008-12-02T22:40:00.003-09:00

Joyful Music in Tune With Heart Health
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By Amanda Gardner

HealthDay Reporter
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TUESDAY, Nov. 11 (HealthDay News) -- Throw on a little Bach, Beatles or Beyonce, and then sit back and relax in the knowledge that your blood vessels are expanding wide open, letting the blood flow freely.

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Nothing could be healthier for your heart, a new study suggests.
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"Listening to music that makes you feel good may also be a good preventive measure for heart health," said study author Dr. Michael Miller, director of the Center for Preventive Cardiology at the University of Maryland Medical Center, in Baltimore. "There's no downside. It's simple, economic and it may pay off dividends in regard to a healthy heart."
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Added Dr. Carl Lavie, medical director of cardiac rehabilitation and prevention director of the Stress Testing Laboratory at the Ochsner Heart and Vascular Institute in New Orleans: "Although this was just an acute [short-term] study, it suggests that laughter and listening to relaxing music may provide cardioprotection or be heart-healthy. I suspect that the authors are correct in this theory. But the important thing to know is whether regular performance of this or similar activity would have long-term benefits on the cardiovascular system, similar to, superior, or additive to such things as regular aerobic exercise that has been extensively studied and proven to have substantial long-term benefits."
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Miller, who presented the findings Tuesday at the American Heart Association's annual scientific sessions, in New Orleans, said many people look at heart health in terms of negative risk factors that need to be overcome. "There are not a lot of positive risk factors," he noted.
Previous studies had found that music could affect heart rate and blood pressure. Prayer has also been shown to improve cardiac performance. And Miller's group previously found that laughter improved vascular health.
For the new study, 10 healthy, nonsmoking volunteers (70% of them men with a mean age of 36) selected music that made them feel good and other music that made them feel anxious. Selections differed according to the person. Participants also were asked to look at humorous video clips and relaxation audio tapes.
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The researchers measured brachial artery flow, in the forearm, using a blood pressure cuff, before and after each "stimulus."
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"In the minute after you release [the rubber bulb], you see how the inner lining of the blood vessel reacts, the endothelial response," Miller said. "People with risk factors for heart disease like smoking and hypertension don't dilate normally. We believe that means that their vasculature is not healthy."
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Among the study participants, brachial artery flow increased 26% during the joyful music phase and decreased 6% after listening to anxiety-producing music.

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Blood flow also increased 19% during the laughter (video clip) phase and 11% during relaxation.

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The increase in dilation seen after listening to joyful music was "about the same level we see after someone does aerobic activity. It's also similar to what we see after taking statin medication," Miller said. "The effect lasts for about an hour."
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The positive effect may come from the release of endorphins, Miller speculated, referring to the body chemicals that block pain and ease anxiety and depression.
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"Clearly, the role of psychological risk factors, and particularly psychological stress, has been neglected in preventive cardiology," Lavie said. "Clearly, extreme emotional stress -- the classic example is public speaking, especially for novice speakers -- has the exact opposite effects as what Miller showed with laughter and relaxing music. Acute and chronic job stress also has deleterious effects which could be countered by laughter or relaxing music."
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SOURCES: Michael Miller, M.D., director, Center for Preventive Cardiology, University of Maryland Medical Center, Baltimore; Carl J. Lavie, M.D., medical director, cardiac rehabilitation, and prevention director, Stress Testing Laboratory, Ochsner Heart and Vascular Institute, New Orleans; Nov. 11, 2008, presentation, American Heart Association's annual scientific sessions, New Orleans

http://www.medicinenet.com/script/main/art.asp?articlekey=94151

Flu Shots Can Help Prevent Cardiac Death

2008-12-01T10:40:00.002-09:00

The three-dimensional structure of influenza virus from electron tomography. The viruses are about 120 nanometers -- about one ten thousandth of a millimeter -- in diameter.

Patients with heart disease ought to get flu shots, say the American Heart Association and the American College of Cardiology. A number of studies over the past few years suggest that patients with underlying heart disease (or even an increased risk of heart disease) who get flu vaccine substantially reduce their risk of cardiac death.

In 2007, the American Heart Association (AHA) and the American College of Cardiology (ACC) joined forces to advise doctors to give flu shots to all their patients with cardiovascular disease. The message is especially aimed at cardiologists -- the doctors who are most likely to see these high-risk patients.

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This advisory is in compliance with guidelines for treating patients with cardiovascular disease, issued by the AHA and ACC in May, where influenza vaccination was recommended as routine preventative therapy for heart patients for the first time. This recommendation follows the results of several studies showing the benefits of flu vaccine in cardiac patients, studies that began appearing several years ago. In some reports, the risk of cardiovascular mortality was reduced as much as 50% in cardiac patients receiving flu shots, leading the AHA/ACC advisory to recommend vaccination "with the same enthusiasm as cholesterol and blood-pressure control." The reduction in deaths is due not only to preventing the increased death rate that the flu itself has in those with cardiovascular disease, but also in preventing flu-triggered heart attacks. .

DrRich Comments:

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The AHA/ACC advisory on influenza vaccine is commendable. Keep in mind, however, that it often takes 5 to 10 years for formal guidelines such as these to penetrate down to the average doctor. Don't wait: If you've got heart disease take the initiative yourself, and get a flu shot.

http://heartdisease.about.com/od/reducingcardiacrisk/a/cardiaflushots.htm

Heart Disease Reversed in Mice

2008-12-01T00:08:00.010-09:00

November 30, 2008

Heart disease 'reversed in mice'
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Tiny fragments of genetic material can play a role in heart disease.

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Scientists have halted the advance of heart disease in mice - and even reversed some of its effects.

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The study provides hard evidence that tiny pieces of genetic material called microRNA can play a key role in the development of heart disease. .
The therapy, featured in the journal Nature, targets and blocks microRNA in heart cells.
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A US specialist said that, with trials under way in other animals, human tests may be only a few years away.
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This is one of the hottest topics in biology at the moment .
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Professor Eric OlsonUniversity of Texas Southwestern Medical Center
The importance of microRNAs to heart disease - and a host of other diseases - has already been suggested by other scientists.
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Their job is to regulate the activity of our genes, but with many different types present in the cell, scientists are trying to establish which plays the biggest role.
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The US and German scientists are focusing on one type labelled microRNA-21, and their role in a type of heart cell called the cardiac fibroblast, which helps provide the structure of the organ, and plays a critical role in the progressive scarring which stops it working properly in heart disease.
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Until recently, that process was thought to be an irreversible one.
The researchers found that cells in a failing heart had higher levels of this microRNA, and linked it to a chemical signalling pathway which leads to the tissue damage found in the condition.
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Animal studies
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In mice, they used a chemical which blocked microRNA-21, and found that not only that this pathway was interrupted, but that cardiac function in the animals improved.
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This, they wrote, proved its potential as a new target for drugs in heart diseased humans.
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Professor Eric Olson, from the University of Texas Southwestern Medical Center, whose own research focuses on microRNAs and heart disease, said that the results were "exciting".
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"This is one of the hottest topics in biology at the moment," he said.
"Micro-RNAs are being very seriously considered as a therapeutic target - there is a lot of promise and potential in this area.
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"This research suggests you can reverse or prevent aspects of heart disease."
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He said: "There are already studies in large animals using micro-RNA inhibitors in heart disease - I can envisage that in a few years we will see this in human trials."

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http://news.bbc.co.uk/2/hi/health/7750855.stm
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MicroRNA Drugs Startup Miragen Nears Close of Series A, Begins Defining Pipeline
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May 15, 2008
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By Doug Macron
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Miragen Therapeutics, a Boulder, Colo.-based startup developing microRNA-targeting drugs for cardiovascular disease and related muscle disorders, is close to closing a Series A round of financing, RNAi News has learned.
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“A big part” of what Miragen will work on over the next six months will be “defining the key microRNAs and … [specific] clinical indication we want to go after,” he added.
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Given the fact that delivery continues to be the biggest hurdle for nucleic acid-based drugs, Marshall said that Miragen will initially focus on developing a therapeutic that can be directly delivered to the heart.
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http://en.wikipedia.org/wiki/MicroRNA

Purkinje Fibers

2008-11-29T10:07:00.001-09:00

Heart muscle with purkinje fibers on the surface of heart muscle fibers. Purkinje fibers are modified cardiac muscle fibers that originate from the atrioventricular node and spread into the two ventricles. They transmit the electrical impulse from the atrioventricular node to the ventricles enabling almost simultaneous contraction. The spread of excitation through the ventricles from the atrioventricular node is extremely rapid, moving at one to four meters per second.

http://www.astrographics.com/GalleryPrintsIndex/GP2084.html

Pericarditis

2008-11-28T10:56:00.002-09:00

Pericarditis is a swelling and irritation of the pericardium, the thin sac-like membrane that surrounds your heart. Pericarditis often causes chest pain and sometimes other symptoms. Pericarditis may be acute or chronic. The sharp chest pain associated with acute pericarditis occurs when the pericardium rubs against the heart's outer layer.

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Mild cases may improve on their own. Treatment for more-severe cases may include medications and, rarely, surgery. Early diagnosis and treatment may help to reduce the risk of long-term complications.

Symptoms

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If you have acute pericarditis, the most common symptom is sharp, stabbing chest pain behind the breastbone or in the left side of your chest. However, some people with acute pericarditis describe their chest pain as dull, achy or pressure-like instead, and of varying intensity. The sharp pain may travel into your left shoulder and neck. It often intensifies when you lie down or inhale deeply. Sitting up and leaning forward can often ease the pain. At times, it may be difficult to distinguish pericardial pain from the pain that occurs with a heart attack.

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Other signs and symptoms often associated with pericarditis include:
Shortness of breath when reclining

Low-grade fever

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An overall sense of weakness, fatigue or feeling sick
Dry cough

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Abdominal or leg swelling

Causes

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Under normal circumstances, the two-layered pericardial sac that surrounds your heart contains a small amount of lubricating fluid. In pericarditis the sac becomes inflamed and the resulting friction from the inflamed sac rubbing against the outer layer of your heart leads to chest pain.

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In some cases the amount of fluid contained in the pericardial sac may increase, causing what is called pericardial effusion.

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The cause of pericarditis is often hard to determine. In most cases doctors are either unable to determine a cause (idiopathic) or suspect a viral infection.

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Pericarditis can also develop shortly after a major heart attack due to the irritation of the underlying damaged heart muscle. In addition, a delayed form of pericarditis may occur weeks after a heart attack or heart surgery because of antibody formation. This delayed pericarditis is known as Dressler's syndrome. Many experts believe Dressler's syndrome is due to an autoimmune response, a mistaken inflammatory response by the body to its own tissues — in this case, the heart and pericardium.
Other causes of pericarditis include:

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Systemic inflammatory disorders. These may include lupus and rheumatoid arthritis.

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Trauma. Injury to your heart or chest may occur as a result of a motor vehicle or other accident.

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Other health disorders. These may include kidney failure, AIDS, tuberculosis and cancer.

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Certain medications. Some medications can cause pericarditis, although this is unusual.

When to seek medical advice

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Seek immediate medical care if you develop chest pain.

http://www.mayoclinic.com/health/pericarditis/DS00505

Importance of Uninterrupted Chest Compressions in Sudden Cardiac Arrest

2008-11-28T09:52:00.006-09:00

(Note: The disco tune "Stayin' Alive) is about 100 beats per minute)

Gasping Helps Cardiac Arrest Victims Survive, New Research Shows
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ScienceDaily (Nov. 26, 2008) — People who witness an individual collapse suddenly and unexpectedly should perform uninterrupted chest compressions even if the patient gasps or breathes in a funny way, research from the Resuscitation Research Group at The University of Arizona Sarver Heart Center shows.
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When an individual breathes abnormally or gasps after collapsing from sudden cardiac arrest there is a greater chance of surviving, the researchers report. Gasping can be thought of as a survival reflex triggered by the brain. .
Each day, about 500 Americans collapse because their hearts suddenly stop beating. Data collected by Sarver Heart Center researchers show that in more than half of witnessed cardiac arrest cases, the patient gasped.
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"Gasping is an indication that the brain is still alive, and it tells you that if you start and continue uninterrupted chest compressions, the person has a high chance of surviving," said Gordon A. Ewy, MD, corresponding author of the study, professor and chief of cardiology at the UA and director of its Sarver Heart Center. "We need people to promptly recognize sudden cardiac arrest, to call 9-1-1 and to start chest compressions right away."
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Gasping has been described as snoring, gurgling, moaning, snorting or agonal or labored breathing. However, bystanders often misinterpret gasping and other unusual vocal sounds as normal breathing and don't call 9-1-1 or begin lifesaving chest compressions quickly enough, Dr. Ewy said.
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The authors hope their findings lead to greater willingness of untrained bystanders to jump in and perform continuous chest compressions. Bystander-initiated CPR has been shown to be a cardiac arrest victim's only chance of survival until an automated external defibrillator or the paramedics get to the scene.
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Many bystanders are hesitant to perform mouth-to-mouth ventilation, and in a case of a witnessed (seen or heard) collapse, so-called rescue breathing is not necessary and may be harmful, Dr. Ewy said. "When the patient gasps, there is a negative pressure in the chest, which not only sucks air into the lungs but also draws blood back to the heart. In contrast, mouth-to-mouth breathing creates overpressure in the chest and actually inhibits blood flow back to the heart. Gasping during cardiac arrest is much better than mouth-to-mouth breathing."
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But what about choking? "That's very different," Dr. Ewy said. "Someone who is choking will be seen to grasp their throat and struggle to breathe, which means they're responsive. These individuals need the Heimlich maneuver." A primary cardiac arrest is the witnessed unexpected collapse of an individual who is not responsive, Dr. Ewy said. "Cardiac arrest will cause the stricken individual to pass out and collapse to the ground within seconds."
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The Arizona researchers examined data from two sources. Transcripts from the Phoenix Fire Department Regional Dispatch Center included information on gasping in patients found by bystanders, whether their collapse was witnessed or not. The department's first-care reports on 1,218 witnessed patients provided the incidence of gasping upon or after the arrival of emergency medical service (EMS) personnel. Among the 481 patients who received bystander CPR, 39 percent of gaspers survived, but only 9.4 percent of those who didn't gasp survived.
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Performing uninterrupted chest compressions (a technique developed at the UA Sarver Heart Center and endorsed by the American Heart Association as "Hands-Only CPR" for lay individuals) may cause a person who has stopped gasping to resume gasping. "This scares many people and they stop pressing on the chest," Dr. Ewy said, "This is bad because gasping is an indication that you're doing a good job."
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The study is set to publish in the Nov. 24 online issue of Circulation, the official journal of the American Heart Association.
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The authors of the study are: Bentley J. Bobrow, MD; Mathias Zuercher, MD; Gordon A. Ewy, MD; Lani Clark, BS; Vatsal Chikani, MPH,; Dan Donahue BS, NREMT-P, Arthur B. Sanders, MD; Ronald W. Hilwig, DVM; Robert A. Berg, MD; and Karl B. Kern, MD.
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Experts continue to promote a combination of rescue breathing and chest compressions for victims of cardiac arrest due to non-cardiac causes, like near drowning or electrocution, and all victims of pediatric cardiac arrest.
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The study was funded in part by a grant from the Arizona Department of Health Services Bureau of Emergency Medical Services.
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http://www.sciencedaily.com/releases/2008/11/081124165125.htm

Gratitude is a vaccine

2008-11-27T11:18:00.008-09:00

The sign for "thank you" is made by touching your lips with the front of the fingers of your right hand.

Your hand should be an "open-b."
Move your hand away from your face, palms upward.
Smile.

Note: If you use two hands with this sign it means you are "very" grateful.

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“Gratitude is a vaccine, an antitoxin,and an antiseptic.”— John Henry Jowett

If you start practicing now, you could be grateful by Thanksgiving. Not only that, your marriage could improve, you might be exercising more, feel less depressed, sleep better, have a healthier heart, more life satisfaction, and increase your chances of living longer.

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This may sound like a late-night ad that comes with a free set of steak knives (…and that’s not all!), but a growing body of research shows that gratitude is truly amazing in its physical and psychosocial benefits. The benefits are so great, in fact, that it’s a wonder “gratitude gyms” aren’t already being franchised.

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Robert A. Emmons, PhD, a professor of psychology at University of California, Davis, pioneer in the research on gratitude and one of the leading scholars in positive psychology, has written a new book on the impressive findings in the field.

Thanks: How the New Science of Gratitude Can Make You Happier is the perfect text for Gratitude 101, a course that could justifiably be part of the core curriculum to leading a happy life. What makes gratitude the “magic ingredient” is that it takes us outside ourselves so that we can see how we are part of the larger, intricate network of sustaining relationships -- relationships that are mutually reciprocal.

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Research on gratitude.

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In one of his first studies on gratitude, conducted with colleague Mike McCullough at the University of Miami, Emmons randomly assigned participants one of three tasks. Some were encouraged to feel gratitude indirectly, others to be indirectly negative and complaining, and a third group to be neutral.

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Every week, participants kept a short journal. They briefly described either five things they were grateful for that had occurred in the past week, or the opposite, five daily hassles from the previous week that displeased them.

The neutral group was asked to list five events or circumstances that affected them, but they were not told to accentuate the positive or negative.

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The results of this study at the end of 10 weeks:
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Participants in the gratitude group felt better about their lives as a whole and were more optimistic about the future than participants in either of the other control conditions -- a full 25 percent happier.
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They reported fewer health complaints and even spent more time exercising than control participants.
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They had fewer symptoms of physical illness than the other two groups.
The gratitude group exercised 1.5 hours more than the hassled group.
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In a second study by Emmons, people were asked to write with daily frequency about things for which they were grateful or when they experienced gratitude. There was evidence that the daily intervention led to greater increases in gratitude than did the weekly practice in the first study.

The results showed another benefit:
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Participants in the gratitude condition also reported offering others more emotional support or help with a personal problem, indicating that the gratitude condition increased “pro-social” motivation.
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A third study on gratitude was conducted with adults having congenital and adult-onset neuromuscular disorders (NMDs), with the majority having post-polio disease (PPS).
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Compared to those who were not jotting down their blessings nightly, participants in the gratitude condition reported more hours of sleep each night, spending less time awake before falling asleep, and feeling more refreshed upon awakening.
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The gratitude group also reported more satisfaction with their lives as a whole, felt more optimism about the upcoming week, and felt considerably more connected with others than did participants in the control condition.
The participants weren’t the only ones believing life was better. According to the researchers, “Spouses of the participants in the gratitude condition reported that the participants appeared to have higher subjective well-being than did the spouses of the participants in the control condition.”
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Several studies have shown depression to be strongly inversely related to gratitude. The more grateful a person is, the less depressed they are. The more depressed, the less likely one is to feel thankful for life. One researcher, Philip Watkins, clinical psychologist at Eastern Washington University, found that clinically depressed individuals showed significantly lower gratitude (nearly 50 percent less) than non-depressed controls.
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One reason may be that people who are grateful tend to show a positive recall bias (conjuring up many more pleasant memories than unpleasant ones) when asked about past life events, just as depressed individuals show a negative recall bias when asked about past life events. Watkins suggests that gratitude may help alleviate depression for three other reasons:

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Gratitude might increase a person’s potential for enjoyment of benefits and “the benevolence of the event.”
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A grateful attitude may provide useful coping skills for dealing with losses and other stressful events, such as appreciating important things that we have previously taken for granted.
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A grateful approach to life can increase one’s focus on their benefits in life.
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Marriage: the 5 to 1 ratio
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Dr. John Gottman at the University of Washington has been researching marriages for two decades. The bottom line of all that research, he concludes, is that unless a couple is able to maintain a high ratio of positive to negative encounters (5:1 or greater), it is likely the marriage will end.
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With 90 percent accuracy, Gottman can predict, often after only three minutes of observation, which marriages are likely to flourish and which will probably flounder. The formula is that for every negative expression (a complaint, frown, put-down, expression of anger) there needs to be about five positive ones (smiles, compliments, laughter).

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So, what’s the best way to create a positivity ratio? No surprises here. Gottman suggests practicing gratitude in marriage and having a goal of counting at least five blessings for every one complaint.
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Gratitude and heart health
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How about the healthy heart benefit? University of Connecticut psychologist Glen Affleck’s research showed that the explanation a person fashions for why he or she has had a heart attack has implications for future cardiac health. He and colleagues at the Department of Community Medicine and Health Care found that cardiac patients who blamed their heart attacks on others were more likely to suffer another heart attack within the next eight years. On the other hand, perceiving benefits and gains from an initial heart attack, including becoming more appreciative of life, was related to a reduced risk for subsequent attack.

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In a study at Duke University Medical Center, 3,000 patients with significant blockage who were more socially isolated were substantially less likely to say they count their blessings by comparing themselves to less fortunate others. The benefit of gratitude extended even to people who had heart transplants. At the University of Pittsburgh, a study of 119 heart transplant patients found “thankfulness and appreciation as an aspect of religious faith was positively related to their perceived physical and mental health at one year post-transplant. Thankfulness also was predictive of greater compliance with the medical regimen and of fewer difficulties with diet and medications.”
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10 steps to gratitude

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So, what’s the best way to make all these great things happen? In his book Thanks, Emmons recommends these 10 steps:

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Keep a gratitude journal daily, recording in writing what you are grateful for.
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Remember the bad. A mental comparison of how bad it was and how much better it is now really helps.
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Three questions to ask yourself:
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What have I received from ______?

What have I given to ________?

What troubles and difficulty have I caused ____?
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Learn prayers or meditations of gratitude.
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Come to your “senses.” Count bodily related blessings: being able to see, hear, walk, eat, etc.
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Use visual reminders, like pictures of loved ones or scenes of nature.
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Make a vow to practice gratitude.
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Watch your language. Negative talk undermines the gratitude practice.
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Go through the motions. Feelings follow words and actions.
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Think outside the box. Think of the non-obvious things to be grateful for.
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Gratitude, with practice, can become not only a habit, but a way of viewing the world. “Ain’t it Awful” is as much learned as “Ain’t it Grand,” and not nearly so much fun. No doctor’s appointment needs to be scheduled to practice gratitude, no deductible on your insurance, no personal trainer required. This amazing health remedy is yours for the taking, right now. So, say, “Thank you!”
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You are more than welcome.
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http://www.healthleader.uthouston.edu/archive/Mind_Body_Soul/2007/gratitude-1121.html
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Change in Heart Rate over Time Predicts Mortality

2008-11-26T11:30:00.003-09:00

Change in heart rate over time predicts mortality

November 21, 2008

Lisa Nainggolan

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Paris, France - In the first study to ever assess the prognostic value of a change in heart rate (HR) over a number of years, French doctors have found that there is a relation between this variable and mortality [1]. Dr Xavier Jouven (Hôpital Européen Georges Pompidou, Paris, France) and colleagues report their findings in a study published online November 7, 2008 in the American Journal of Cardiology.

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They found that in a cohort of healthy policemen, HR at rest and its change over five years were both predictors of death, independent of the standard cardiovascular risk factors. Those whose HR rose by more than three beats per minute (bpm) over this time period had an almost 20% increased mortality risk compared with men whose HR remained unchanged.

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Jouven told heartwire that this is "an important paper and the second step" in a jigsaw. "We knew before that a person with a high heart rate has a high mortality. Now this article shows we are advancing in the research concerning the potential association between HR and mortality."

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Change in HR over a five-year period conferred additional information beyond HR at rest and the usual risk factors.

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Dr Franz Messerli (St Luke's-Roosevelt Hospital, New York) commented to heartwire: "The present study is unique in that it shows that patients whose heart rate increased during a five-year period had an . . . increased mortality risk. Of note, the policemen who did best were the ones who had a low heart rate at the beginning of the Paris Prospective Study 1 and whose heart rate remained unchanged."Reduced HR associated with 14% lower risk of death

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The observational, although prospective, study followed 5139 asymptomatic men (aged 42 to 53 years) who were recruited from 1967 to 1972 and had their HRs measured at rest in standardized conditions every year for five consecutive years. HR change was defined as the difference between HR at examination 5 and HR at inclusion. Subjects were divided into the following tertiles: decrease >4 bpm; unchanged (from -4 to +3 bpm); or increase >3 bpm.

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After adjustments were made for confounding factors, including baseline HR at rest, compared with subjects with unchanged HRs, those with decreased HRs during the five years had a 14% decreased mortality risk (RR 0.86, 95% CI 0.74-1.00; p=0.05), whereas men with increased HRs during the five years had a 19% increased mortality risk (RR 1.19, 95% CI 1.04-1.37; p<0.012).>

"We found that change in HR over a five-year period conferred additional information beyond HR at rest and the usual risk factors [and] was an independent predictor of mortality in middle-aged men," they observe. Exercise keeps heart rate low Messerli told heartwire that "the most common reason for a slow heart rate in young to middle-aged subjects, such as in the present study, is regular conditioning. Conceivably, therefore, subjects in this group were the ones who exercised regularly and continued to exercise regularly throughout the five-year period, thereby keeping heart rate slow.

As expected, [body-mass index] BMI was lowest in this group. "It is of little surprise, then, that these slow-heart-rate policemen had a drastically lower mortality than those who started out with an increased heart rate [that] accelerated . . . even more during the five-year period," he added. Jouven told heartwire that the next step to prove an association will be with some kind of interventional trial aimed at investigating whether an induced HR decrease—with, for example regular exercise—is associated with a decrease in mortality risk. "If we change HR, do we change mortality?" he wondered.

Source

.Jouven X, Empana JP, Escolano S, et al. Relation of heart rate at rest and long-term (>20 years) death rate in initially healthy middle-aged men. Am J Cardiol 2008; DOI:10.1016/j.amjcard.2008.08.071. Available at: http://www.ajconline.org/.

http://www.theheart.org/article/923023.do

What the News Media Did Not Reveal About Bill Clinton's Heart Problem

2008-11-25T23:50:00.003-09:00

BILL CLINTON’S CHOLESTEROL, LDL, AND BLOOD PRESSURE

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One of the unique aspects of being president of the United States is that details of your medical history are made public every year. According to the results of the last exam performed before he left the White House, Bill Clinton’s total cholesterol was 233 mg/dL, which is not outrageously high. Since optimal cholesterol levels are now considered below 200 mg/dL,1 the news media made a big deal over the fact that Clinton’s cholesterol was too high.

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A more significant problem that the news media only touched on was that the former president’s LDL level was a dangerous 177 mg/dL. New guidelines call for LDL to be below 100 mg/dL, and some doctors want LDL to be below 70 mg/dL in those suffering from coronary artery disease.

The Life Extension Foundation was first to advocate that LDL levels should be below 100 mg/dL. Until recently, most mainstream doctors believed that an LDL of 130 mg/dL was all right.

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Clinton’s blood pressure of 136/84 used to be considered acceptable, but conventional medicine has finally realized that blood pressure over 119/79 exposes one to greater risks of coronary artery disease, stroke, kidney failure, and other diseases.

One of the drawbacks of being president is that you get free health care provided by government doctors who are not always up to date on new disease risk factors.

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Interestingly, Clinton was prescribed cholesterol-lowering medication before he left the White House, but decided on his own to stop taking the drug after losing some weight. Without first verifying that LDL and cholesterol levels are in safe ranges using a simple blood test, discontinuing any lipid-lowering therapy is a risky strategy. Regrettably, side effects from cholesterol-lowering drugs cause some patients to stop taking them without informing their doctors.

(This is only an excerpt from the comprehensive and well-written article)

http://www.lef.org/magazine/mag2004/nov2004_awsi_01.htm

Using Stem Cells for Heart Failure

2008-11-25T00:18:00.004-09:00

Symptoms of Heart Failure

University of Utah researchers to use patient's own stem cells to treat heart failure

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Bone marrow cells may prove effective in regenerating heart muscle, improving function
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SALT LAKE CITY – Nov. 17, 2008 – Researchers at the University of Utah are enrolling people in a new clinical trial that uses a patient's own stem cells to treat ischemic and non-ischemic heart failure.
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The one-year Cardiac Repair Cell Treatment of Patients with Dilated Cardiomyopathy (IMPACT-DCM) study will look at the safety of injecting Cardiac Repair Cells (CRC) and their ability to improve heart function.
Patients enrolled in IMPACT-DCM will have their own bone marrow cells drawn (about 3 tablespoons worth), which will then be grown in a culture to expand the number of cells that will help the heart muscle and improve blood flow. Two weeks later, the patient's stem cells will be injected directly into the left ventricle of the heart during a minimally invasive surgery developed by Amit N. Patel, M.D., national principal investigator for the IMPACT-DCM trial and director of cardiovascular regenerative medicine at the University of Utah School of Medicine.
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"Heart failure affects about 5 million Americans, with more than half a million new cases diagnosed each year. A subset of these patients has dilated cardiomyopathy (DCM), a condition that leaves the heart weakened, enlarged and unable to pump blood efficiently. For most of these patients, the only option has been a heart transplant," said David A. Bull, M.D., professor and division chief of Cardiothoracic Surgery in the U's medical school and site principal investigator for the trial.
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"This is the first trial of its kind in the United States, providing patients who have limited to no other options with a viable treatment," said Patel, professor of surgery. "By using a patient's own cells, we eliminate the concern of rejection and the need for potentially harmful immunosuppressive drugs. We hope these cells will help with new blood vessels and support the heart muscle in order to improve the heart's function, thereby greatly improving the patient's quality of life."
Patients who have been diagnosed with congestive heart failure (NYHA Class 3 or 4) and are between the ages of 18 and 86 may be eligible to participate in the trial. The University of Utah is one of five nationwide sites conducting the IMPACT-DCM study, sponsored by Aastrom Biosciences, Inc., a company specializing in autologous cell products. IMPACT-DCM is a randomized, controlled, Phase II study that will enroll 40 patients nationwide: 20 patients with ischemic DCM and 20 patients with nonischemic DCM.

http://www.eurekalert.org/pub_releases/2008-11/uouh-uou111708.php
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Heart Failure Symptoms

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Heart failure symptoms are not always apparent. Some people in the very early stages of heart failure may have no symptoms at all. And others dismiss feeling tired and experiencing shortness of breath as signs of growing older.

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But some heart disease symptoms are more obvious. When the heart is not pumping properly or efficiently, daily activity can cause shortness of breath or difficulty in breathing when lying down. The legs and ankles may swell because the body is retaining water. Feeling weak and tired is common. Ordinary daily activities like going to the grocery store or even walking up a flight of stairs can be exhausting.

Because of the heart’s inability to efficiently pump blood and supply your organs, such as the kidneys and the brain, you may experience a number of symptoms including:

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Shortness of breath
Swelling of the feet and legs
Lack of energy, feeling tired
Difficulty sleeping at night due to breathing problems
Swollen or tender abdomen, loss of appetite
Cough with "frothy" sputum
Increased urination at night
Confusion, impaired memory

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Your heart failure symptoms will help your doctor classify the severity of your heart failure and monitor the effects of drug and/or device therapy.
Are you at risk for heart failure? Take the Heart Failure Assessment.

http://www.hearthelp.com/heartfailure/symptoms-heart-failure.html

New Test to Predict Imminent Heart Attack

2008-11-23T09:25:00.005-09:00

Test for Imminent Heart Attacks Cardiologists Discover New Enzyme that Predicts Risk of Heart Attack

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August 1, 2005 — MPO, or myeloperoxidase,is an enzyme produced by white blood cells. High levels of MPO predict a heart attack, the need for invasive intervention, or cardiac death within the next six months with 95-percent accuracy. The FDA has recently approved a simple blood test for MPO.
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CLEVELAND--For many people the first sign of heart disease is a heart attack ... And one out of three people who have a heart attack die. The problem? Current blood tests only tell doctors if a heart attack has already happened. Now a new blood test could let doctors know who needs aggressive heart help, before a heart attack happens.

Fifty-four year old David Lesesky exercises every day with his young family. He has a lot to live for, but not too long ago, his family nearly lost him. "I thought I was running out of wind," he says. "I couldn't catch my breath."

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Lesesky was having a heart attack He knows he is lucky to be alive. He says, "I worked out. I tried to do all the right things. So I thought, if anything, I'm in great shape." This former triathlete's doctors thought so, too. Heart and stress tests didn't pick up a thing, but a dangerous blockage was forming.

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MPO, or myeloperoxidase is produced by white blood cells, the body's defense system. When there's a dangerous blockage, MPO levels in the blood increase.

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Cardiologist Stanley Hazen, of Cleveland Clinic, says, "We were able to show that this enzyme called MPO ... that elevated levels of it are seen in patients who are at risk not only for having a heart attack when they present, but also a heart attack or needing bypass surgery or needing angioplasty or dying in the next one-month to six-month period."
A simple blood test -- when performed on patients with the highest MPO levels -- predicted a heart attack, the need for invasive intervention, or cardiac death within the next six months with 95-percent accuracy.
The cardiac MPO test was recently approved by the FDA. It's not widely available yet, but it should start appearing in hospitals across the country soon.
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BACKGROUND: Doctors at the Cleveland Clinic in Ohio have developed a new test to identify those who are in imminent danger of a heart attack by measuring the level of a disease-fighting enzyme in the bloodstream. A start-up company called PrognostiX has received FDA approval to sell the diagnostic test.
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HOW IT WORKS: Enzymes are proteins in the body that control metabolism: they convert nutrients into energy and new cell tissue. Enzymes can speed up chemical processes that would otherwise take longer. They are also very specific: each type of enzyme only reacts with one specific compound. High levels of an enzyme called myeloperoxidase (MPO) in the bloodstream can signal a person's near-term risk for heaving a heart attack within months.

WHAT CAUSES HEART ATTACKS: Heart attack is the leading cause of death in North and South America and in Europe. It is usually the result of prolonged hardening and narrowing of the arteries that direct blood into the heart. When blood vessels are healthy, oxygen-rich blood flows easily to all the muscles and organs of the body. But if they become clogged by the buildup of fatty deposits on vessel walls, blood can be cut off, killing heart muscle cells. This is called coronary heart disease, and it can lead to heart attacks or strokes.
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SIGNS OF A HEART ATTACK:
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Pressure, tightness, or burning chest pain. May extend into the jaw, shoulders, back, or arms
Nausea or vomiting
Sweating
Shortness of breath
Dizziness

http://www.sciencedaily.com/videos/2005/0812-test_for_imminent_heart_attacks.htm

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Blood Protein Offers Clues To Heart Attack In Seemingly Healthy People

ScienceDaily (July 9, 2007) — We've all wondered how a seemingly healthy person can actually be at high risk for heart disease or a heart attack. Now researchers have uncovered a new clue to this mystery. The culprit: myeloperoxidase (MPO), a protein secreted by white blood cells that both signals inflammation and releases a bleach-like substance that damages the cardiovascular system.
See also:
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Although MPO is intended to kill harmful bacteria, it may instead inflame the body's arteries and cripple protective substances in the blood, according to a study published in the July 10, 2007, issue of the Journal of the American College of Cardiology (JACC). As a result, long before conventional risk factors set off alarms, elevated MPO levels signal that harmful plaque has been building up.

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"We were surprised to find that many years before a cardiovascular event actually occurs, MPO is increased," said Matthijs Boekholdt, M.D., Ph.D., a resident in cardiology at Academic Medical Center in Amsterdam, the Netherlands. "This could open up completely new areas of research and diagnosis. As we learn more about these processes, we hope to be able to identify 'vulnerable blood' as a reliable tool for detecting vulnerable patients."

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Not only does MPO change low-density-lipoprotein (LDL) cholesterol into a harmful oxidized form that can cause atherosclerosis, the "bleach" produced by MPO damages the arteries directly, causing cell death and erosion of the arterial lining, a process that can create unstable plaques. MPO also hampers the protective effects of high-density-lipoprotein (HDL) cholesterol and reduces the availability of nitric oxide, a natural chemical that relaxes the blood vessels.
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Earlier studies in patients with chest pain and heart disease have shown that elevated levels of MPO identify those at highest risk for a heart attack. "The novelty of the present study is that it is the first large-scale study to examine the relationship of MPO to cardiovascular risk in apparently healthy individuals," Dr. Boekholdt said.
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For the study Dr. Boekholdt and colleagues recruited healthy people living in Norfolk, United Kingdom, between 1993 and 1997, as part of a larger community-based research program known as the European Prospective Investigation Into Cancer and Nutrition (EPIC). They took baseline blood samples from each participant and froze the samples for future analysis.

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After an average of eight years, 1,138 EPIC-Norfolk participants had been admitted to the hospital or died from the effects of coronary artery disease (CAD), including heart attack. The researchers matched these patients with study participants who remained healthy throughout the follow-up period, selecting those of the same gender and similar ages and enrollment times.

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The average blood levels of MPO were significantly higher in those who developed heart disease than in those who remained healthy. In fact, when MPO levels were divided into four groups, patients in the highest fourth were 1.49 times as likely as those in the lowest fourth to develop CAD or have a heart attack. When traditional risk factors--blood pressure, LDL and HDL cholesterol levels, body mass index, smoking and diabetes--were taken into account, an MPO level in the highest fourth increased the risk of heart disease by 1.36 times.
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Equally important, elevated MPO levels signaled increased risk even in those with acceptable levels of LDL cholesterol, HDL cholesterol or C-reactive protein, a widely acknowledged marker of inflammation.
"MPO levels help to identify individuals at increased risk for CAD when traditional risk screening fails," Dr. Boekholdt said.
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The search for blood tests to help identify patients at risk for heart attack is a very important one, said Christopher Cannon, M.D., F.A.C.C., who did not participate in the study and is an associate professor of medicine at Harvard Medical School, Boston, MA. "One fascinating aspect of this study is that this marker of inflammation precedes by nearly a decade the development of clinical coronary disease," he said. "This suggests MPO could be used to catch the disease in a very early stage and help in true prevention of CAD.
.

"Another interesting aspect of MPO is that it may be a marker for unstable plaque. Even more than the number or severity of coronary plaques, we want to know the risk of plaque rupture, and this evolving new marker may help in that regard. More study is needed, but among the hundreds of markers tested to date, MPO looks like a "keeper" that will one day become part of clinical care," Dr. Cannon said.

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Researchers are continuing to assess the value of MPO in different patient groups as well as in relation to other biomarkers, Dr. Boekholdt said. Key questions include whether, and under what circumstances, MPO should be added to the laboratory tests used to screen for cardiovascular disease, and whether blocking MPO could prevent cardiovascular disease.
The EPIC-Norfolk study is supported by program grants from the Medical Research Council UK and Cancer Research UK, with additional support from the European Union, Stroke Association, British Heart Foundation, and the Wellcome Trust. Some of the measurements in this study were supported by Wyeth. One of the study's authors, Stanley L. Hazen, M.D., Ph.D., is named as a co-inventor on pending patents filed by the Cleveland Clinic Foundation relating to the use of myeloperoxidase as a biomarker for cardiovascular disease.
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http://www.sciencedaily.com/releases/2007/07/070703172506.htm

CardioMPO

http://www.prognostix.com/

Longevity Runs in Families

2008-11-22T10:56:00.005-09:00

Children Of Centenarians Live Longer, Have Lower Risk Of Heart Disease, Stroke, Diabetes

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ScienceDaily (Nov. 21, 2008) — A recent study appearing in the November issue of Journal of American Geriatrics Society revealed that centenarian offspring (children of parents who lived to be at least 97 years old) retain important cardiovascular advantages from their parents compared to a similarly-aged cohort. The study is the first to assess the health of centenarian offspring over time and could be important for future research, as the subjects may be used as a model of healthy aging.
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The findings show that centenarian offspring have a 78 percent lower risk for heart attacks, 83 percent lower likelihood of stroke and an 86 percent lower risk of developing diabetes mellitus.

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Additionally, the study found that centenarian offspring who were followed in the study were 81 percent less likely to die than the reference group of similarly-aged patients during the follow-up period. The survival rate is evidence that longevity runs in families, and the results reinforce the notion that there may be physiological and genetic reasons that longevity runs in families.
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The results are consistent with previous research, which suggested that the avoidance or delay of cardiovascular disease and cardiovascular risk factors, including high blood pressure and diabetes, runs strongly in the families of centenarians, particularly amongst their children.
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Dellara F. Terry, co-author of the study, points out that offspring of centenarians maintain these cardiovascular advantages throughout their lives. "These advantages persisted over the several years of the study when they are compared to a similarly-aged group whose parents did not survive to very old age," Terry said.

http://www.sciencedaily.com/releases/2008/11/081120122159.htm

The word from the world's oldest person

December 11, 2005
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Maria Capovilla was born in 1889.Photo: Reuters
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A 116-YEAR-OLD Ecuadorean woman has been declared the oldest person in the world, lifting the title from a US woman previously thought to be the oldest.
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Maria Esther Capovilla was confirmed as the oldest living person after her family sent details of her birth and marriage certificates to Guinness World Records. "We hadn't heard of her before," Kate White, brand manager at the book's publisher, said. "She's in very good health, she's got good sight … and doesn't walk with a stick."
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Ms Capovilla was born in Guayaqull in western Ecuador on September 14, 1889.
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She had five children, and has four grandchildren, nine great-grandchildren and two great-great-grandchildren.
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Asked what she thought about the changes she had seen, Ms Capovilla said "she disliked the fact that presently it's acceptable for women to pursue men", White said.
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REUTERS

http://www.theage.com.au/articles/2005/12/10/1134086848291.html

Stem Cells FAQ

2008-11-20T21:10:00.004-09:00

Drawing of catheter injecting stem cells into the heart

Frequently Asked Questions

What are stem cells?

Stem cells are unspecialized cells that have the amazing potential to develop into many different cell types in the body. Serving as a sort of repair system for the body, they can potentially divide without limit to replenish other cells that have been damaged. When a stem cell divides, each new cell has the potential to either remain a stem cell or become another type of cell with a more specialized function, such as a muscle cell, a red blood cell, or a heart cell.

Where can one find stem cells?
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Stem cells can be found in many tissues in the body such as bone marrow, fat, blood, and other organs like the heart. More immature stem cells can be found in the embryo, as well as the blood found in the umbilical cord of a newborn baby. The Stem Cell Center only uses adult stem cells in its research.

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Do you conduct research using embryonic stem cells?
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No. Embryonic stem cells are not used in our research.
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What diseases do stem cells treat?
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Stem cells, depending on where they come from, have been studied as a possible treatment strategy in numerous diseases such as diabetes, Parkinson’s disease, burns, spinal cord injury, and more specifically heart disease. Recently, numerous studies have shown the potential benefit of implanting stem cells into the heart. The treatment of heart disease is the focus of the Stem Cell Center at the Texas Heart Institute. (Stem cell therapy is an investigational therapy and therefore no definitive claim can be made on the benefit for any single disease.)

How do stem cells work?
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It is not clear how stem cells work exactly. They may differentiate into the cells that surround them (a stem cell placed in the heart may become another heart cell), they may release hormones that help the surrounding tissue function more efficiently, or they may wake up the dormant stem cells in the tissue.
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Even though we do not fully understand how stem cells work, one of the goals of our research at the Stem Cell Center is to further our knowledge in this area.
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How do you use stem cells to treat cardiovascular diseases?
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Stem cells can be injected into the veins, arteries, or directly into the heart muscle. After over 400 injections done safely using direct injection of stem cells from inside the chamber of the heart, the investigators at the Stem Cell Center now perform countless procedures for people all over the world.

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In peripheral vascular disease, stem cells may be injected into the veins, arteries, or directly into the lower leg muscles in hopes of regenerating new blood vessels.

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Updated November 2008

http://www.texasheart.org/Research/StemCellCenter/Stem_Cell_Basics.cfm

Can Stem Cells Repair a Damaged Heart?

2008-11-19T10:31:00.004-09:00

Can Stem Cells Repair a Damaged Heart?

Heart attacks and congestive heart failure remain among the Nation's most prominent health challenges despite many breakthroughs in cardiovascular medicine. In fact, despite successful approaches to prevent or limit cardiovascular disease, the restoration of function to the damaged heart remains a formidable challenge. Recent research is providing early evidence that adult and embryonic stem cells may be able to replace damaged heart muscle cells and establish new blood vessels to supply them. Discussed here are some of the recent discoveries that feature stem cell replacement and muscle regeneration strategies for repairing the damaged heart.

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Introduction

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For those suffering from common, but deadly, heart diseases, stem cell biology represents a new medical frontier. Researchers are working toward using stem cells to replace damaged heart cells and literally restore cardiac function.

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Today in the United States, congestive heart failure—the ineffective pumping of the heart caused by the loss or dysfunction of heart muscle cells—afflicts 4.8 million people, with 400,000 new cases each year. One of the major contributors to the development of this condition is a heart attack, known medically as a myocardial infarction, which occurs in nearly 1.1 million Americans each year. It is easy to recognize that impairments of the heart and circulatory system represent a major cause of death and disability in the United States [

5].

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What leads to these devastating effects? The destruction of heart muscle cells, known as cardiomyocytes, can be the result of hypertension, chronic insufficiency in the blood supply to the heart muscle caused by coronary artery disease, or a heart attack, the sudden closing of a blood vessel supplying oxygen to the heart. Despite advances in surgical procedures, mechanical assistance devices, drug therapy, and organ transplantation, more than half of patients with congestive heart failure die within five years of initial diagnosis. Research has shown that therapies such as clot-busting medications can reestablish blood flow to the damaged regions of the heart and limit the death of cardiomyocytes. Researchers are now exploring ways to save additional lives by using replacement cells for dead or impaired cells so that the weakened heart muscle can regain its pumping power.

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How might stem cells play a part in repairing the heart? To answer this question, researchers are building their knowledge base about how stem cells are directed to become specialized cells. One important type of cell that can be developed is the cardiomyocyte, the heart muscle cell that contracts to eject the blood out of the heart's main pumping chamber (the ventricle). Two other cell types are important to a properly functioning heart are the vascular endothelial cell, which forms the inner lining of new blood vessels, and the smooth muscle cell, which forms the wall of blood vessels. The heart has a large demand for blood flow, and these specialized cells are important for developing a new network of arteries to bring nutrients and oxygen to the cardiomyocytes after a heart has been damaged. The potential capability of both embryonic and adult stem cells to develop into these cells types in the damaged heart is now being explored as part of a strategy to restore heart function to people who have had heart attacks or have congestive heart failure. It is important that work with stem cells is not confused with recent reports that human cardiac myocytes may undergo cell division after myocardial infarction [1]. This work suggests that injured heart cells can shift from a quiescent state into active cell division. This is not different from the ability of a host of other cells in the body that begin to divide after injury. There is still no evidence that there are true stem cells in the heart which can proliferate and differentiate.

[Article is much longer.]

http://stemcells.nih.gov/info/scireport/chapter9.asp

National Institutes of Health

http://www.nih.gov/

Stem Cells after a Heart Attack: I

2008-11-19T10:17:00.002-09:00

(0ne of the most exciting areas of heart research is the use of stem cells to repair damage after a heart attack: this will be one of a number of articles. It is a fairly technical article, but you get the idea from reading it. As someone who lost a lot of heart muscle after a heart attack (www.heartak.com), this research is near and dear to my heart, as they say -- sparker)

Cardiosphere-Derived Stem Cells More Effective At Treating Heart Attack Than Purified Stem CellsMain Category

Capricor Inc. announced today the results from preclinical studies showing that its cardiosphere-derived stem cells (CDCs), when transplanted into a well-established mouse model of myocardial infarction (MI), protect the heart significantly better against progressive degeneration following MI or heart attack than do highly purified cardiac stem cells or heart derived mesenchymal like progenitor cells. Cardiac degeneration after a heart attack leads to progressive loss of cardiac function ending in heart failure and death. This promising study was conducted by Dr. Rachel Ruckdeschel Smith, Project Leader Regenerative Medicine, at Capricor, will be presented today at the American Heart Association's 2008 Scientific Sessions. The presentation will take place at the session entitled, Human Progenitor Cells and Myocardial and Vascular Regeneration, located in room 271-273, at the Ernest N. Morial Convention Center in New Orleans."This study confirms our previously published preclinical work that CDCs have a strong therapeutic effect when applied to animal models of heart attack," said Oliver Foellmer, President and CEO at Capricor.

"Preparations for a clinical trial testing CDCs in patients with recent heart attack are already underway and we hope to file an IND with the FDA by the end of this year to investigate the beneficial impact that CDCs can have in patients."In this preclinical study, Dr. Ruckdeschel Smith and research collaborators at Johns Hopkins Medical Center as well as the University of Rome, compared transplantation of human CDCs, highly purified human cardiac stem cells, and human heart derived mesenchymal like progenitor cells into immunodeficient mice that had induced myocardial infarcts. Many questions remain to be answered on how various stem cells act when delivered into a damaged heart. "Capricor's CDCs represent a mixed population of multiple progenitor lineages, acting synergistically to regrow heart muscle as well as cardiac vasculature," said Dr. Ruckdeschel Smith. "In contrast, purified cardiac stem cells and mesenchymal like cells from the heart, while maintaining an individual effect showed significantly less benefit than the CDCs, which contain both these progenitor populations."

About Cardiosphere-derived Stem CellsCPI-003, Capricor's lead product candidate, is an autologous adult stem cell product for the treatment of myocardial infarction. The product contains multiple progenitor cells from the patient themselves, and is derived from a small heart muscle biopsy in an outpatient procedure. The cells are multiplied in the laboratory, and then reintroduced to the patient. This elegant autologous therapy represents the ultimate personalized medicine matching the patient both genetically and immunologically. CDCs have an excellent safety profile and clinical trials in cardiovascular indications are expected to initiate in 2009. About Capricor Inc.Capricor Inc., headquartered in Los Angeles, California, is a leading biotechnology company that specializes in discovering, developing, and commercializing biotherapeutics for the treatment of heart diseases. Capricor's mission is to revolutionize the treatment of cardiac disease by translating novel stem cell science into therapeutics that halt and reverse the disease process for patients, their families, and society in general. Further information can be found at the company's web site at http://www.capricor.com.

http://www.medicalnewstoday.com/articles/129653.php

Optical Frequency Domain Imaging

2008-11-18T11:58:00.002-09:00

Technology Gives 3-D View Of Human Coronary Arteries

OFDI fly-through view of same patient's right coronary artery, white arrowheads indicate area of white dotted line in image at right. (Credit: Massachusetts General Hospital)

ScienceDaily (Nov. 18, 2008) — For the first time researchers are getting a detailed look at the interior of human coronary arteries, using an optical imaging technique developed at the Wellman Center for Photomedicine at Massachusetts General Hospital (MGH). In their report in the journal JACC: Cardiovascular Imaging, the research team describes how optical frequency-domain imaging (OFDI) gives three-dimensional, microscopic views of significant segments of patients' coronary arteries, visualizing areas of inflammation and plaque deposits.
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"This is the first human demonstration of a technique that has the potential to change how cardiologists look at coronary arteries," says Gary Tearney, MD, PhD, of the MGH Pathology Department and the Wellman Center for Photomedicine at MGH, the study's lead author. "The wealth of information that we can now obtain will undoubtedly improve our ability to understand coronary artery disease and may allow cardiologists to diagnose and treat plaque before it leads to serious problems."
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OFDI is an advance over optical coherence tomography (OCT), another imaging technology developed by the MGH investigators. While OCT examines tissues one point at a time, OFDI can look at over 1,000 points simultaneously using a device developed at MGH-Wellman. Inside a fiberoptic probe, a constantly rotating laser tip emits a light beam with an ever-changing wavelength. As the probe moves through the structure to be imaged, measuring how each wavelength is reflected back allows rapid acquisition of the data required to create the detailed microscopic images. Besides providing three-dimensional images of an artery's microstructure in seconds, the increased speed also reduces signal interference from blood, which had plagued the first-generation technology. In 2006 members of the MGH-Wellman team reported the successful use of OFDI to image the esophagus and coronary arteries of pigs.
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The current study enrolled three patients scheduled to have stents placed in their coronary arteries at the Lahey Clinic in Burlington, Mass. After the completion of stent placement, OFDI was used to image 3- to 7-centimeter-long segments of the patients' coronary arteries including the stented areas. OFDI provided detailed images along the length of the arteries – visualizing lipid or calcium deposits, immune cells that could indicate inflammation, and the stents – and dramatic "fly-through" views looking down the artery's interior. More detailed, cross-sectional images of narrowed vascular segments revealed features associated with the type of atherosclerotic plaques that are likely to rupture and cause a heart attack.
Tearney and his colleagues note that these findings need to be duplicated in a larger group of patients, and the time required to process the "fly-through" images – currently several hours – needs to be reduced to provide the real-time information most useful for clinical applications. Combining OFDI with intravascular ultrasound might help with another of the technique's limitations, the inability to penetrate deep into tissues.
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"While more work remains, the technology is advancing at a rapid pace. We expect to see commercial devices available in a one- to two-year time frame," says Brett Bouma, PhD, of the Wellman Center, senior author of the report. "Our goal now is to help put the pieces in place to ensure that this technique will be widely available to interventional cardiologists." Bouma is an associate professor of Dermatology, and Tearney an associate professor of Pathology at Harvard Medical School.
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Additional co-authors of the JACC: Cardiovascular Imaging report are Milen Shishkov, PhD, Ben Vakoc, PhD, Melissa Suter, PhD, Adrien Desjardins, PhD, Wang-Yul Oh, PhD, Lisa Bartlett and Mireille Rosenberg, PhD, MGH-Wellman; and Sergio Waxman, MD, and Mark Freilich, MBBS, Lahey Clinic. The MGH has licensed cardiovascular applications of OFDI to Terumo Corporation, which has supported nonclinical OFDI studies by Tearney and Bouma. The current study was supported by a grant from the National Institutes of Health.

http://www.sciencedaily.com/releases/2008/11/081117192809.htm

Pacemakers affected by MP3 Headphone

2008-11-13T22:46:00.004-09:00

November 10, 2008

Implantable Defibrillators, Pacemakers Affected By MP3 Headphones

Headphones for MP3 players placed within an inch of pacemakers and implantable cardioverter defibrillators (ICDs) may interfere with these devices, according to research presented at the American Heart Association's Scientific Sessions 2008.
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Researchers investigated the effects of MP3 player headphones, most of which contain the magnetic substance neodymium, on the operation of implanted cardiac devices (abstract P662). An MP3 player is a popular digital music player.
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Earlier this year an FDA report concluded that interactions between MP3 players, such as the popular iPod®, and implanted cardiac devices are unlikely to occur. "We became interested in knowing whether the headphones which contain magnets - not the MP3 players, themselves - would interact with implanted cardiac devices," said William H. Maisel, M.D., M.P.H., senior author of the study and director of the Medical Device Safety Institute at Beth Israel Medical Center in Boston, Mass.
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Maisel said doctors traditionally use magnets in the clinical setting to test pacemakers, which treat slow heart rhythms. When exposed to magnets, these devices automatically pace, sending low-energy signals to the heart to make it beat. Defibrillators, which treat slow and dangerously fast heart rhythms, send either low- or high-energy signals to the heart.
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However, ICDs near magnets may temporarily stop looking for abnormal heart rhythms. Implanted cardiac devices that react in these ways to magnets outside the clinical setting can be potentially dangerous for patients who rely on their lifesaving technologies. Researchers tested eight different models of MP3 player headphones (including both the clip-on and earbud variety) with iPods® on 60 defibrillator and pacemaker patients. "We placed the headphones on the patients' chests, directly over where their devices are located, monitoring them for evidence of an interaction," Maisel said.
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The researchers found a detectable interference with the device by the headphones in 14 patients, (23 percent). Specifically, they observed that 15 percent of the pacemaker patients and 30 percent of the defibrillator patients had a magnet response, Maisel said. "For patients with pacemakers, exposure to the headphones can force the device to deliver signals to the heart, causing it to beat without regard to the patients' underlying heart rhythm," he said. "Exposure of a defibrillator to the headphones can temporarily deactivate the defibrillator."
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In most cases, removal of the headphones restores normal device function. The researchers also tested the magnetic field strengths of each of the headphone models using a gauss meter, which measures the units of magnetic charge produced. Field strength of 10 gauss at the site of the pacemaker or defibrillator has the potential to interact with the implantable device. The researchers found that some of the headphones had field strengths as high as 200 gauss or more. "Even at those high levels, we did not observe any interactions when the headphones were at least 3 cm, or about 1.2 inches, from the skin's surface," Maisel said. "Patients should not focus on the brands we tested but instead should simply be instructed to keep their headphones at least 3 cm from their implantable devices."
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Instead, patients should not place headphones in their pocket or drape them over their chest. "For family members or friends of patients with implantable defibrillators, they should avoid wearing headphones and resting their head right on top of someone's device," he said. In two unrelated studies, researchers did not report adverse heart-related effects on implantable cardiac devices from other devices.
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Researchers in Hyannis, Mass., found that cell phones equipped with wireless technology known as Bluetooth® and pills swallowed to view internal organs are unlikely to interfere with pacemakers or ICDs (abstract P651). Likewise, California researchers determined that electromagnetic interference from personal devices including iPod®, iPod® nano, iPhone, some cell phones (with and without Bluetooth® technology), electric blankets and hand-held airport security metal detectors did not cause adverse effects to patients with pacemakers or ICDs (abstract P663).
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http://www.medicalnewstoday.com/articles/128723.php

Source of Image

http://www.bloomberg.com/apps/news?pid=20601103&sid=aqEpbLqyVSeU&refer=news

Large Versus Small LDL

2008-11-13T00:33:00.005-09:00

A Cross Section of a Typical LDL-Cholesterol Molecule

Large vs. small LDL

It is now a rare person who does not have at least some proportion of their LDL cholesterol as small particles. I estimate that, of the people who come to the office or report their data on the Track Your Plaque website, 90% have at least 40-50% small LDL particles. Some people have 100% small LDL particles. The nutritional approach for small vs. large LDL differs. Small LDL particles are most sensitive to carbohydrate intake; large LDL particles are more sensitive to saturated fats. The conventional "heart healthy" diet that restricts saturated fat reduces large LDL but exerts no effect on small LDL. Thus, a diet that is restricted in saturated fat and weighed more heavily with "healthy whole grains" triggers small LDL particles. Followers of the conversations here recognize that small LDL particles are flagrant triggers for coronary plaque; they have, in fact, become the number one most common cause for heart disease in the U.S. When you have lipoproteins tested, you can therefore gauge the likely result obtained when specific dietary changes are made. Follow the low saturated fat advice, large LDL will drop modestly, but small LDL skyrockets. Eliminate sugars, wheat, and cornstarch and you will see small LDL plummet (along with total LDL). As an aside, my personal observation is that the "need" for statin cholesterol drugs can be reduced dramatically by paying attention to this important LDL size distinction.
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Dr. William Davis

http://heartscanblog.blogspot.com/

Source of Image

http://www.souzaoenterprises.com/Omegacin.html

Sleep Apnea and Sudden Cardiac Arrest

2008-11-12T08:35:00.005-09:00

Mayo Clinic

10 Nov 2008

After studying the sleep characteristics of nearly 11,000 adults in an overnight sleep laboratory, Mayo Clinic researchers suggest that obstructive sleep apnea (OSA) - and, in particular, the low nighttime oxygen saturation of the blood it causes - may be a risk factor for sudden cardiac death (SCD).

OSA is a condition that disrupts breathing during sleep and is associated with obesity. The study identified OSA as one of two traits that contribute to the highest risk of SCD. The other is age - patients who are 60 years old or older. SCD can happen when the heart's electrical system malfunctions; if treatment - cardiopulmonary resuscitation and defibrillation - is not administered quickly, a person dies.

If further studies validate these findings, OSA would join established risk factors such as smoking, obesity, high cholesterol and high blood pressure. Mayo Clinic cardiologist Apoor Gami, M.D., the lead researcher on the study, presents the findings today at the American Heart Association's Scientific Sessions 2008 in New Orleans.

Significance

Physicians have suspected for years that OSA might be implicated in SCD because of evidence that low oxygen alters the blood vessels in a way that promotes heart disease. This is the first large study to rigorously test the hypothesis, Dr. Gami says. "Nighttime low oxygen saturation in the blood is an important complication of obstructive sleep apnea," says Virend Somers, M.D., Ph.D., the study's principal investigator. "Our data showed that an average nighttime oxygen saturation of the blood of 93 percent and lowest nighttime saturation of 78 percent strongly predicted SCD, independent of other well-established risk factors, such as high cholesterol.

These findings implicate OSA, a relatively common condition, as a novel risk factor for SCD." Dr. Somers says these early results are relevant to clinical care. He urges physicians to watch for OSA in their heart patients and consider treating severe cases. "It is possible that diagnosing and treating sleep apnea may prove to be an important opportunity to advance our efforts at preventing and treating heart disease," he says. Obstructive sleep apnea and public healthOSA is a common breathing disorder associated with frequent and repeated instances of upper airway obstruction during sleep.

Restless sleep and extremely loud snoring are typical symptoms. Obstruction can be caused by excess tissue in the airway, a large tongue or large tonsils, or nasal passage irregularities that diminish airflow.

Obesity is a major cause of the condition. Treatments are available, such as a customized appliance worn during sleep to stabilize tissues. Given the rising incidence of obesity in children and adults, OSA is also becoming more common, Dr. Somers says. So concerned are major heart physicians' groups about this emerging public health trend that last summer the American Heart Association and the American College of Cardiology issued a joint statement calling for studies probing the link between OSA and SCD, says Dr. Somers. He chaired the committee that wrote the statement. About the study

.The researchers reviewed data from 10,701 consecutive adults who underwent an initial diagnostic sleep laboratory analysis session between 1987 and 2003. During a follow-up period of up to 15 years, researchers assessed cases where patients had sudden cardiac arrest, and either died (SCD) or were resuscitated, in relationship to the presence of OSA and other data, including nighttime levels of oxygen saturation in the blood. Results showed that during an average follow-up of 5.3 years, 142 patients had suffered SCD and either died or were resuscitated. Collaboration and support.

Other researchers from Mayo were Eric Olson, M.D.; Win Shen, M.D.; R. Scott Wright, M.D.; Karla Ballman, Ph.D.; Daniel Howard; Dave Hodge and Regina Herges. The study was funded by grants from the National Institutes of Health and Mayo Foundation for Medical Education and Research

Article URL: http://www.medicalnewstoday.com/articles/128795.php

Brown Seaweed Gel Reduces Heart Attack Scarring

2008-11-10T13:20:00.007-09:00

(As a heart attack survivor with arrhythmias and reduced heart function from a severe heart attack (www.heartak.com), this is good news for the rest of you out there who are candidates for a heart attack.)
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Tue, 12 Aug 2008:
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It’s an amazing news for the heart patients as a team of Israeli scientists have developed a miracle gel which could save thousands of life suffering from major heart attacks.
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A gel derived from ordinary brown seaweed can be used for saving the heart patients from further heart attacks as researchers cim.

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The team of Israeli scientists led by Professor Smedar Cohen has claimed to discover such an incredible gel which substances can be used for strengthening the scar tissues of heart when it is injected in the heart through groin vein in liquid form.
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The liquid transforms into thick gel when it meets with the scar tissues of heart and also leads the tissues to be thick, which in general are found to be in thin form in heart patients.
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The thick heart tissues heal gradually and function as normal tissues, which shrinks the chances of further heart attack and enhance the life-term of patients.
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Usually, in heart patients, the tissues of the heart become week and left ventricle also becomes dangerously enlarged after first heart attack. As a result it has to work harder for pumping blood around the body thereby multiplying the chances of further heart attacks.
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At present, there is no treatment of healing the scar tissues of heart.
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According to British Doctors, after entering in the market commercially that is expected to arrive by 2011, this miracle gel can save as much as 20,000 lives every year.
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The researchers have tested it on the animals and found amazing result. According to them, 90 per cent of animals injected with the gel survived a heart attack compared to just 40 per cent who received no treatment at all.
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The trial on human has been initiated in Germany, Belgium and Israel, as per sources.

http://www.newstrackindia.com/newsdetails/11369

Source of Image

http://flickr.com/photos/bestrated1/298449143/#DiscussPhoto

Risk of Sudden Cardiac Arrest After a Heart Attack

2008-11-06T12:02:00.005-09:00

Community Study Of Heart Attack Survivors Finds Risk Of Sudden Cardiac Death Highest Early After Attack

People who survive a heart attack face the greatest risk of dying from sudden cardiac death (SCD) during the first month after leaving the hospital, according to a long-term community study by Mayo Clinic researchers of nearly 3,000 heart attack survivors.Sudden cardiac death can happen when the heart's electrical system malfunctions; if treatment - cardiopulmonary resuscitation and defibrillation - does not happen fast, a person dies.After that first month, the risk of sudden cardiac death drops significantly - but rises again if a person experiences signs of heart failure. The research results appear in the Nov. 5 edition of Journal of the American Medical Association.

This study emphasizes the need for physicians to stay in close contact with their heart attack patients, forming a partnership to recognize symptoms, says Veronique Roger, M.D., M.P.H., a Mayo Clinic cardiologist and lead author of the study. Physicians and patients - and their family members - need to be keenly alert for the symptoms of heart failure, as described by the American Heart Association, Dr. Roger says.

Heart failure symptoms that require immediate attention include:

-- Shortness of breath

-- Persistent cough or wheezing

-- Bloating and swelling-

-- Fatigue

-- Confusion

...

"There are three key findings here that can be immediately applied to heart attack patients today," Dr. Roger says. "One is that the first month post-heart attack is the highest risk period for patients to suffer sudden cardiac death - and acute surveillance is warranted. A second is that the risk drops rapidly after the first month, but this does not mean the patient is out of danger. Surveillance is still required after the first month because our third finding shows that even though the risk drops after the first month, the onset of symptoms of heart failure at any time after the heart attack markedly increases the risk of SCD."

The study is one of the largest and longest comprehensive community studies performed by reviewing medical records. Drawing on data from the Rochester Epidemiology Project, the study analyzed the records of 2,997 men and women who had heart attacks in Olmsted County, Minn. - the county where Mayo Clinic is located - between 1979 and 2005. The patients' average age was 67 years. Patients were followed until death or the last recorded medical exam. Investigators were able to identify out-of-hospital deaths whose primary cause was listed as coronary heart disease. This enabled them to analyze sudden cardiac death trends. Housed at Mayo Clinic, the Rochester Epidemiology Project is one of the largest long-term, integrated databases of patient records in the world.

Another major finding of this study identifies a long-term, positive trend in the reduction of sudden deaths by nearly 40 percent over this time. This reflects medical advances in the care of heart patients, Dr. Roger says.These include the use of rapid restoration of blood flow during the initial phase of the heart attack, treated by emergency care and the adoption of "secondary prevention" measures. These measures include diet and lifestyle changes, such as taking medications to lower cholesterol levels and blood pressure. The measures help keep heart disease from developing or progressing, Dr. Roger says.

The Mayo Clinic research team also includes Susan Weston; Bernard Gersh, M.B.Ch.B., D.Phil.; and Terry Therneau, Ph.D. Collaborating in the research was A. Selcuk Adabag, M.D., from the Veterans Affairs Medical Center in Minneapolis. Their work was funded by the U.S. Public Health Service, the National Institutes of Health, and the Veterans Affairs Clinical Science Research & Development Service.Mayo Clinic200 First St. SWRochesterMN 55902United States

http://www.medicalnewstoday.com/articles/128165.php

Source of Image:

http://www.lex-co.com/Departments/PublicSafety/EMS/Public%20Access%20Defibrillation/Lexington%20County%20EMS%20Public%20Access%20Defibrillation%20Page.html

Links:

http://www.heart-links.blogspot.com/

Inflammation and heart disease

2008-11-02T23:47:00.004-09:00

Inflammation and heart disease

by Dr Norman Swan

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Over the last couple of months there have been papers that reinforce evidence that heart researchers have had for years - that inflammation plays an important role in heart disease.
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Over the last couple of months there have been papers that reinforce evidence that heart researchers have had for years - that inflammation plays an important role in heart disease.

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There are a few lines of evidence. One is that people with immune diseases like rheumatoid arthritis and lupus have a raised risk of heart attacks. It's also known that white blood cells and immunological hormones assist cholesterol damage in arteries.
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And it's also known that statins - cholesterol-lowering medications - reduce the risk of heart attacks more than you'd expect from their cholesterol reduction, and they have immune effects.
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Summarising the findings from the three recent papers, they suggest that while cholesterol lowering is still vital, reducing inflammation - the immune reaction in arteries - is important too.
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In one study of people on statins, the lower the inflammation, the lower the heart attack risk.
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In another study of people on a statin, the lower the bad form of cholesterol and inflammation, the slower artery blockage progressed.
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And a third study of markers of inflammation showed an association with the risk of heart disease.
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Some lifestyle changes may help lower inflammation, like exercise and diet if you don't like fancy medications, but that's yet to be proven conclusively.
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For Reference

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Title: New England Journal of MedicineAuthor: Nissen S et al, Statin therapy, LDL cholesterol, C-reactive protein and coronary heart disease.URL: http://content.nejm.org/2005, vol 352, pp 29-38.
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Title: New England Journal of MedicineAuthor: Ridker PM et al, C-reactive protein levels and outcomes after statin therapy. URL: http://content.nejm.org/2005, vol 352, pp 20-28.
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Title: New England Journal of MedicineAuthor: Ehrenstein MR et al, Statins for atherosclerosis - a good as it gets?URL: http://content.nejm.org/2005, vol 352, pp 73-75.
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Title: New England Journal of MedicineAuthor: Pai J et al, Inflammatory markers and the risk of coronary heart disease in men and women.URL: http://content.nejm.org/2004, vol 351, 2599-2610.

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http://www.abc.net.au/health/minutes/stories/2005/01/27/1290235.htm

Source of image

http://www.flameez.com/files/2177936/uploaded/diagram2.jpg

CRP does not cause Heart Disease

2008-11-02T14:24:00.012-09:00

Recent reseach suggests that while increased CRP levels are an indicator for increased risk for heart disease and stroke, they are not cause of the heart disease. Many drug companies are trying to find drugs that reduce CRP; they are barking up the wrong tree. (sparker, November 2008)

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Treatments Aimed Directly at Protein in Blood Won't Affect Heart Disease

By Daniel J. DeNoon, WebMD Health News

Oct. 29, 2008 -- C-reactive protein is linked to heart disease, but it's an innocent bystander and not a cause of disease, a new study shows.

People with high levels of C-reactive protein (CRP) in their blood are at high risk of heart disease. The protein is part of the body's inflammatory immune response.

Inflammation swells cholesterol-crammed artery walls, making the lining of those arteries vulnerable to breaking down or bursting. When the lining of an artery wall is disrupted, a cascade of events is set off culminating in the formation of a blood clot, which can go on to cause a potentially deadly heart attack or strokes. Earlier studies have suggested that CRP plays a key role in this process.

Drug companies already are racing to make drugs that target CRP. But taking aim at CRP will miss the real causes of heart disease, suggests new evidence from Borge Nordestgaard, MD, DMSc, professor and chief physician at Copenhagen University Hospital, Denmark, and colleagues.
"There is nothing wrong with using CRP as a marker of higher risk for heart disease and stroke," Nordestgaard tells WebMD. "We just say it is not causing the disease."

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CRP and Heart Disease

Scientists know cholesterol directly causes heart disease because in clinical trials, people taking cholesterol-lowering drugs have less heart disease. Yet there's no drug that directly targets CRP.

Fortunately, nature has provided its own version of a clinical trial. Some people carry variant CRP genes that make more or less CRP than the normal CRP gene. Do people with naturally high CRP levels have more heart disease and stroke?

First, Nordestgaard's team measured CRP levels in more than 10,000 people. They found that high levels of CRP increased risk of heart disease by 60% and risk of stroke by 30%. That's the same degree of risk seen in previous studies.

Then the researchers analyzed CRP genes and measured CRP levels in more than 31,000 people. They found that people with certain CRP genes made 64% more CRP than people with the least active CRP genes. This allowed them to calculate that if CRP caused disease, people with the most active CRP genes should get up to 32% more heart disease and up to 25% more strokes.

Finally, the researchers looked at people who actually had heart disease or stroke and compared them to people who remained disease free. The big surprise: People with the most active CRP genes were at no higher risk for heart disease and stroke than were people with the least active CRP genes.

To make sure their calculations were correct, the researchers also studied people with variant cholesterol genes. Those with genes that made the most cholesterol were indeed at highest risk of heart disease and stroke -- almost exactly as their calculations predicted.

This means CRP does not cause heart disease, says cardiologist Heribert Schunkert, MD, director of Germany's Luebeck University Hospital and professor of cardiology at the University of Leicester, England.

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"It is pretty definitive. Genetic markers that increase CRP don't increase disease," Schunkert tells WebMD.

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Also convinced is Thomas A. Pearson, MD, PhD, MPH, senior associate dean for clinical research at the University of Rochester Medical Center. Pearson led a recent study group that evaluated CRP research for the CDC and the American Heart Association.

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"This is a nail in the coffin for the idea that CRP is a causal factor in heart disease," Pearson tells WebMD. "This is a very useful study, and cleverly done, and their conclusion is right on the money."

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That conclusion: CRP is an indicator of heart disease and stroke risk, but not a cause.

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The Nordestgaard study and an editorial by Schunkert and colleague Nilesh J. Samani, MD, FmedSci, appear in the Oct. 30 issue of The New England Journal of Medicine.

http://www.webmd.com/heart-disease/news/20081029/crp-not-cause-of-heart-disease