Dynamic LVOT obstruction

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 

Stress Echocardiography

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?

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.

ECG tips in acute coronary syndromes

•  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.

Contrast agents for coronary angiography

Assessment of coronary plaques

Hemodynamics in cathlab

discussion

Bifurcational lesions - basics of coronary angiobraphy

Selection of catheters - basics of coronary angiography

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

coronary lesion assessment - basics of coronary angiography

Angiographic views - Basics of coronary angiography

Allergic Angina

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.

Cardiology case presentation

Cardiology case 1 from Mohammed Khayyal

Biochemical markers of myocardial necrosis

The Damage of myocytes results in release of several proteins into the circulation. The estimation of the serum level of these proteins can be used as a marker of myocardial necrosis. These proteins include:

• Myoglobin
• Creatine kinase (CK) and its isozyme myocardial band creatine kinase (CK-MB)
• Cardiac troponins I and T (cTnI and cTnT)
• Lactate dehydrogenase
• Aspartate aminotransferase (AST) or (SGOT)
• Ischemia modified albumin
• Heart Fatty acid binding protein
• Myosin light chain

The criteria for ideal biomarker for myocardial necrosis are:

1. High sensitivity: abundant in myocardial tissue.
2. High specificity: not present in extramyocardial tissues.
3. Rapid release from damaged cells
4. Cost effective detection
5. Can be detected precisely

Elevation of biochemical markers is essential for diagnosis of myocardial infarction. From the definition of myocardial infarction "it is the typical rise and fall of biomarkers of myocardial ischemia with at least a single value above the 99^th percentile of the upper reference limit, combined with the presence of any of ischemia symptoms, ischemic ECG changes (Q-waves, ST elevation or ST depression) or coronary intervention". However this definition considers only 2 of the cardiac biomarker, namely troponins and CK-MB. Due to the lag between the onset of chest pain and appearance of biochemical markers in blood, a second sample should be obtained and tested after 6 hours of the presentation before exclusion of myocardial infarction.

Myoglobin:

• It is a small heme protein found in myocardium and skeletal muscles.
• The earliest marker to rise (within 1-2 hours) because of its small molecular weight that facilitates its diffusion from the damaged tissue to circulation.
• Peaks after 6-8 hours
• Returns to normal after 24 hours
• It is highly sensitive.
• It is not specific to myocardium because it is found also in greater amounts in the skeletal muscles. So, not used in clinical practice to detect myocardial necrosis.
• Normal level is 30-90 ng/ml in males and 10-55 ng/ml in females.

Creatine kinase (CK) and its isoenzyme (CK-MB):

• It is found within the striated muscle (skeletal and cardiac) cells and is essential for ATP production (creatine phosphate shuttle).

• It is a dimer formed of two subunits. In the skeletal muscle the two subunits are of M type. In the cardiac muscle there is one M subunit and the other is of B type.
• The CK-MB isozyme is abundant in the cardiac myocytes (40%). The CK-MM isozyme is dominant in skeletal muscle (97%).
• Detection of total CK is less sensitive and less specific than detection of CK-MB.
• Both CK and CK-MB are elevated in other causes than MI, e.g. rhabdomyplysis. In such cases, CK-MB to total CK fraction of >10% is diagnostic of MI.
• CK-MB is detectable after 4-6 hours of onset of chest pain in MI, peaks after 24 hours and remains elevated for 3-4 days.
• CK-MB is more useful in detection of re-infarction because of its faster return to normal value as compared with troponins.
• Normal CK: 15-170 U/L
• Normal CK-MB: 0-15 U/L

Troponins:

• Troponin complex is a regulatory protein responsible for regulation of myocyte contraction. It is formed of 3 subunits. Troponin C binds to the calcium, troponin T binds to tropomyosin and troponin I inhibits actin and myosin interaction.

• The bulk of troponin is found within the contractile apparatus but a small fraction is found free in the cytoplasm (cytosolic) and it is the first part that detected in the plasma.
• Normal cTnI is <0.1>
• - It is elevated 4-6 hours after the onset of MI.
• It peaks after 24 hours.
• It remains elevated for 1-2 weeks after onset (TnT longer than TnI).
• It is highly sensitive and specific for myocardial damage.
• It adds prognostic value to the diagnosis as patients with negative troponins are considered of low risk. Also, the level of elevation is correlated to the risk. Patients with elevated troponins <6>
• Troponins are not useful for diagnosis of re-infarction because it takes long duration to return to the normal value. So, concomitant estimation of CK-MB is needed.
• Elevation of troponins with normal CK-MB levels identifies the patients who will gain greatest benefits of GP IIb/IIIa inhibitors.

• other conditions that cause elevation in cardiac troponins are:

- other causes of cardiac injury:

cardiac contusion

Pulmonary embolism

Acute decompensated heart failure

Coronary spasm

Hypertensive crisis

Myocarditis

DC cardioversion/defibrillation/ablation procedures

- Renal failure: elevated troponins level is found in high percentage of asymptomatic patients with end stage renal disease. cTnI is much more specific than cTnT in this group of patients.

- Other infrequent causes:

Subarachnoid hemorrhage and cerebrovascular accidents.

Endocrinal diseases.

Hematological malignancies.

Skeletal muscle diseases: dermatomyositis and polymyositis.

Sepsis

Lactate dehydrogenase (LDH):

• This enzyme is widely distributed in many tissues and organs.
• It is not specific for myocardial injury as it is found also in RBCs WBCs, lungs, kidneys, liver, skeletal muscles, pancreas, placenta and other tissues.
• It is elevated in MI after 24 hours, peaks after 3-4 days and returns to normal after 14 days.
• The isoenzyme LDH₁ is the form found in cardiac myocytes and RBCs. Normally LDH₂ is the abundant form. So, flipped LDH pattern (LDH₁>LDH₂) is found in MI and hemolytic and megaloblastic anemias.
• Normal LDH range: 100-225 U/L

Aspartate aminotransferase (AST also SGOT):

• This enzyme is found in myocardial cell, skeletal muscle cells and liver cells. It is elevated in injury to any of these tissues, so, it is not specific to myocardial injury.
• In MI, the AST level is increased after 6-8 hours of onset, peaks after 24 hours and returns to normal within 5-7 days. The AST level reaches 4-10 times the upper limit of normal in MI.
• The normal value is 5-30 U/L.

Heart Fatty acid binding protein (H-FABP):

• It is a small protein (14.5 KDa) responsible for transport of hydrophobic long chain fatty acids from cell membrane to mitochondria. The H-FABP is immunologically different from the corresponding protein found in liver and intestines.
• It is released rapidly (1-3 hours) and appears early in urine. Its urinary level correlates to the extent of infarction.
• It peaks at 6-8 hours from onset.
• It returns rapidly to normal level after 24-36 hours (excellent for detection of re-infarction and perioperative infarction).

Myosin light chain 1 (MLC1):

• Myosin is a part of the sarcomere (the basic contractile unit of the skeletal and cardiac muscles).
• Myosin is heteropolymer formed of 2 heavy chains and 2 pairs of light chains. There are 2 types of myosin light chains: MLC1 and MLC2.
• MLC2 is very labile and can not be measured clinically. Thus, it is not clinically significant.
• MLC1 appears after 3-6 hours and peaks after 4 days. It remains elevated for 10-14 days.
• Its peak level correlates to the infarction size and prognosis.
• It can not be used as a marker of reperfusion or re-infarction.

Ischemia modified albumin (ILA):

• Albumin loses its ability to bind some metals such as cobalt, after exposure to ischemic myocardium due to some conformational changes to its N-terminus.
• This test poorly discriminates between myocardial ischemia with and without infarction.

N.B.: The normal levels mentioned above may vary with different methods of estimation and between different populations.

Systolic and diastolic currents of injury

Why and How myocardial ischemia causes the ST segment changes?

Did you ask yourself this question before?

To answer such a question you need to go back to the physiological basics of electrocardiography. You must remeber that the ECG is the surface recording of electrical changes caused by electrical activity of the heart. At the culluar level those electrical changes are known as the action potential, which represents the potential differences across the cellular membrane as a result of a proper stimulus. The ischemia causes less negative resting membrane potential and loewr amplitude and longer duration of the action potential.



The ischemia is affecting a localized area and the rest of the myocardium is healthy and has normal action potential. This generates an electrical difference between the ischemic myocardium and the nearby healthy myocardium.

Systolic injury current:

During electrical systole (QT interval) the ischemic myocardium is less positive than the healthy myocardium (due to less amplitude of the action potential. This causes the electrical current to run from the healthy myocardium (more positive) to the ischemic myocardium. This is known as the systolic injury current. It is reflected in the ECG tracing as ST-segment elevation or depression according to the thickness and location of the ischemic area. If the ischemia affects the subendocardial area then the systolic injury current will be running from epicardium towards the endocardium (i.e. away from the body surface). The result will be ST-segment depression in the ECG leads corresponding to the ischemic territory. If the injuried area is whole thickness (transmural), then the systolic injury current will be running from the neighboring healthy myocardium towards the injured area. The summation vector of the resultant current will be directing outwards and causes ST-segment elevation in the leads representing the affected area.

Diastolic injury current:
The theory of diastolic current of injury is somewhat different. It is based on the fact that the resting membrane potential in the ischemic area is less negative in comparison with the healthy areas. This generates the diastolic injury current during the electrical diastole (TQ-interval). The direction of this current is from the ischemic area towards the healthy area. Thus it causes elevation of the TQ-segment in case of subendocardial infarction and depression of of TQ-segment in transmural infarction. But the TQ-segment is representing the base line for the ECG recording. So the net result will be apparent ST-segment depression and elevation respectively.


Images are from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.