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

Why being a doctor is a great thing

Basic course in pediatric echocardiography for congenital heart disease

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

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.

New ACC recommendation system

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

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.

Carotid sinus massage

Carotid sinus massage (CSM)

It is a vagal maneuver with diagnostic and therapeutic values.

How to do CSM?

- The patient is placed in supine position with neck extended by a pillow under his shoulders. The head is turned away from the side to be massages.

- Palpate the carotid artery pulsation at the angle of the mandible.

- Auscualtate the artery to be massaged looking for bruit.

- While monitoring ECG, apply gentle pressure with rolling from side to side for no more than 5 seconds. The artery is pressed aganist the transverse process of the opposite cervical vertebra.

- The test can be repeated on the opposite side but never do the test on both sides simultaneously.

Effects of CSM:

- cardioinhibitory response: decreasing both sinus rate, atrial rate and AV-nodal conduction.

- Vasodepressor response.

Value of CSM:

A) Diagnostic:

- In arrhythmias: Termination of arrhythmia indicates that in involves the AV node as a part of its reentry circuit (i.e. AV node dependent tachycardia) such as AVNRT and AVRT. In other supraventricular tachycardias, the heart rate will slow down temporarily due to the increase of the AV nodal block. This slowing of ventricular response may reveal hidden flutter waves or abnormal P waves in cases of atrial tachycardias. Gradual and temporary decrease of heart rate occurs with sinus tachycardia. Abrupt and temporary decrease of the heart rate occurs with atrial tachycardias. There will be no effect in ventricular tachycardias. In ventricular tachycardia with retrograde atrial activation, the CSM will cause the retro grade P waves to disappear or to decrease in frequency (due to increased V-A block). (Thanks to my dear colleague, Dr. Mohammed Saber for adding the last sentence).

- In syncope: inducibility of the syncope by CSM is very important unless there is another clear cause. Blood pressure should be monitored during the test. The protocol is different from the above mentioned. A sinus pause of 3 seconds or more, or a drop in blood pressure of 50 mmHg or more are diagnostic of cardotid sinus hypersensitivity.

- In ACS: relieve of chest pain by CSM is diagnostic for angina pectoris (Levine's test). This can be applied also for several minutes. Also, in the presence of LBBB, CSM may cause disappearance of the LBBB and reveal underlying ST elevation.

B) Therapeutic:

- CSM can be used for termination of AVNRT and AVRT.

- CSM may be applied for several minutes to treat acute pulmonary edema with hypertension and myocardial ischemia.

When not to do CSM?

- In patients with know or highly suspected carotid artery disease such as patients with history of stroke or TIA's or carotid artery bruit.

- Patients with previous unfavorable outcome with CSM.

- Be very cautious with elderly patients.

N.B.: The CSM may provoke exaggerated response in cases of digitalis toxicity, even before any other sign of toxicity.

Is IST a form of dysautonomia?

IST = inapropriate sinus tachycardia

Back in the 19th century, there used to be a condition called “neurasthenia”. Young women (the beautiful but delicate ones, according to the romance novels of the time) would find themselves suddenly unable to function due to a host of inexplicable symptoms, often including fatigue, weakness, strange pains, dizziness, and passing out. Doctors would not find anything to explain these symptoms, so they were attributed to a “weak nervous system”, or neurasthenia. Victims were often confined to their beds, where they would either recover or, eventually (and tragically) die. And while nobody knew what caused this condition, everyone —doctors and laymen alike—took it seriously; the condition and its sufferers were treated with great respect.

Today’s doctors shake their heads in wonder at the notion of such a condition, and tend to put neurasthenia in the same bucketas the witchcraft hysteria of a few centuries earlier. But patients who would have been called neurasthenics 150 years ago are still around; they’re just given different labels. These labels include chronic fatigue syndrome (CFS), vasovagal or neurocardiogenic syncope, panic attacks, anxiety, irritable bowel syndrome (IBS), postural orthostatic tachycardia —and, quite possibly, IST. While most syndrome (POTS), fibromyalgia doctors still tend to think of these various syndromes as stand-alone conditions, they are all part of a general class of conditions called the dysautonomias.

In dysautonomia the autonomic nervous system loses its normal balance, and at various times the parasympathetic or sympathetic systems inappropriately predominate. Symptoms can include frequent, vague but disturbing aches and pains, faintness or frank syncope, fatigue and inertia, severe anxiety attacks, sinus tachycardia, hypotension, poor exercise tolerance, gastrointestinal disturbances, sweating, dizziness, blurred vision, numbnessand tingling, anxiety and (quite understandably) depression.

Sufferers of dysautonomia can experience all these symptoms or just a few of them. They can experience one cluster of symptoms at one time—and another at other times. And since people with dysautonomia are usually normal in every other way, a physical exam most often does not reveal any abnormalities. Patients are often labeled hysterical and are accorded little of the respect they received during the 19th century. (Fortunately, doctors no longer prescribe bed rest, so the risk of mortality is now very low.) When patients do get an actual diagnosis, the one they receive does often depend on their recently dominant symptoms and on which specialist they are referred to.

What causes dysautonomia? The dysautonomias do not have a single cause. Some patients inherit the propensity to develop dysautonomia syndromes, and variationsof dysautonomia often run in families. Viral illnesses can trigger a dysautonomia syndrome. So can exposure to chemicals. (Gulf War Syndrome is, in effect, dysautonomia—low blood pressure, tachycardia, fatigue and other symptoms—that, government denials aside, appears to have been triggered by exposure to toxins.) Dysautonomia can result after various types of trauma, especially trauma to the head and chest. (It has been reported to occur for example after breast implant surgery.) Dysautonomias caused by viral infections, toxic exposures, or trauma often have a rather sudden onset. CFS, for instance, most classically begins following a typical viral-like illness (sore throat, fever, muscle aches, and so on), but any of the dysautonomia syndromes can have a similar onset.

Is IST one of the dysautonomias? Obviously we do not know for sure, but it certainly shares many of the characteristics of dysautonomia, including that its onset is frequentlypreceded by a viral illness or trauma; that the patient profile is typical; and that “extra” symptoms frequently occur which are consistent with other forms of dysautonomia. (Indeed, many IST patients might have beenlabeled as suffering from IBS, POTS or CFS if they had seen someone other than an electrophysiologist.) Further, the fact that something stimulates the successfully ablated SA nodes to regenerate in IST patients suggests a more systemic problem than intrinsic SA nodal disease. And finally, electrophysiologists have noted that symptoms consistent with dysautonomia often persist even after successful SA nodal ablation (i.e., during the period of time that normal heart rates have been restored).

From: Richard N. Fogoros, Electrophysiologic testing, 4th ed.,2006.

Assessment of the Left ventricular function in the presence of mitral regurge

The assessment of the rate of rise of LV pressure (dP/dt) can predict the intrinsic left vemtricular systolic function in a load-independent from. Thus it can be used in the assessment of left ventricular systolic function in the presence of mitral regurge. In fact, this method is under utilized in the daily practice.

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To take this measure you must have good picture of the maximum regurgitant jet. Then take a continuous wave doppler spectral profile with high sweep speed (100mm/sec or more). Then measure the time taken for the velocity to rise from 1m/sec to 3m/sec. From Bernolli equation: the pressure change in this time is 32mmHg (4(3)² – 4(1) ² = 36 – 4 = 32). Then dP/dt = 32/the measured time in seconds. Normally this value is > 1200. A dP/dt value from 800-1200 suggests mild systolic impairment. A dP/dt value <800>

LV systolic function	dP/dt	Time taken by LV to generate 32 mmHg
Normal	>1200	<27 br="" msec="">
Mild-moderate impairment	800 – 1200	27 – 40 msec
Sever impairment	<800 o:p="">

>40 msec

(click on the images to view full size)

The major advantage of this method is that it is independent from changes in the afterload as the measures are taken in the isovolumetric contraction phase (before the opening of the aortic valve. Also, this method is well-validated in comparison with cardiac catheterization results. Unfortunately this method is unreliable in cases of left ventricular dysynchrony as in cases of LBBB. Also, it is affected by left atrial compliance. So, it can not be used in cases of acute mitral regurge as the left atrial pressure is elevated and the left atrium is noncompliant. If the regurgitant jet is eccentric, excess care should be taken to make the cursor line at the direction of the jet and at its center to avoid false measurements. However sever aortic stenosis and systemic hypertension was found to affect the reliability of this method.

The dP/dt was found to have prognostic value in the course of chronic heart failure. It is also used to predict the postoperative left ventricular function before valve repair and replacement.

The same principle can be used in the assessment of the right ventricular systolic function with some modification. On the tricuspid valve the time is measured time interval is between the velocities 0 and 2 m/sec (due to the lower pressures on the right side). Thus the dP/dt value on the right side is calculated by dividing 16 on the time interval taken to raise the tricuspid regurge velocity from 0 to 2 m/sec. But this method is not well-validated to assess RV systolic function.

On the opposite side the –ve dP/dt, which is the rate of decline of left ventricular pressure, can be used as a measure for diastolic dysfunction.

References:

1- http://www.criticalecho.com/content/tutorial-5-assessment-lv-systolic-function

2- Feigenbaum's Echocardiography, 6th Edition

3- Echocardiography: the normal examination and echocardiographic measurements, by Bonita Anderson 2002.

4- The practice of clinical echocardiography, by Catherine M. Otto‏, 2007

5- Echocardiography Review Guide, by Catherine M. Otto and Rebecca Gibbons Schwaegler, 2007

6- Doppler-derived dP/dt and –dP/dt predict survival in congestive heart failure, Theodore J. Kolias, Keith D. Aaronson, and William F. Armstrong, 2000;36;1594-1599 J. Am. Coll. Cardiol.

7- A new method for estimating left ventricular dP/dt by continuous wave Doppler-echocardiography. Validation studies at cardiac catheterization, GS Bargiggia, C Bertucci, F Recusani, A Raisaro, S de Servi, LM Valdes-Cruz, DJ Sahn and L Tronconi, 1989;80;1287-1292 Circulation

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.

Smoking paradox

Do you know about smoking paradox?

I first heard of this was during a clinical round a week ago. The professor asked us about it and nobody knew the answer. He told us the answer. It was noted that the incidence of in-stent stenosis following PCI was lower in smokers than non-smoker. He explained that by activation of CYP450 by smoking. This enzyme is responsible for transformation of clopidogrel to its active form. This lowers in-stent thrombosis and also lowered clopidogrel resistance.

However I have done my own search on the web to know more about that topic. I found some additional information. There are more explanations not mentioned by our professor. One explanation is the younger age of smokers in the studies revealing that paradox. Another one is the relectunce of smokers toseek medical advice when such problems occur. However, the long term mortality is still higher in smokers despite this claimed paradox.

I found two other paradoxes related to smoking. One was the lower mortality of somkers hospitalized for heart failure in OPIMIZE-HF study compared with non-smokers. However, the age of the smokers in the study was also younger, and this may be a resonable explanation. Another explanation is the difference in drug handling by smokers due to enzyme induction and inhibition. The third paradox related to smoking was noted in the study of lung cancer. It was noted the Japanese population has lower incidence of lung cancer compared with western populations, despite the higher incidence of smoking in the Japanese. This time the explanations were multiple. The main explanations were genetic difference, the different cigarette types and different filters, and the more healthy lifestyles led by the Japanese (less fat and less alcohol consumption).

The term "Paradox" may be deceiving or misleading. It gives the false impression that smoking is benfitial in this disease. The fact is exactly the opposite. Smoking causes the disease process to happen in an earlier age. And the real cause for the paradox is the younger age of the smokers, not the smoking itself, I guess. However it is still established that nonsmokers have longer and more healthy lives.

If you would like to read in more details follow these links:
1, 2 and 3.

Another case

Here is another case met by our hospital few weeks ago. The patient is a 25 year old male admitted to our hospital because of comminuted fracture of the humerus in a motor vehicle accident and internal fixation by plate and screws was done. 2 days after operation, the patient suffered of dyspnea and tachypnea of sudden onset. His blood pressure was 80/40 and heart rate was 145 bpm. He was transferred to the ICU. His oxygen saturation was low (in 80's) and the chest exam revealed generalized sibilant rhonchi. The followinf ECG was obtained.






Pulmonary embolism was suspected but, unfortunately there was no availible CT or echocardiography in our hospital by that time. The attending physician thought he might loose the patient if he referred him to another hospital because the patient's condition was getting worse despite i.v. fluids oxygen inhalation and bronchodilators. He decided to give thrombolytic therapy. After receiving the streptokinase the patient's condition improved markedly. Here is the ECG obtained after finishing streptokinase infusion.

A case of arrhythmia

50-year old male patient came to our hospital complaining of palpitations. He had steted that the onset was about 45 minutes ago and was relater to a fall from a ladder. The patient showed no dyspnea or chest pain. He was not on any medications. There was no signs of distress. His BP was 100/60 and heart rate was 140 bpm and irrregularly irregular. 12-lead ECG was done and here it is:
Click on it to enlarge







What do you thin is the diagnosis and what should we do?


Update: see the tracing after cardioversion below

Uncommon case of chest pain CME on medscape

Here is a new CME case from CME medscape.
It is a nice case of chest pain due to an uncommon cause. Just try to guess the answer without looking at the multiple choices at the bottom and see if you can expect it. Look carefully in the X-ray. The link is here.

http://cme.medscape.com/viewarticle/702661