This is a link to the AVOID study results.
Thursday, May 19, 2016
This is a link to the AVOID study results.
Friday, May 13, 2016
- Echocardiographic features of constrictive pericarditis include:
- 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:
Wednesday, May 11, 2016
- 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?
- 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.
- 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.
Friday, April 22, 2016
Thursday, April 21, 2016
Tuesday, April 12, 2016
Thursday, January 28, 2016
Sunday, November 15, 2015
Here is a series of 17 videos that represent a basic course for beginners in pediatric echocardiography for congenital heart disease.
Saturday, October 3, 2015
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)
- 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.
Thursday, October 1, 2015
Monday, March 25, 2013
Tuesday, February 16, 2010
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:
- 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:
- High sensitivity: abundant in myocardial tissue.
- High specificity: not present in extramyocardial tissues.
- Rapid release from damaged cells
- Cost effective detection
- 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 99th 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.
- 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
- 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:
Acute decompensated heart failure
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.
Skeletal muscle diseases: dermatomyositis and polymyositis.
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.
Monday, February 8, 2010
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:
- 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.
- 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.
Thursday, December 3, 2009
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.