Cardiology Database

Strain fundamentals made easy

2017-03-16T03:26:00.000+02:00

Basic course in transesophageal echocardiography

2016-12-17T04:53:00.000+02:00

Importance of appraisal of published papers

2016-12-07T12:26:00.001+02:00

A must-see video by the amazing medical educator Dr. Eric Strong. Here he is exploring the defects in our scientific publishing system leading to wrongful perception of medical evidence guiding the medical practice.

Echocardiography in obstructive shock

2016-12-04T11:56:00.000+02:00

Embryology for the cardiologist

2016-12-03T09:30:00.000+02:00

A very informative concised lecture on the embryology of the heart. A must-see lecture before studying congenital heart disease.

Dynamic LVOT obstruction

2016-12-02T06:43:00.000+02:00

Dynamic LVOT obstructin can occur due to several causes:
1. The most well-known cause is hypertrophic cardiomyopathy (HCM). The hypertrophied basal septal (the most common cause of HCM) causes narrowing of LVOT that is dependant on the preload and afterload. Sometimes the obstruction is not obvious and requires provocation with Valsalva's maneuver or vasodilators.
2. Narrowing of LVOT due to other causes (e.g.: subaortic membrane) can cause dynamic obstruction. So, with subaortic membrane part of the obstruction is fixed due to the presence of membrane itself. but sometimes there is a dynamic component due to the associated systolic anterior motion (SAM) of the anterior mitral leaflet. This is due to the Venturi effect, as increased velocity in the LVOT bulls the anterior mitral leaflet causing further narrowing of the LVOT.
3. With increased contractility of the basal portions of LV. This can occur in different situations. For example compensatory hypercontractility of the basal segments in cases of acute myocardial infarction involving the apical and mid segments. Another example is in case of stress cardiomypathy that typically involves the apical segments with the famous apical ballooning picture. The basal parts usually tries to compensate with increased contractility to keep the cardiac output unaffected. The third condition is increased contractility due to dminstration of dobutamine as during dobutamine stress echocardiographym, dynamic LVOT obstruction can occur and is one of the possible causes of hypotension that is worsened by the vasodilator effect of dobuamine. The presence of concentric LVH with small cavity is predisposing condition in all the three situation given here.
4. Cardiac amyloidosis should be suspected in dynamic LVOT obstruction. It can cause septal hypertrophy in association with reduced LV filling. Both togeather may lead to LVOT obstruction.
5. Mitral valve repair with ring: Here the anterior mitral leaflet is pushed rather than pulled into the LVOT in contrary to the other types of LVOT obstruction. Small LV cavity and long posterior leaflet predisposes to this situation.
6. Increased velocity in the LVOT with increase flow as in exercise, sepsis and severe anemias has been shown to cause LVOT obstruction in some cases. Here there is reduction of the afterload associated with tachycardia that causes reduced filling time and smalled LV cavity predisposing to dynamic LVOT obstruction.
7. Aortic valve replacement for treatment of aortic stenosis. Long standing aortic stenosis causes significant LVH. But as there is increased afterload due to the fixed obstruction at the valve level, this keeps the LV walls apart and no dynamic component is present. As the fixed obstruction is relieved with aortic valve replacement, the dynamic obstruction is unmasked. Dynamic obstruction here is more commen to happen at the midcavity level rather than LVOT.
8. Sigmoid septum in elderly patients can cause dynamic LVOT obstruction due to abnormal aortic angle but yet the exact mechanism is unclear.
9. In cases of L-TGA, the LVOT is open into the low pressure pulmonary circulation while the right ventricle is exposed to the systemic higher pressure circulation. This causes bulging of the interventricular septum to the left ventricle and subsequently may cause dynamic LVOT obstruction of a unique mechanism

The source is here

Acute right sided heart failure

2016-12-01T06:06:00.001+02:00

Stress Echocardiography

2016-05-24T04:25:00.000+02:00

Here is a quick tip about stress echocardiography. During stress echocardiography, both left ventricular dilatation and decline in global systolic function are indicative for severe coronary artery disease. Both are less common to occur with dobutamine stress echo rather than exercise echocardiography. However, hypotension is also a marker of severe coronary artery disease that is more likely to occur during dobutamine stress echocardiography. his may be due to the vasodialtor effect of dobutamine or due to dynamic left ventricular outflow tract obstruction with increased contractility.

Is oxygen beneficial in patients with myocardial infarction?

2016-05-19T21:42:00.001+02:00

In classic teaching in medical school, we were told to give supplemental oxygen to patients with myocardial infarction. But in the era of evidence based medicine this may be not true for everyone. The AVOID trial has addressed tis issue. The AVOID investigators has found that oxygen in the non-hypoxic STEMI patients was associated with increased infarction size (detected by CMR), increased rate of re-infarction and increased incidence of ventricular arrhythmias. So, it is not recommended to give supplemental oxygen if the patient is not hypoxic on room-air, i.e. the patient has SO2 above 94%. This may be explained by the increased formation of oxygen free radicles that are associated with more myocardial injury (chemical rather than ischemic).

This is a link to the AVOID study results.

Tips on echocardiography for constrictive pericarditis

2016-05-13T08:19:00.000+02:00

Echocardiographic features of constrictive pericarditis include:

- Septal bounce

- dilated IVC

- dilated hepatic veins with diastolic flow reversal on expiration

- absence of normal sliding motion between the RV and the liver

- respiratory varitions of mitral E velocity with more than 25% increase with expiration

Respiratory variations of mitral inflow (E-wave) is not always present in constrictive pericarditis. It can be masked by increased left ventricular end diastolic pressure. However, it can be unmasked by imaging in the sitting up position. Also some diuretics may unmask it. Howeverm its absence does not exclude constriction.

Respiratory variations of mitral E-wave velocity can occur also with COPD. in cases of COPD, the highest E-wave is at onset of expiration, while in constriction, the highest E-wave is at end expiration. Another useful tip, use SVC flow to differentiate COPD from constriction. In COPD SVC systolic flow increases markedly with inspiration. But in case of constriction, SVC diastolic flow shows limited increase with inspiration (less than 20cm/sec).

Using Tissue Doppler Imaging to differentiate constriction from restriction:

- medial mitral e' velocity less than 8 cm/sec is associated with restriction.

- constriction is associated with "Annulus Reversus" on TDI. This means that the medial annular e' velocity is higher than that of lateral annulus. Normally, the lateral mitral annular e' velocity is higher than the medial by more than 20%. This annulus reversus disappears after pericardiectomy.

ECG tips in acute coronary syndromes

2016-05-11T04:47:00.001+02:00

Wellens' syndrome: This is characterized by symmetrical T-wave inversion in the precordial leads during the chest pain free periods in the setting of ACS. This occurs without Q waves,o ST-elevation. The cardiac enzymes are not or minimally elevated. During the chest pain episoes, this T-wave inversion may be normalized (pseudonormalization). The presence of Weelens' syndrome indicates the presence of critical lesion in the proximal segment of the left anterior descending artery (LAD). Early intervention is advised in this settings.

De Winter's T waves: This is charachterized by an upsloping ST depression (>1mm at J point) followed by a tall symmetric T-wave. This was present in precordial leads. It is associated with 0.5-1 mm elevation in aVR. This pattern is present in 2% of anterior MI. It may precede or follow the usual pattern of anterior STEMI. It was associated with LAD occlusion. Presence of this sign should prompt activation of cathlab immediately.

aVR - Does it have any diagnostic value?

Actually it has. In the setting of diffuse ST-depression (more than 7 of the other11 leads), ST elevation in the aVR indicates the presence of either left main coronary stenosis or multivessel disease.

Localization of the culprit leion in the setting of inferior STEMI: You may compare the amplitude of ST-segment elevation in the inferior leads. If the highest elevation is in the lead II, LCX occlusion is expected. If lead III shows the highest ST-segment elevation, RCA occlusion is more common.

Acute MI with LBBB: We all know that LBBB causes changes in ST-segment, rendering the diagnosis of STEMI difficult. some useful tips are presented here. Actually new LBBB in the setting of STEMI is the result of proximal total occlusion of LAD or left main coronary artery occlusion. These are sites of obstruction before the 1st septal branch that supplies the left bundle branch. An infarction due to occlusion in this site is usually associated with severe pain and hemodynamic compromise due to large area of infarction involved. Those patients may present with acute heart failure or cardiogenic shock. The interpretation of ECG with understanding this clinical tips is somewhat helpful in making the diagnosis. Another point is the Sgarbossa diagnostic criteria.

concordant ST elevation >1mm is given 5 points. Concordant ST depression >1mm is given 3 points. Discordant ST elevation >5mm is given 2 points. The higher the Sgarbossa score the patient hasm the more likely he has a myocardial infarction. However, Dr. Smith has found some modification on these criteria to be more useful. He suugested that the discordant ST elevation to be considered positive if it reaches >25% of the depth of the preceding S wave.

After coronary reprefusion we should monitor for the signs of myocardial reperfusion, one of which is reperfusion arrhythmias. The most specific arrhythmia for reperfusion is accelerated idioventricular rhythm, also known as slow VT. It is a ventricular rhythm at rate of 60-120 bpm.

Basic course in transesophageal echocardiogeaphy

2016-04-22T09:39:00.000+02:00

Echocardiographic Workshop on Congenital Heart Disease

2016-04-21T01:38:00.001+02:00

Here is a playlist that contains a workshop on echocardiography in congenital heart disease.

Contrast agents for coronary angiography

2016-04-12T06:34:00.000+02:00

Assessment of coronary plaques

2016-04-12T06:32:00.002+02:00

Hemodynamics in cathlab

2016-04-12T06:31:00.002+02:00

discussion

Bifurcational lesions - basics of coronary angiobraphy

2016-04-12T06:29:00.002+02:00

Selection of catheters - basics of coronary angiography

2016-04-12T06:26:00.000+02:00

https://www.youtube.com/watch?v=tkkds9YsWYI

coronary lesion assessment - basics of coronary angiography

2016-01-28T14:30:00.001+02:00

Angiographic views - Basics of coronary angiography

2016-01-28T14:28:00.000+02:00

Why being a doctor is a great thing

2015-11-30T04:34:00.000+02:00

Basic course in pediatric echocardiography for congenital heart disease

2015-11-15T10:41:00.002+02:00

Here is a series of 17 videos that represent a basic course for beginners in pediatric echocardiography for congenital heart disease.

Allergic Angina

2015-10-03T01:53:00.000+02:00

Allergic angina
Also known as "Kounis syndrome"
Named after the greek cardiologist "Nicholas Kounis" who has first described it in 1991.
- It is an acute coronary syndrome (may be STEMI) that is precipitated by an allergic reaction (e.g., bee sting)
Pathophysiology:
- Allergic insults resulting in mast cell degranulation and release of inflammatory mediators e.g, histamine, neutral proteases, arachidonic acid derivatives, platelet activating factors and a variety of cytokines and chemokines. These substances cause coronary vaso spasm and plaque rupture.
- Tryptase release leading to plaque rupture through activation of interstitial collagenase, gelatinase and stromelysin.
Diagnosis: clinical condition with confirmation by increased serum tryptase level.
Treatment consideration: The usual anti-anginal medication with the following treatment changes:
- Antianaphylactic measures: epinephrine, corticosteroids and antihistaminics.
- Pain control by Fentanyl not morphine as morphine is associated with histamine release.
- Avoid beta blockers. Even reverse beta blockers if given with glucagon. Do not give epinephrine if beta blockers are give except after reversal due to fear of unopposed alfa action.

New ACC recommendation system

2015-10-01T15:42:00.000+02:00

Here is the new recommendation and level of evidence system adobted for the ACC guidelines.

Cardiology case presentation

2013-03-25T19:28:00.000+02:00

Cardiology case 1 from Mohammed Khayyal