What are the indications for aortic valve replacement in patients with aortic stenosis?The simple answer is that aortic valve replacement is indicated whenever symptoms develop related to the aortic stenosis. The classic triad of symptoms is dyspnea on exertion (from heart failure), angina on exertion, and syncope on exertion.Aortic valve replacement is also indicated if the left ventricular systolic function starts to decline from the pressure overload caused by the aortic stenosis.The clinical significance of a patient with aortic stenosis exhibiting symptoms cannot be underemphasized since the onset of symptoms is accompanied by a dramatic increase in mortality. According to one large series, if aortic valve replacement is not performed, patients presenting with dyspnea have a mean life expectancy of 2 years, those with syncope 3 years, and presenting with angina have an average of 5 years.

What are the signs and symptoms of digoxin toxicity?The most common symptoms are gastrointestinal and include nausea, vomiting, abdominal pain and diarrhea.The cardiac manifestations are the most concerning and can be life-threatening. Digoxin toxicity can induce literally every arrhythmia except for rapidly conducted atrial arrhythmias (atrial fibrillation or atrial flutter with ventricular rates > 100). Cardiac arrest and death can occur.Neurologic symptoms including altered mental status can occur even without hypoperfusion of the brain. Ocular manifestation includes xanthopsia (seeing yellow). Most experts believe that the famous artist Vincent van Gogh was using foxglove (the flower that digoxin is derived from) and this explains his yellow paintings toward the end of his life.

What are the causes of acute heart failure exacerbations?The etiology of a heart failure exacerbation is crucial to determine in order to direct medical therapy in the right direction not only to improve the current heart failure symptoms, but to prevent recurrence. Every heart failure patient presenting to the emergency room or the hospital ward should be evaluated for the following:1. Dietary non-compliance: Consuming large amounts of fluids and/or sodium can result in volume overload causing symptoms of heart failure and eventual pulmonary edema.2. Medication non-compliance: Frequently, diuretics are not taken as prescribed due to the urinary side-effects. Also, uncontrolled hypertension from not taking other cardiovascular medications can contribute.3. Ischemia: Acute coronary syndromes or progression of ischemic heart disease can cause heart failure exacerbations. All heart failure patients in the hospital should have at least one ECG performed as well as cardiac enzymes.4. Arrhythmia: Multiple different arrhythmias can occur in heart failure patients resulting in volume overload from reduced cardiac output. These include atrial fibrillation and ventricular tachycardia.5. Progression of the heart failure: Worsening of the cause of the patients heart failure, such as progression of valvular heart disease or further LV systolic decline in ischemic or non-ischemic cardiomyopathies cause trigger heart failure exacerbations.6. Non-cardiac illness: Pneumonia, severe sepsis, and gastrointestinal bleeding are examples of conditions that require a higher cardiac output. In patients with already reduced heart function, these can trigger clinical heart failure.

What are the potential fatal complications of an ascending aortic dissection?Aortic regurgitation: Acute aortic regurgitation can result from dilation of the aortic root. This may cause acute left heart failure with hypotension and pulmonary edema. Respiratory failure can ensue and again, surgical repair/replacement is required urgently.Inferior myocardial infarction: When the ascending aortic dissection involves the ostium of the right coronary artery, an inferior myocardial infarction can occur. This is diagnosed on the 12-lead ECG where ST elevation is seen in leads II, III and aVF with reciprocal ST depression in the high lateral leads I and aVL. Treatment is emergent coronary bypass surgery.Carotid artery dissection: When the carotid artery is involved in the ascending aortic dissection, symptoms of carotid artery dissection may occur which include headache, neck pain and Horner’s syndrome (ptosis - drooping eyelid, miosis - constriction of the pupil, and hemianhidrosis - lack of sweating on one side of the face), tinnitus and focal neurologic deficits.Cardiac tamponade: An acute pericardial effusion can occur causing cardiac tamponade if the proximal portion of the ascending aortic dissection ruptures into the pericardium. In this situation physical exam findings include:- Sinus tachycardia- Elevated jugular venous pressure- Pulsus paradoxus (see below)- Pericardial friction rub (from pericarditis if present)- Distant heart sounds (from heart sound muffling related to the pericardial effusion)- Kussmaul’s sign (rarely) - increase in jugular venous pressure during inspiration"Pulsus paradoxus" which is present in cardiac tamponade reflects a decrease in systolic blood pressure with inspiration of more than 12 mmHg. Pulsus paradoxus also occurs in severe asthma or COPD exacerbations.

What would a new left bundle branch block indicate in a patient with chest pain?A new left bundle branch block in a patient with chest pains would be concerning for an acute myocardial infarction. Sgarbossa criteria, Chapman’s sign and Cabrera’s sign can be helpful to make the diagnosis of an acute myocardial infarction in the setting of a left bundle branch block. See the review of a left bundle branch block for more details.

What is the long-term complication of childhood Kawasaki’s disease?Coronary aneurysms. When a coronary arterial wall becomes weakened it can dilate and form a coronary artery aneurysm. This can occur as post-stenotic dilation during ahteroslcerotic coronary disease or can occur as a part of a vasculitis. Kawasaki's disease (a form of vasculitis) during childhood can lead to coronary aneurysms in adulthood causing ischemic heart disease and angina. When the coronary aneurysms are large. the pathophysiologic mechanism of ischemia is thought to be due to microemboli and thus anticoagulation with warfarin is frequently utilized although there is no clinical data to support this therapy.

What is the classic triad of symptoms in aortic valve stenosis and how do they predict mortality if the patient remains untreated?The classic triad of symptoms in patients with aortic stenosis is exertional angina, exertional syncope and dyspnea from congestive heart failure.The development of aortic stenosis takes many years and is initially asymptomatic. Dyspnea is the first symptom of aortic stenosis in about 50% of the cases while syncope and angina account for 35% and 15% of initial symptoms respectively.The clinical significance of a patient with AS exhibiting symptoms cannot be underemphasized since the onset of symptoms is accompanied by a dramatic increase in mortality. According to one large series, if aortic valve replacement is not performed, patients presenting with dyspnea have a mean life expectancy of 2 years, those with syncope 3 years, and presenting with angina have an average of 5 years.

What is the definition of sustained ventricular tachycardia versus non-sustained ventricular tachycardia?Sustained ventricular tachycardia VT is defined as lasting greater than 30 seconds or symptomatic. Non-sustained is less than 30 seconds and asymptomatic.There is a big difference in the management of sustained versus non-sustained ventricular tachycardia (VT). Sustained VT requires immediate attention with either Cardioversion or medication therapy depending on the stability of the patient. Non-sustained VT is present in most patients with systolic heart failure and is usually asymptomatic.

What are the contraindications to using dronedarone?Dronedarone is contraindicated if left ventricular systolic dysfunction is present since clinical trials showed an increase in deaths from heart failure.Dronedarone is not indicated if atrial fibrillation or atrial flutter is permanent.Dronedarone is not used for ventricular arrhythmias.Dronedarone (Multaq) is a class III antiarrhythmic drug used in the treatment of paroxysmal and persistent atrial fibrillation and atrial flutter. There are structural similarities to amiodarone, however no iodine is present in the chemical structure of dronedarone which has resulted in dramatically reduced toxicity compared to amiodarone (see amiodarone toxicity), however a lower efficacy than amiodarone.

What are the three causes of holosystolic murmurs?The three main causes of holosystolic murmurs are mitral valve regurgitation, tricuspid valve regurgitation, and a ventricular septal defect. On rare occasion, Gallavardin dissociation from aortic stenosis can radiate to the cardiac apex where it may sound holosystolic and mimic the murmur of mitral regurgitation. Using handgrip exercises would increase the murmur of mitral regurgitation, but not change that of aortic stenosis which is helpful to distinguish these two.

What is cardiac amyloidosis, what are the causes, and what are the common pathologic findings?Amyloid cardiomyopathy is a form of restrictive cardiomyopathy and can result in significant progressive diastolic congestive heart failure.The familial form of amyloid cardiomyopathy is caused by a gene mutation resulting in a form of amyloid deposition called transthyretin. This can progress rapidly and can result in end-stage diastolic heart failure. Senile amyloid cardiomyopathy occurs much more slowly and is from the “wild type” or naturally occurring transthyretin amyloid protein. Diagnosis is made by myocardial biopsy.The only major therapy for familial amyloid cardiomyopathy is combined heart-liver transplantation (the liver is included since it is the location of the transthyretin production). Medical management is unsuccessful and is directed at improving symptoms.

How long does troponin I, creatine kinase (CK) and myoglobin remain detectable after a myocardial infarction?Cardiac enzymes (a.k.a. cardiac biomarkers) include myoglobin, troponin and creatine kinase. Historically, LDH (lactate dehydrogenase) was used as well however is non-specific. Cardiac enzymes are released into the circulation when myocardial necrosis occurs as seen in myocardial infarction.Myoglobin: Myoglobin is released into circulation with any damage to muscle tissue, including myocardial necrosis. Since skeletal muscle contains myoglobin, this measurement in quite non-specific for myocardial infarctions. The benefit lays in the fact that a detectable increase is seen only 30 minutes after injury occurs, unlike troponin and creatine kinase which can take 3-4 hours.Troponin: The enzymes troponin I and troponin T are normal proteins important in the contractile apparatus of the cardiac myocyte. They are released into the circulation about 3-4 hours after myocardial infarction and are still detectable for 10 days afterwards. The long half-life allows for the late diagnosis of myocardial infarction, however makes it difficult to detect re-infarction as can occur in acute stent thrombosis after percutaneous coronary intervention. There are a number causes of troponin elevation not related to myocardial infarction, however troponin elevation is much more sensitive than myoglobin and even CK.Creatine kinase (CK): Creatine kinase (a.k.a. creatine phosphokinase or CPK) is a muscle enzyme which exists as isoenzymes. The MB type is specific to myocardial cells while MM and BB are specific to skeletal muscle and brain tissue respectively. The CK level will increase approximately 3-4 hours after a myocardial infarction and stays elevated for 3-4 days. This makes it useful for the detection of re-infarction in the 4-10 day time window after the initial insult since troponin remains elevated for 10 days making it less useful for this purpose.

What are the complications of a left ventricular aneurysm?A left ventricular aneurysm can form after a transmural myocardial infarction. Most commonly, the apex of the heart is involved however, the inferior wall can form an aneurysm as well.The four main concerns in patients with left ventricular aneurysm are:1. Heart failure: The portion of the heart that contains the aneurysm is not contractile and is frequently “dyskinetic”. This results in overall decrease in heart function and the development of congestive heart failure.2. Left ventricular thrombus formation: When blood stagnates in any area of the body, there is a risk of platelet aggregation and thrombus formation. The aneurysmal portion of the LV is no different. Embolization of left ventricular thrombi can lead to embolic stroke or other systemic embolisms.3. Ventricular tachycardia: The scar within the left ventricular aneurysm is a focus for ventricular arrhythmias which can lead to sudden cardiac death.4. Angina pectoris: The aneurysmal tissue can still cause symptoms of angina, even if revascularized.An LV aneurysm can be diagnosed on ECG when there is persistent ST segment elevation occurring 6 weeks after a known transmural MI (usually anterior). Without knowing the persons past medical history, the ECG changes of an aneurysm may mimic an acute ST segment elevation MI. With an anterior or apical aneurysm, the persistent ST elevation is in lead V1 and V2. In an inferior aneurysm it would be in lead II, III and aVF. The only way to be sure of an LV aneurysm diagnosis on an ECG (not from an acute MI) is to have the patient’s history of a prior heart attack and cardiac imaging to document the presence of an aneurysm.There is a surgical procedure during which the surgeon resects the aneurysm and uses a Dacron patch. This is called the “Dor procedure” or the EVCPP (endoventricular circular patch plasty). This procedure is indicated when medical therapy fails to control or acceptably improve the above mentioned complications/symptoms from the left ventricular aneurysm.

Which statin significantly raises the levels of cyclosporine?Lovastatin significantly raises levels of cyclosporine. Historically, cyclosporine was quite expensive and yet a crucial medication for patients after cardiac transplantation to prevent rejection. In order to reduce the amount of cyclosporin needed and the cost, lovastatin was the statin of choice.

What causes a fixed split S2 heart sound?The second heart sound is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2 and the sound produced by the closure of the pulmonic valve is termed P2. When these sounds are distinguishable from each other a split S2 can be heard. The patterns of splitting of the S2 heart sound include physiologic splitting, paradoxical splitting, widened splitting and fixed splitting.A fixed split S2 is a rare finding on cardiac exam, however, when found it almost always indicated the presence of an atrial septal defect (ASD). A fixed split S2 occurs when there is always a delay in the closure of the pulmonic valve and there is no further delay with inspiration (compare this to a widened split S2 as described above).

To explore why an ASD results in a fixed split S2, we must considered the altered cardiac hemodynamics present in this situation which result in a fixed delay in PV closure. During inspiration, as usual there is an increase in venous return to the right side of the heart and thus increased flow through the PV delaying its closure. Where the alteration occurs in a person with an ASD is during expiration. As the person expires, the pressure in the right atrium decreases (since there is less venous return). The decreased pressure allows more blood to flow abnormally through the ASD from the high pressured left atrium to the right atrium ultimately resulting again in increased flow through the pulmonic valve again delaying its closure.

When is digoxin indicated for patients with heart failure?Digoxin therapy gets a class I indication for the treatment of symptomatic systolic congestive heart failure. The DIG (Digitalis Intervention Group) trial showed no mortality benefit, however there was improvement in symptoms and fewer hospitalizations for heart failure.Commonly, if systolic heart failure is present in combination with atrial fibrillation and an uncontrolled ventricular rate, digoxin therapy is utilized.Digoxin is only used in diastolic heart failure if atrial fibrillation is present with uncontrolled ventricular rates.Digoxin does have a class IIa indication to control heart rates in atrial fibrillation when used in conjunction with a beta-blocker or non-dihydropyridine calcium channel blocker.Digoxin has a class IIb indication to be used a sole agent to control heart rates in patients with atrial fibrillation and a class III indication (may be harmful) to be used as a sole agent to control heart rates in patients with paroxysmal atrial fibrillation.

What are the main factors to consider when choosing AV blocking agents to control heart rates in patients with atrial fibrillation?Selecting the appropriate AV blocking agent requires the knowledge of other indications and contraindications for these drugs, specifically, knowledge of the left ventricular systolic function is important. AV blocking agents used in AF include beta-blockers, non-dihydropyridine calcium channel blockers and digoxin.Beta-blockers (atenolol, metoprolol, carvedilol and others) antagonise beta-receptors (see review of beta-adrenergic blockers) which result in decreasing conduction through the AV node reducing the heart rate in atrial fibrillation patients. Caution is advised in patients with asthma since antagonizing beta-2 receptors can cause bronchospasm. In severe left ventricular systolic dysfunction (reduced ejection fraction), beta-blockers can acutely decrease cardiac output leading to severe hypotension, acute heart failure and even cardiogenic shock. Despite this, beta-blockers are considered safe when used cautiously in this setting.Non-dihydropyridine calcium channel blockers (diltiazem, verapamil) decrease AV conduction by antagonizing voltage gated calcium channels decreasing intracellular calcium. Since these drugs reduce left ventricular inotropy (contractility) via the same mechanism, they are in general not advised to be used in the setting of left ventricular systolic dysfunction (reduced ejection fraction).Digoxin blocks the sodium/potassium ATPase pump. The mechanism by which this decreases AV conduction is not clear however is perhaps due to increased vagal tone. Intracellular calcium within the cardiac myocytes is increased by digoxin resulting in increased inotropy (contractility) and thus digoxin is frequently used when AF and left ventricular systolic dysfunction coexist. Digoxin is effective to reduce ventricular rates at rest, however not effective during physical activity and thus it is recommended to use digoxin in combination with a beta-blocker or non-dihydropyridine calcium channel blocker.Rarely, the above medications are not able to adequately reduce the ventricular rate and AV nodal ablation with permanent pacemaker implantation is needed.

What is Brugada Syndrome?Brugada syndrome is a genetic disorder that results in sudden cardiac death from polymorphic ventricular tachycardia or ventricular fibrillation in the setting of a structurally normal heart. This is most commonly from a mutation in the sodium channel gene SCN5A. Unlike other genetic syndromes that results in sudden cardiac death, the QT interval is normal in Brugada syndrome.There are three types of ECG findings in Brugada syndrome patients:Type I: Lead V1 has a “coved” ST segment elevation of at least 2 mm followed by a negative T waveType II: There is a “saddleback” appearance of the ST segment in lead V1 with ST elevation of at least 2 mm. This can be present in normal individuals as well.

Type III: Features of type I (coved) or type II (saddleback) with < 2 mm of ST segment elevationThese ECG changes can be provoked in the electrophysiology lab by infusing ajmaline or procainamide.The treatment for Brugada syndrome is an implantable cardioverter defibrillator (ICD).

What is the definition of unstable angina?Unstable angina is an acute coronary syndrome characterized by an unstable coronary plaque causing symptoms of myocardial ischemia in one of three patterns:1. Exertional angina of new onset. Even if relieved with rest and requiring a consistent amount of exertion to

procedure symptoms, when angina first occurs it is considered unstable.2. Exertional angina that was previously stable and now occurs with less physical exertion.3. Anginal symptoms at rest without physical exertion. 

What is the ECG criteria for a 1st degree AV block?A first degree AV node block occurs when conduction through the AV node is slowed, thus delaying the time it takes for the action potential to travel from the SA node, through the AV node, and to the ventricles.A first degree AV block is indicated on the ECG by a prolonged PR interval. Recall that the P wave indicates atrial depolarization (initiated by firing of the SA node). The atrial depolarization eventually spreads to the AV node where there is a slight delay before the electrical impulse is conducted to the ventricles. If the AV nodal conduction (dromotropy) is decreased, it will take longer for the impulse to reach the ventricles, so there will be a greater distance between the P wave and the QRS complex (remember the QRS complex indicates ventricular depolarization). Thus the PR interval will be prolonged.The PR interval is normally 0.12-0.20 seconds or 120 to 200 milliseconds. A PR interval consistently longer than 0.20 seconds (greater than 5 small boxes) indicates a 1st degree AV block. Note: There is a 1:1 ratio between P waves and QRS complexes, unlike 2nd degree AV nodal block and 3rd degree AV nodal block.In general, a 1st degree AV block is a benign finding that does not require any treatment, however it may be an indicator of higher degree AV block in the future. Higher doses of AV blocking medications should be avoided.

What is hibernating myocardium and what are the imaging modalities that can detect this?Hibernating myocardium occurs when significantly reduced blood flow effects a segment of the myocardium causing dysfunction on a chronic basis. If blood flow is restored via percutaneous coronary intervention (PCI) or surgical bypass grafting, the function can return to normal. Viability testing can help determine if myocardium is hibernating or completely infarcted. Viability testing is best performed using magnetic resonance imaging (MRI), but can also be achieved with PET scanning (positron emission tomography), thallium myocardial perfusion imaging and dobutamine stress echocardiography.

How can hemochromatosis affect the heart?Hemochromatosis most commonly causes a restrictive cardiomyopathy, however can cause left ventricular systolic dysfunction and a dilated cardiomyopathy as well.A restrictive cardiomyopathy results in severe diastolic congestive heart failure with intact systolic function. This is due to significantly impaired left ventricular relaxation which results in increased cardiac pressures and clinical manifestations of congestive heart failure. See the review of restrictive cardiomyopathy and diastolic dysfunction for more details.

What are the ECG findings of a left ventricular aneurysm?A left ventricular aneurysm (LV aneurysm) can be diagnosed on ECG when there is persistent ST segment elevation occurring 6 weeks after a known transmural MI (usually anterior). Without knowing the persons past medical history, the ECG changes of an aneurysm may mimic an acute anterior myocardial infarction. With an anterior or apical aneurysm, the persistent ST elevation is in lead V1 and V2. In an inferior aneurysm it would be in lead II, III and aVF. The only way to be sure of an LV aneurysm diagnosis on an ECG (not from an acute MI) is to have the patient’s

history of a prior heart attack and cardiac imaging to document the presence of an aneurysm. The shape of the ST elevation is also relatively unique and has been described as “coving”.

What is the most common ECG finding of a pulmonary embolus?The most common ECG finding in the setting of a pulmonary embolism is sinus tachycardia, however the "S1Q3T3" pattern of acute cor pulmonale is classic. This is termed the McGinn-White sign.A large S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III indicates acute right heart strain. This pattern only occurs in about 10% of people with pulmonary embolisms and is similar to the ECG findings in a left posterior fascicular block (LPFB).

What are the potential side effects of ACE inhibitors?A non-productive cough is common with ACE inhibitors and is due to increased bradykinin in the lungs. This cough does not occur with angiotensin receptor blockers (ARBs).Angioedema is a life-threatening reaction relatively common with ACE inhibitors.A rash is common with ACE inhibitors.Hypotension can occur with ACE inhibitors causing dizziness and weakness.Hyperkalemia can occur due to the aldosterone inhibition.Renal failure can occur due to efferent arteriolar vasodilation.Angiotensin converting enzyme inhibitors (ACE inhibitors) are a class of oral medications that act primarily through blockade of the angiotensin converting enzyme (ACE). This enzyme converts angiotensin I to angiotensin II. Angiotensin II causes vasoconstriction increasing afterload thus increasing systemic blood pressure. Angiotensin contributes to the production of aldosterone which normally acts to retain sodium and water. 

What are the indications for valve replacement in patients with bacterial endocarditis?The indications for valve replacement in patients with endocarditis are:1. Congestive heart failure from valvular regurgitation2. Failure of antibiotic therapy to successfully suppress the infection or infection with difficult to treat organisms

(fungal, Pseudomonas, Brucella, drug-resistant organisms)3. Valvular annular abscess4. Peripheral embolism of vegetation5. Size of vegetation > 1.0 cm

Describe the Law of Laplace how it relates to cardiac hemodynamics?The left ventricular wall stress is the force acting against the myocardial cells. This is directly proportional to the left ventricular pressure and radius. Wall stress is indirectly proportional to two times the wall thickness. This was described with the Law of LaPlace which is quite important in order to understand which disease states can alter oxygen demand resulting in angina and which therapies can relieve angina:

Left ventricular pressure increases with states that increase “afterload” of the heart including systemic hypertension and aortic valve stenosis.Left ventricular radius increases in valvular heart disease (especially aortic regurgitation) or cardiomyopathies causing systolic heart failure.Left ventricular wall thickness increases in chronic hypertension or aortic valve stenosis as a compensatory mechanism to decrease wall stress (inversely proportional to wall stress) thus decreasing oxygen demand (since the

stress will be distributed over a larger mass). Hypertrophic obstructive cardiomyopathy (HOCM) similarly increases wall thickness. After myocardial infarction, the wall thins during remodeling which increases wall stress.

What is the classification system used for aortic dissections (name two and describe)?There are two classification systems used to describe thoracic aortic dissections:The DeBakey classification:Type I: Dissection originating in the ascending aorta extending a variable length frequently into the aortic arch and/or descending thoracic aortaType II: Dissection originating in the ascending aorta remaining confined to this area.Type III: Dissection originating in the descending thoracic aorta. This is further classified as IIIa which is confined to the thoracic aorta and IIIb which extends to the abdominal aorta.The Stanford classification:Type A: Dissection involving any part of the ascending aortaType B: Dissection remaining confined to the descending thoracic aorta

What is the treatment or “antidote” for a beta-blocker overdose?Beta blocker overdose can be life threatening. The three main features include bradycardia, hypotension and hypoglycemia. Hypothermia can occur as well.Treatment includes intravenous fluids to correct hypotension, glucagon to correct hypoglycemia and inotropes such as dobutamine or milrinone to correct bradyarrhythmia.Charcoal can be used to bind the beta-blocker. Ipecac is contraindicated.

How do the heart sounds and murmur of mild mitral stenosis (MS) differ from that of severe mitral stenosis?As MS worsens, left atrial pressure increases forcing the mitral valve open earlier in diastole. Thus, in severe MS, the opening snap occurs earlier as does the initial decrescendo part of the murmur.The mobility of the valve leaflets is a major factor influencing the intensity of M1 component of the first heart sound (S1). In mild to moderate mitral stenosis, the increased left atrial pressure causes the mobile portions of the mitral valve leaflets to be more widely separated, thus resulting in an accentuated M1 sound. In severe to critical mitral stenosis, the valve leaflets are so calcified and immobile that the M1 sound is diminished or absent.Mitral stenosis results in a uniquely shaped, low-pitched diastolic murmur best heard at the cardiac apex. The opening of the mitral valve produces an "opening snap" due to the high LA pressures, which is immediately followed by a decrescendo murmur as blood flows passively from the left atrium to the LV through the stenosed mitral valve creating turbulence. Immediately before the S1 sound, active LV filling occurs when the left atrium contracts and forces more blood through the stenosed mitral valve creating a late diastolic decrescendo murmur. In the presence of atrial fibrillation, the active LV filling phase does not take place and the latter part of the MS murmur disappears.

Historically, which medication is the safest to use during pregnancy to treat hypertension and what are the potential side effects?Methyldopa has been used safely to treat hypertension during pregnancy. Methyldopa is a centrally acting alpha-2 receptor agonist. When these receptors are stimulated, norepinephrine release is inhibited thus the heart rate decreases and there is a decrease in peripheral vascular resistance leading to decreased afterload and decreased systemic blood pressure.

What do the ACC/AHA guidelines say about the use of non-steroidal anti-inflammatory drugs (NSAIDs) during an acute coronary syndrome?These agents (ibuprofen, naproxen, rofecoxib) have many negative effects on the heart during and after STEMI. They can interfere with the beneficial actions of aspirin, increase the risk of myocardial infarction (COX-2 selective inhibitors), exacerbate heart failure, and increase blood pressure. These drugs should be discontinued immediately when STEMI is diagnosed according to ACC/AHA guidelines.

What are the cardiovascular implications of cocaine use (acute and chronic)?

Cocaine has a number of harmful cardiovascular effects. The main mechanism by which cocaine exerts these effects is via activation of the sympathetic nervous system. This results in profound hypertension and tachycardia at times leading to coronary vasospasm. The result can lead to acute myocardial infarction from increased oxygen demand or coronary vasospasm. Chronic cocaine use enhances the development of atherosclerosis. Treatment includes calcium channel blockers and the avoidance of beta-blockers so unopposed alpha agonism does not occur. Cocaine cardiomyopathy is similar to that of Takotsubo cardiomyopathy (stress induced cardiomyopathy).

What are the Jones Criteria?The Jones criteria are used to diagnose acute rheumatic fever:

What are the ECG findings of a secundum type atrial septal defect versus the primum type of atrial septal defect?The ECG of a patient with an atrial septal defect (ASD) should show a right bundle branch block (sometimes incomplete) partially due to the right ventricular volume/pressure overload that occurs.When an ostium primum atrial defect is present, the ECG reveals left axis deviation. When an ostium secundum atrial septal defect is present, the ECG reveals right axis deviation.

What is arrhythmogenic right ventricular dysplasia?Arrhythmogenic right ventricular dysplasia (ARVD) or arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic condition (autosomal dominant) affecting the desmosomes of the cardiac myocyte. This results in fatty replacement of the right ventricular myocardium.As the name implies, the predominant feature of ARVD is arrhythmia, usually in the form of ventricular tachycardia. This ventricular tachycardia is frequently from the right ventricular outflow tract also known as adenosine sensitive ventricular tachycardia. Premature ventricular contractions are common. Sudden cardiac death from ventricular fibrillation is a primary concern.

What are the indications to close an atrial septal defect?Closure of an atrial septal defect can be done either percutaneously with a closure device or surgically. ASD closure is indicated when right heart enlargement is present, however not in the presence of severe pulmonary hypertension and Eisenmenger’s syndrome.

What are the contraindications to using flecainide/propafenone?Flecainide and propafenone are class IC antiarrhythmic drugs. Significant coronary artery disease is a contraindication to the use of class IC antiarrhythmics as this increases the risk of proarrhythmia and sudden cardiac death.These drugs may be proarrhythmic in the setting of left ventricular hypertrophy (wall thickness > 1.4 cm) and are contraindicated in this setting.These agents must be used in combination with an AV blocking agent in order to prevent rapid atrial fibrillation or atrial flutter conduction (1:1 conduction) through the AV node resulting in very fast ventricular rates if a breakthrough episode occurs since class IC drugs also act to increase AV nodal conduction.

What medical therapy has a class I indication in the treatment of patients with chronic diastolic congestive heart failure?The ACC/AHA guidelines give three class I recommendations to medically treat chronic diastolic congestive heart failure.The first is to control the heart rate in patients with atrial fibrillation in order to improve diastolic filling. Tachycardia shortened diastolic filling time and so keeping heart rates < 100 beats per minute and preferably between 60-80 beats per minute will improve cardiac output when significant diastolic heart failure is present. Rate control can be achieved using beta-blockers, non-dihydropyridine calcium channel blockers, or digoxin.The second is to control systolic and diastolic blood pressure and the third is to use diuretics to control pulmonary congestion and peripheral edema.

What are the different types of ventricular septal defects?Membranous VSDs are the most common type and originate inferior to the crista supraventricularis, yet still towards the left ventricular outflow tract.Perimembranous VSDs are also inferior to the crista supraventricularis, however extend into the muscular septum.Supracristal VSDs occur just beneath the aortic valve at the left ventricular outflow tract. A Venturi effect can occur from the left to right shunt causing the aortic valve leaflet to prolapse into the VSD resulting in significant aortic valve regurgitation.Muscular VSDs occur in the mid to apical interventricular septum and do not involve cardiac valves.A Gerbode defect is technically a type of ventricular septal defect, although this results in a left ventricular to right atrial shunt.

What is “Prinzmetal's angina” and what is the treatment?Prinzmetal’s angina (a.k.a. variant angina or angina inversa) occurs with coronary artery vasospasm resulting in myocardial ischemia. The smooth muscle in the coronary wall contracts without explanation resulting in decreased blood flow the the myocardium causing symptoms of angina (chest pain).More common in young women, the etiology remains unclear. Symptoms usually occur at rest and are thought to be due to endothelial cell dysfunction. Coronary angiography will show normal coronary arteries (no atherosclerotic stenosis), however the infusion of ergonovine can reproduce the spam. Ergonovine is not commonly used any longer for this purpose since the spasm can be severe resulting in infarction.Coronary vasospasm can cause ST elevation on the ECG, however only during symptoms. Once the vasospasm resolves, the ECG changes will as well making it a challenge to diagnose this condition.The treatment for coronary vasospasm includes dihydropyridine calcium channel blockers (such as amlodipine or nifedipine), alpha blockers, and avoiding the use of beta-blockers. Animal studies have shown these to be effective, however no human trials have been performed. Beta-blockers are thought to cause “unopposed alpha receptor agonism”. Since the beta receptors would be occupied by the beta-blockers, substances (epinephrine, norepinephrine etc...) can stimulate the alpha receptors more easily causing worsened vasospasm. Avoidance of alpha agonists are important to treat coronary vasospasm. These include pseudoephedrine and oxymetazoline.

What are the contraindications to using thrombolytic therapy to treat an acute myocardial infarction?When the decision to treat a STEMI patient with fibrinolytic therapy is made (since primary PCI is not available in a timely fashion), contraindications to fibrinolytic therapy must be considered . Suspected aortic dissection, active bleeding (excluding menses) or a bleeding diathesis are contraindications to fibrinolytic therapy. In general, if there is high risk of intracranial hemorrhage (ICH) defined as  > 4%, then fibrinolytic therapy is contraindicated as well and primary PCI is preferred (class I).The following would place a patient in the high ICH risk category:1. Prior intracranial hemorrhage2. Ischemic stroke within 3 months3. Known cerebrovascular abnormality such as aneurysm or arteriovenous malformation4. Known malignant intracranial tumor5. Significant closed head trauma or facial trauma within 3 months

Relative contraindications (not absolute) to fibrinolytic therapy include:1. Uncontrolled hypertension (blood pressure > 180/110) either currently or in the past2. Intracranial abnormality not listed as absolute contraindication (i.e. benign intracranial tumor).3. Ischemic stroke > 3 months prior4. Bleeding within 2-4 weeks (excluded menses)5. Traumatic or prolonged cardiopulmonary resuscitation (CPR)6. Major surgery within 3 weeks7. Pregnancy8. Current use of anticoagulants9. Non-compressible vascular puncture10. DementiaNote that advanced age is not listed as an absolute or relative contraindication to fibrinolytic therapy in the ACC/AHA guidelines.

Name the four properties that vary between beta-blockers? Give examples.The four different properties of beta-blockers are cardioselectivity, lipid solubility, intrinsic sympathomimetic activity and membrane stabilization. Each beta-blocker has a different amount of these properties and it is important to

consider these when selecting a beta-blocker for a specific condition. The chart below summarizes which beta-blockers possess each property.

Cardioselectivity: All beta-blockers act upon both beta-1 and beta-2 receptors. The “Cardioselective” beta-blockers act upon beta-1 receptors much more than the beta-2 receptors. For this reason, the cardioselective  beta-blockers are safer to use in patients with asthma or reactive airway diseases.Lipid solubility: Beta-blockers that are lipid soluble, such as propranolol or metoprolol, can cross the blood-brain barrier easily. These medications are commonly used for migraine headaches, stage fright and panic attacks for these reasons.Intrinsic sympathomimetic activity (ISA): Beta-blockers with ISA only partially antagonize while actually causing a small degree of activation of the beta receptors. So they will have some beta-blocking effects, but not to the degree of beta-blockers without ISA. These are commonly used in younger patients or in athletes where heart rates need to elevate (allowing overall increased cardiopulmonary effort) in order to compete in sports. Examples include pindolol and acebutolol.Membrane stabilization: Stabilizing membranes decreases the propagation of action potentials. This is also the mechanism that local anesthetics work (lidocaine). Class I antiarrhythmic drugs possess this characteristic as well. The importance of this is not clear in clinical medicine in regards to beta-blockers. Perhaps this is partially an explanation for propranolol treating migraine headaches.

What is left ventricular non-compaction?Left ventricular non-compaction (a.k.a. LVNC, spongy myocardium or hypertrabeculation syndrome) is a pathologic cardiac condition in which the myocytes exhibit a “spongy” appearance. This is considered a genetic cardiomyopathy and is somewhat rare. The left ventricular myocardium exhibits pronounced trabeculae with intracavitary recesses (similar to diverticulum).Diagnosis is made either via echocardiography or pathologically. The Jenni Criteria has been proposed as a 2:1 ratio of non-compacted cells to compacted cells in end-systole on the parasternal short axis echocardiographic view.Manifestations include heart failure (frequently systolic), thromboembolism, arrhythmia and sudden cardiac death. Anticoagulation is recommended in all patients with LVNC with ejection fractions < 40% or if they develop atrial fibrillation. Medical therapy otherwise consists of standard heart failure therapy. Monitoring for arrhythmia is important and avoiding vigorous exercise is recommended.

What are the Duke criteria for endocarditis?Major criteria:1. Positive blood cultures defined as below:Typical organism isolated from two separate blood cultures Streptococcus viridans species or Streptococcus gallolyticus HACEK group organisms Staphylococcus aureus Community-acquired enterococci in the absence of another focus Persistently positive blood cultures from organism not mentioned above Two blood cultures positive drawn 12 hours apart Three of four blood cultures positive even if drawn together2. Evidence of endocardial involvementEchocardiographic evidence of endocarditis Vegetation defined as “oscillating intracardiac mass on a valve or supporting structure, in the path of a regurgitant

jet, or on implanted material”. Intracardiac abscess Dehiscence of a prosthetic heart valveNew valvular regurgitation (new murmur does not meet criteria)Minor criteria:Predisposing heart condition or IV drug use

Fever (38.0 C or 100.4 F)Vascular phenomena Arterial embolism Septic pulmonary infarctions Mycotic aneurysm Intracranial hemorrhage or conjunctival hemorrhages Janeway lesions Immunologic phenomena Glomerulonephritis Osler’s nodes Roth spots Positive rheumatoid factorMicrobiologic evidence (positive blood cultures not meeting major criteria)

What are the contraindications to using sotalol?Sotalol is proarrhythmic in the setting of left ventricular hypertrophy (wall thickness > 1.4 cm) and left ventricular systolic dysfunction and thus is contraindicated in these settings.Sotalol can prolong the QT interval. It is recommended that sotalol be initiated in the inpatient setting in a  majority of cases in order to monitor the QT interval after each dose to prevent polymorphic ventricular tachycardia (Torsades de Pointes) from occurring which can be fatal.Sotalol can cause severe bradycardia necessitating drug discontinuation.Sotalol is a class III antiarrhythmic drug and acts by blocking cardiac potassium channels. Sotalol also has non-selective beta-blocker properties. Sotalol exhibits “reverse use-dependence” meaning at faster heart rates (when potassium channels are being used more), the antiarrhythmic effect is less.

What are the causes of low voltage on an ECG?Low voltage is defined as peak-to-peak QRS amplitude of < 5 mm in the limb leads and/or < 10 mm in the precordial leads. Low voltage may be present in the following situations:1) Obesity2) COPD3) Pericardial effusion4) Severe hypothyroidism5) Subcutaneous emphysema6) Massive myocardial damage/infarction7) Infiltrative/restrictive diseases (such as amyloid cardiomyopathy)Note: If the gain indicated at the left of the ECG is turned down accidently, the voltage will be falsely low (pseudo-low voltage). The indicator should be set to 10 mm amplitude.

What are the symptoms of lidocaine toxicity?Side effects of intravenous lidocaine can be neurologic, cardiovascular or gastrointestinal.Neurologic side effects include tremor (usually the first sign of toxicity), dizziness, dysarthria, agitation, hallucinations and drowsiness. Seizures can be caused by higher lidocaine levels since the first neurons that lidocaine suppresses are considered inhibitory neurons (inhibiting inhibitory neurons leads to neuronal overactivity and seizures).Cardiovascular side effects include bradycardia, hypotension and asystole. These are all relatively uncommon.Gastrointestinal side effects include nausea, vomiting, and poor appetite.

What is the appropriate method(s) to evaluate a patient with 2:1 AV block?2:1 AV block (a form of second degree AV nodal block) occurs when every other P wave is not conducted through the AV node to get to the ventricles. 2:1 AV block may be either second degree type I AV nodal block (Wenckebach) or second degree type II AV nodal block. This distinction is crucial since the former is usually benign while the later requires implantation of a permanent pacemaker.A general rule to remember is that if the PR interval of the conducted beat is prolonged AND the QRS complex is narrow, then it is most likely second degree type I AV nodal block (Wenckebach). Alternatively, if the PR interval is normal and the QRS duration is prolonged (such as a left or right bundle branch block pattern), then it is most likely second degree type II AV block and a pacemaker is probably warranted. Remember that second degree type I AV nodal block is an issue in the AV node itself which is subject to sympathetic and parasympathetic tone while second degree type II AV block is "infranodal" conduction disease of the His/Purkinje system, therefore altering AV nodal conduction would have no effect.In order to distinguish between the two potential rhythms when an ECG reveals 2:1 AV nodal block, a couple different maneuvers can be employed:

1. Carotid sinus massage or adenosine (slows the sinus rate allowing the AV node more time to recover, thus reducing the block from 2:1 to 3:2 and unmasking any progressing prolonging PR intervals that would indicate second degree type I AV nodal block)2. Atropine administration (enhances AV nodal conduction and could eliminate second degree type I AV nodal block since it is due to slowed AV nodal conduction)3. Exercise ECG testing (enhances AV nodal conduction and could eliminate second degree type I AV nodal block since it is due to slowed AV nodal conduction)

What are the indications to close a ventricular septal defect?The indications to close a ventricular septal defect either percutaneously or surgically are:1. When the Qp/Qs is > 1.5 and there is LV systolic or diastolic dysfunction causing clinical heart failure.2. Prior endocarditis3. When the Qp/Qs is > 1.5 and the pulmonary pressures are no more than two thirds of systemic pressure.4. When the Qp/Qs is > 2 and there is evidence of volume overload of the LV5. When acute VSD develops after myocardial infarctionIf Eisenmenger’s syndrome is present, closure of a VSD is NOT recommended and can be fatal. In this situation, the only remedy is heart-lung transplantation.

What are the stages of ECG changes of hyperkalemia? Include the potassium level and the change that it would correlate to on the ECG tracing.The ECG findings of hyperkalemia change as the potassium level increases. From earliest to latest the ECG findings include:1. Peaked T waves best seen in the precordial leads, shortened QT interval, and sometimes ST segment depression.2. Widening of the QRS complex occurs (usually requires a potassium level of 6.5 or greater). This frequently appears as in "intraventricular conduction delay" or IVCD which is characterized by a widened QRS complex of > 120 ms that does not meet the criteria for a left or right bundle branch block. Frequently an IVCD will look like a left bundle branch block in lead V1 with a rS complex or monomorphic S wave and it appears like a right bundle branch block in leads I and V6 with a broad, slurred S wave.3. Decreased amplitude of the P waves, an increase in the PR interval, and bradycardia in the form of AV blocks occur as the potassium level exceeds 7.0.4) Absence of the P waves and eventually a "sine wave" pattern (see below) which is frequently a fatal rhythm.

Giving intravenous calcium is "cardioprotective" in the setting of hyperkalemia. You will frequently see instant reversal of all hyperkalemic ECG changes within seconds of administration. Calcium does not decrease the potassium levels, so other therapy like bicarbonate or insulin is needed to do this.

Name the direct thrombin inhibitors and their differences.There are a number direct thrombin inhibitors, the most common are as follows:1. Lepirudin (Refludan)

- Intravenous administration only.- Used for the treatment of HIT (heparin induced thrombocytopenia).- Monitored by aPTT - goal is 1.5 to 3.0 times above baseline.- Renally cleared.- Not easily reversed.

2. Argatroban- Intravenous administration only.- Used for the treatment of HIT (heparin induced thrombocytopenia).- Monitored by aPTT - goal is 1.5 to 3.0 times above baseline.- Dosing adjustment in hepatic dysfunction. NOT renally cleared.

3. Bivalirudin (Angiomax)- Intravenous administration only.- Short half-life of 25 minutes.- Used during PCI (percutaneous coronary intervention).- May be used in ST elevation myocardial infarction.

4. Dabigatran (Pradaxa)- Oral administration- Used for stroke prophylaxis in patients with non-valvular atrial fibrillation and atrial flutter.- Standard dose 150 mg PO twice daily.- Renally cleared. Dose reduction to 75 mg PO twice daily if creatinine clearance is 15-30 mL/min.- Not easily reversed.- No monitoring required if aPTT or PT due to predictable pharmacokinetics

5. Rivaroxiban (Xarelto)- Actually a direct factor Xa inhibitor, not direct thrombin inhibitor.- Oral administration- Used primarily for stroke prophylaxis in patients with non-valvular atrial fibrillation and atrial flutter. Also used for

DVT prophylaxis after orthopedic surgery.- Standard dose is 20 mg PO once daily- Renally cleared. Dose reduction to 15 mg PO daily with renal impairment. Not recommended in severe renal

impairment.- Not easily reversed.

6. Apixaban (Eliquis)

What are the indications for percutaneous mitral balloon valvuloplasty in patients with mitral stenosis?New York Heart Association functional class III-IV symptoms with moderate or severe mitral stenosis and a favorable valve morphology (Class I)New York Heart Association functional class II symptoms and moderate or severe mitral stenosis with favorable valve morphology (Class I)New York Heart Association functional class II symptoms and mild mitral stenosis when exercise increases the pulmonary artery systolic pressure to > 60 mmHg and valve morphology is favorable (Class IIb)

Which medications lower serum triglyceride levels?Hypertriglyceridemia contributes to the atherosclerotic process and maintaining normal serum triglyceride levels have some support to lower the risk of heart attack, stroke and cardiovascular death. Lifestyle changes, including diet, weight loss, exercise, controlling diabetes mellitus and controlling hypothyroidism all can help lower triglyceride levels.1. HMG-CoA reductase inhibitors:Many authorities consider “statins” or inhibitors of the HMG-CoA reductase enzyme to be considered first line therapy for hypertriglyceridemia since they have the strongest evidence in primary prevention trials to reduce cardiovascular mortality. High doses of atorvastatin (80 mg) and rosuvastatin (40 mg) can reduce serum triglyceride levels up to 40% in some trials. If unsuccessful, then another agent can be added to achieve goal triglyceride levels (< 150 mg/dL).2. FibratesThe drugs fenofibrate and gemfibrozil can reduce serum triglycerides by as much as 50% in some studies. The mechanism of action is complex. Fibrates activate peroxisome proliferator-activated receptor alpha which in turn activates lipoprotein lipase. This increases lipolysis and the elimination of triglycerides from the plasma. Fibrates must be used with caution in patients on HMG-CoA reductase inhibitors due to potential myalgias and rhabdomyolysis. Pravastatin or fluvastatin are the safest to use in combination with fibrates due to their elimination via the CYP3A4 system. While rosuvastatin also uses this system, doses should not exceed 10 mg daily while taking fibrates concomitantly.3. Nicotinic acid (Niacin)Niacin can reduce triglycerides by as much as 25%, however the predominant effect is to raise HDL levels. Niacin works by stimulating a G-protein coupled receptor (GPR109A) which inhibits lipolysis in adipose tissue resulting in decreased VLDL (which is used to make LDL) and increase HDL levels. The predominant side-effect is flushing which can be quite severe. Strong data to support the use of niacin is lacking as there has been few studies showing mortality benefit. Specifically, the AIM-HIGH trial was halted in 2011 since there was no cardiovascular benefit and stroke risk was higher in the niacin group. This study specifically evaluated patients with their LDL levels already at goal on statin therapy.4. Fish oil or omega-3 fatty acidsFish oil in higher doses (> 3 g daily) can reduce serum triglycerides by about 50%. The mechanism of action is not clearly defined.

What are the grades diastolic dysfunction measured by echocardiography and what are the clinical ramifications of each?Diastolic dysfunction occurs when the left ventricular myocardium is non-compliant and not able to accept blood return in a normal fashion from the left atrium. This can be a normal physiologic change with aging of the heart or result in elevated left atrial pressures leading to the clinical manifestations of diastolic congestive heart failure. There are four grades of diastolic dysfunction as described below. Echocardiography is the gold standard to diagnose diastolic dysfunction.Grade I (impaired relaxation): This is a normal finding and occurs in nearly 100% of individuals by the age of 60. The E wave velocity is reduced resulting in E/A reversal (ratio < 1.0). The left atrial pressures are normal. The deceleration time of the E wave is prolonged measuring > 200 ms. The e/e’ ratio measured by tissue Doppler is normal.Grade II (pseudonormal): This is pathological and results in elevated left atrial pressures. The E/A ratio is normal (0.8 +- 1.5), the deceleration time is normal (160-200 ms), however the e/e’ ratio is elevated. The E/A ratio will be < 1 with

Valsalva. A major clue to the presence of grade II diastolic dysfunction as compared to normal diastolic function is the presence of structural heart disease such as left atrial enlargement, left ventricular hypertrophy or systolic dysfunction. If significant structural heart disease is present and the E/A ratio as well as the deceleration time appear normal, suspect a pseudonormal pattern. Valsalva distinguishes pseudonormal from normal as well as the e/e’ ratio. Diuresis can frequently reduce the left atrial pressure relieving symptoms of heart failure and returning the hemodynamics to those of grade I diastolic dysfunction.Grade III (reversible restrictive): This results in significantly elevated left atrial pressures. Also known as a “restrictive filling pattern”, the E/A ratio is > 2.0, the deceleration time is < 160 ms, and the e/e’ ratio is elevated. The E/A ratio changes to  < 1.0 with Valsalva. Diuresis can frequently reduce the left atrial pressure relieving symptoms of heart failure and returning the hemodynamics to those of grade I diastolic dysfunction.Grade IV (fixed restrictive): This indicates a poor prognosis and very elevated left atrial pressures. The E/A ratio is > 2.0, the deceleration time is low and the e/e’ ratio is elevated. The major difference distinguishing grade III from grade IV diastolic dysfunction is the lack of E/A reversal with the Valsalva maneuver (no effect will be seen with Valsalva). Diuresis will not have a major effect on the left atrial pressures and clinic heart failure is likely permanent. Grade IV diastolic dysfunction is present only in very advanced heart failure and frequently seen in end-stage restrictive cardiomyopathies such as amyloid cardiomyopathy.

What is the classic ECG finding of a pulmonary embolus?A large S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III indicates acute right heart strain. This pattern only occurs in about 10% of people with pulmonary embolisms and is similar to the ECG findings in a left posterior fascicular block (LPFB).The most common ECG finding in the setting of a pulmonary embolism is sinus tachycardia, however the "S1Q3T3" pattern of acute cor pulmonale is classic. This is termed the McGinn-White sign.

What medical therapy is indicated to delay the need for surgery in the presence of severe mitral valve regurgitation?There is no medical therapy that can delay the need for surgical repair/replacement of the mitral valve in severe mitral regurgitation. Studies have been performed using ACE inhibitors and dihydropyridine calcium channel blockers. Only one small study using nifedipine showed a potential benefit. Certainly, control of afterload with the above medications with improve hemodynamics and cardiac output in the presence of severe mitral regurgitation, but has not been shown to delay the need for valve repair/replacement.

What is the classic surgical treatment for recurrent tricuspid valve endocarditis in intravenous drug users?Historically, excision of the tricuspid valve was used without inserting a valve prosthesis. The right atrium and right ventricular combine to form one right heart chamber. Most patients tolerate this fine without significant right heart failure, although a small percentage do go on to develop RV enlargement and pressure overload which can be problematic.

What is myocardial bridging and what are its implications?Myocardial bridging occurs when a coronary artery takes a deep course within the myocardium of the left ventricle itself. This is thought to be a benign finding not resulting in any clinical manifestations, however it can be seen angiographically. Severe cases have been reported to cause stable angina symptoms and bypass grafting using a mammary artery to the left anterior descending (the most commonly affected coronary vessel) has been performed. Tachycardia worsens the coronary perfusion in patients with myocardial bridging since the coronary arteries fill during diastolic any tachycardia shortens diastolic filling time. Myocardial bridging is also associated with coronary vasospasm.

What causes the third heart sound (S3)?The third heart sound (S3), also known as the "ventricular gallop", occurs just after S2 when the mitral valve opens allowing passive filling of the left ventricle. The S3 sound is actually produced by the large amount of blood striking a very compliant left ventricle (LV).If the left ventricle is not overly compliant (as in most adults), a S3 will not be loud enough to be auscultated. A S3 can be a normal finding in children, pregnant females, and well trained athletes, however a S4 heart sound is almost always abnormal.

A S3 can be an important sign of systolic heart failure, since in this setting the myocardium is usually overly compliant resulting in a dilated LV (see image below).S3 is a low pitched sound. This is helpful to distinguish a S3 from a split S2 which is high pitched. A S3 heart sound should disappear when the diaphragm of the stethoscope is used and should be present while using the bell. The opposite is true for a split S2. Also, the S3 sound is heard best at the cardiac apex while a split S2 is best heard at the pulmonic listening post (left upper sternal border). To best hear a S3, the patient should be in the left lateral decubitus position.

What are the three most common indications for permanent pacemaker implantation?Sick sinus syndrome, which includes more than one rhythm presentation, is the most common indication for permanent pacemaker implantation. This is followed by AV nodal blocks and then less common indications (neurocardiogenic syncope and post-AV node ablation).

What are the contraindications to using fibrinolytic therapy (thrombolytic therapy) to treat an acute myocardial infarction?Absolute contraindications are:

- Prior intracranial hemorrhage- Ischemic stroke within 3 months- Acute gastrointestinal bleeding- Known intracranial tumor/AV malformation- Significant closed head/facial trauma within 3 months- Suspected aortic dissection

Relative contraindications are:- Uncontrolled hypertension (defined as systolic blood pressure > 180 mmHg)- Ischemic stroke more than 3 months prior- Dementia or other intracranial abnormality (not mentioned in absolute contraindications)- Recent internal bleeding (within 4 weeks)- Trauma or prolonged cardiopulmonary resuscitation or recent surgery (within 3 weeks)- Prior allergic reaction or recent use of streptokinase- Current use of anticoagulants

- Non-compressible vascular puncture- Pregnancy

The age of the patient is controversial. In general, age > 75 is at higher risk, but still considered safe to use thrombolytics.

What classification system can be used to predict mortality in the setting of an acute myocardial infarction?The Killip Classification is frequently used during acute myocardial infarction. First published in 1967, this system focuses on physical examination and the development of heart failure to predict risk as described below:Class I: No evidence of heart failure (mortality 6%)Class II: Findings of mild to moderate heart failure (S3 gallop, rales < half-way up lung fields or elevated jugular venous pressure (mortality 17%)Class III: Pulmonary edema (mortality 38%)Class IV: Cardiogenic shock defined as systolic blood pressure < 90 and signs of hypoperfusion such as oliguria, cyanosis, and sweating. (mortality 67%)The original data from 1967 showed the above mortality rate in each class. This was before reperfusion therapy (thrombolytics and/or PCI). With advances in therapy, the mortality rates have declined about 30-50% in each class.

What is the New York Heart Association functional class?The New york Heart Association (NYHA) functional class helps to classify patients based on their symptoms of heart failure.Class I: No symptoms of heart failureClass II: Symptoms of heart failure with moderate exertion such as ambulating 2 blocks or 2 flights of stairsClass III: Symptoms of heart failure with minimal exertion such as ambulating 1 block or 1 flight of stairs, but no symptoms at restClass IV:  Symptoms of heart failure at restNote that the NYHA functional class differs from the ACC/AHA heart failure classification system in that the former allows movement from one class to the other while the ACC/AHA classification does not (see below).

What causes a paradoxically split second heart sound?A paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspiration, the opposite of the physiologic split S2. A paradoxical split S2 occurs in any setting that delays the closure of the aortic valve, such as severe aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM) or in the setting of a left bundle branch block (LBBB).

What are the causes of atrial fibrillation and atrial flutter?The most common cause of atrial fibrillation/flutter is hypertension. Age is the second most common cause. Obstructive sleep apnea is present in about 40% of patients with atrial fibrillation/flutter, however the exact proportion that it causes is not well defined. There are multiple other causes of atrial fibrillation/flutter that can be remembered with the below pneumonic “PIRATES”:Pulmonary embolism, pericarditisIschemia, intravenous line (central line advanced too far into the right atrium)Rheumatic valvular heart disease (specifically mitral valve stenosis)Alcohol, anemiaThyroid (hyperthyroidism)Elevated blood pressure (hypertension)Sleep apnea, sepsis, surgery

What are the four stages of the ECG findings in patient with acute pericarditis?

Pericarditis, or inflammation of the pericardium, has typical ECG findings. These findings occur in progressive stages, all of which are seen in about 50% of cases of pericarditis.Stage I (acute phase): Diffuse concave upward ST segment elevation in most leads, PR depression in most leads (may be subtle), and sometimes notching at the end of the QRS complex.Stage II: ST segment elevation and PR depression have resolved. T waves may be normal or flattened.Stage III: T waves are inverted and the ECG is otherwise normal.Stage IV: The T waves return to the upright position thus the ECG is back to normal.Note: The ECG changes of pericarditis must be distinguished from those of early repolarization. The ST elevation seen in early repolarization is very similar; diffuse and concave upward. However three things may help to distinguish pericarditis from early repolarization:1. The ratio of the T wave amplitude to the ST elevation should be > 4 if early repolarization is present. In other

words, the T wave in early repolarization is usually 4 times the amplitude of the ST elevation. Another way to describe this would be that the ST elevation is less than 25% of the T wave amplitude in early repolarization.

2. The ST elevation in early repolarization resolves when the person exercises.3. Early repolarization, unlike pericarditis, is a benign ECG finding that should not be associated with any symptoms.

What is sick sinus syndrome? Include all of the rhythm manifestations.Sick sinus syndrome (SSS) occurs from sinoatrial node dysfunction and may manifest in multiple different ways including:

- Tachycardia-bradycardia syndrome (i.e. pauses after converting to sinus rhythm)- Severe sinus bradycardia- Sinus pauses/sinus arrest- Sinoatrial nodal exit block- Chronotropic incompetence (failure of heart rate to increase during exercise)

Clinical symptoms depend on the mechanism. Severe bradycardia results in dizziness, fatigue, generalized weakness and dyspnea on exertion. Pauses can result in syncope and even sudden death. Sick sinus syndrome is the leading indication for permanent pacemaker implantation. Withholding drugs that suppress the sinoatrial nodal function, if possible, can frequently improve the symptoms and potentially avoid the need for pacemaker insertion. These drugs include beta-blockers, calcium channel blockers amiodarone, digoxin, anti-arrhythmic drugs and some older drugs (reserpine, guanethidine, clonidine, cimetidine, lithium).The actual cause of sick sinus syndrome is related to replacement of the sinus node with fibrinous tissue. This usually occurs concomitantly with similar changes throughout the entire conduction system including the AV node and increases with age. On rare occasions, ischemia to the SA node or other infiltrative disease can cause SSS.

What are the indications for an early invasive strategy during a non-ST segment myocardial infarction (when should an angiogram be done early)?An early invasive strategy refers to proceeding to coronary angiography with possible percutaneous coronary intervention (PCI or coronary stenting) within 4 to 24 hours of hospital admission. An initial conservative management consists of medical therapy only without plans to proceed to coronary angiography and PCI.Factors that would warrant an early invasive strategy include:1. Increased cardiac biomarkers (troponin, CK-MB)2. New ST segment depression3. Signs or symptoms of congestive heart failure (rales on examination, hypoxia with pulmonary edema on chest x-

ray)4. Hemodynamic instability5. Sustained ventricular tachycardia or ventricular fibrillation6. Recent coronary intervention within 6 months7. Prior coronary artery bypass grafting8. High TIMI risk score9. Reduced left ventricular systolic function (EF < 40%)10. Recurrent angina at rest or with low level activity11. High risk findings from non-invasive testingThe ICTUS trial showed no difference in the above approaches in 3 years. The RITA-3 trial showed no difference at 1 year, but there was a reduction of death or myocardial infarction at 5 years in the early invasive arm, mainly in high risk patients which justifies the above approach (only performing angiography/PCI on high risk patients).

What are the HACEK organisms that can cause “culture negative endocarditis”?Haemophilus aphrophilus

Actinobacillus actinomycetemcomitansCardiobacterium hominisEikenella corrodensKingella kingaeThese organisms can cause “culture negative endocarditis” meaning infection of the endocardium with vegetation formation despite blood cultures not showing evidence of bacteremia. The above organisms require special medium or prolonged incubation to be isolated. The most common causes of culture negative endocarditis are actually Streptococcus species in patients who already received antibiotic therapy (rendering the blood cultures negative) and fungi.

What are the indications for transesophageal echocardiography?According to the appropriateness criteria from the American Society of Echocardiography, the indications for transesophageal echocardiography (TEE) are:1. When visualization of cardiac structures in not adequate with transthoracic echocardiography2. To evaluate valvular structure and function in preparation for an intervention (surgery)3. To diagnose infective endocarditis when there is a moderate or high pre-test probability4. To evaluate patients with atrial fibrillation/flutter to facilitate clinical decision making in regard to anticoagulation,

cardioversion or ablation.5. Evaluation of acute aortic pathology (such as ascending aortic dissection)6. Evaluation for cardiovascular source of embolus (frequently causing an embolic stroke) with no identifiable non-

cardiac source7. Re-evaluation of a prior TEE finding (i.e. resolution of a thrombus or endocarditis)8. Guidance during percutaneous non-coronary interventions (i.e. atrial septal defect closure)

What is the tetralogy of Fallot?The tetralogy of Fallot is a rare congenital cyanotic heart condition that consists of the following:

1. Right ventricular hypertrophy2. Ventricular septal defect3. Overriding aorta (aorta displaced to the right, near the VSD)4. Pulmonic valve stenosis (right ventricular outflow tract obstruction)

This results in a net right to left cardiac shunt. Depending on the severity of right ventricular outflow tract obstruction, symptoms may be present at birth or delayed into early childhood. Tetralogy of Fallot accounts for about 10% of all congenital heart defects. Surgery is required to repair the defect in most individuals. The Blalock-Taussig shunt (subclavian artery surgically attached to pulmonary artery) was initially used in 1945. Currently, surgery includes closing the VSD and enlargement of the right ventricular outflow tract (by relieving pulmonary stenosis). Chronic pulmonic regurgitation can result as a complication of repair.

What are the physical exam findings of cardiac tamponade?- Sinus tachycardia- Elevated jugular venous pressure- Pulsus paradoxus (see below)- Pericardial friction rub (from pericarditis if present)- Distant heart sounds (from heart sound muffling related to the pericardial effusion)- Kussmaul’s sign (rarely) - increase in jugular venous pressure during inspiration

"Pulsus paradoxus" which is present in cardiac tamponade reflects a decrease in systolic blood pressure with inspiration of more than 12 mmHg. Pulsus paradoxus also occurs in severe asthma or COPD exacerbations. 

What determines the dominance of the coronary arteries (left versus right dominance)?Coronary dominance refers the which vessel the posterior descending coronary artery arises from.In approximately 80% of individuals the posterior descending artery (PDA) arises from the right coronary artery and is referred to as a “right dominant” system. In approximately 10% of individuals the left circumflex coronary artery is

considered dominant and it supplies a left posterior descending artery. This is considered a “left dominant” system. The remaining 10% have a “co-dominant” coronary system meaning both the right coronary artery and the left circumflex contribute to the PDA.

What are the ECG findings of a true posterior myocardial infarction?The ECG findings of a posterior wall MI are different than the typical ST elevation seen in other myocardial infarctions. A posterior wall myocardial infarction occurs when posterior myocardial tissue (now termed inferobasilar), usually supplied by the posterior descending artery (a branch of the right coronary artery in 80% of individuals), acutely loses blood supply due to intracoronary thrombosis in that vessel. This frequently coincides with an inferior wall MI due to the shared blood supply. The ECG findings on an acute posterior wall MI include:1. ST segment depression (not elevation) in the septal and anterior precordial leads (V1 to V4). This occurs since

these ECG leads will see the MI backwards (since the leads are placed anteriorly, but the myocardial injury is posterior).

2. The ratio of the R wave to the S wave in leads V1 or V2 is > 1.3. ST elevation in the posterior leads of a posterior ECG (leads V7 to V9). Suspicion for a posterior MI must remain

high, especially if inferior ST elevation is also present.4. ST elevation in the inferior leads (II, III, and aVF) may be seen if an inferior MI is also present.

What increases or decreases the intensity of the first heart sound?Four factors affect the intensity of the first heart sound. Since the M1 portion of S1 is much louder than T1, it is only important to discuss what affects the intensity of M1. The first factor is the thickness of the chest wall. Obese individuals will have a soft S1 while a thin person will have a more intense S1 heart sound. The greater the distance separating the leaflets of the mitral valve at the beginning of systole, the louder the S1. This is affected by the duration of the PR interval on the ECG. Remember that the PR interval represents part of diastole, so a longer PR interval would result in a longer diastolic filling time. As the left ventricle fills, the pressure gradually increases. This gradual increase in pressure causes the mitral valve leaflets to slowly drift together. Therefore, when ventricular systole occurs in the setting of a long PR interval, the leftist will be separated by a smaller distance and the S1 sound will be softer. The converse is also true. A short PR interval results in an accentuated S1 since the mitral valve leaflets will be further apart at the onset of ventricular systole.The mobility of the valve leaflets in the second factor influencing the intensity of M1. In mild to moderate mitral stenosis, the increased left atrial pressure causes the mobile portions of the mitral valve leaflets to be more widely separated, thus resulting in an accentuated M1 sound. In severe to critical mitral stenosis, the valve leaflets are so calcified and immobile that the M1 sound is diminished or absent.The rate of ventricular contraction also affects the intensity of S1. The faster the heart rate and the faster the rise in ventricular pressure, the louder the S1. Thus, high flow states such as anemia, thyrotoxicosis, or sepsis results in an accentuated S1. Also, during exercise or any other setting of tachycardia, the S1 will be accentuated.

What is the coronary calcium score (CCS) used for?The coronary calcium score (CCS) is used to risk stratify patients in regards to the presence of atherosclerotic coronary disease. The scan is quick, no intravenous access or IV contrast required, and results take only minutes. Calcium can be reliably detected and the amount of calcium present correlates with the risk of significant angiographic stenosis. CCS is available at many centers without a physician's order or appointment for a cash fee.The Agatston score is used to compute a number score. A score of 0 means no calcium was detected. When the score is > 400, there is a 90% chance of an angiographically significant stenosis. Coronary calcium scoring may be reasonable, according to the American Heart Association, in asymptomatic individuals at intermediate risk for heart disease. Screening low risk populations will result in false positives and screening high risk populations is not recommended since aggressive risk factor reduction should already be taking place in these individuals. Identifying coronary calcium in intermediate risk populations will allow the clinician to not only educate the patient regarding their risk of cardiovascular disease, however also be more aggressive with using anti-platelet therapy (aspirin) and statin therapy to prevent progression/reduce the risk of myocardial infarction and stroke.

What is the plasma N-terminal pro-BNP and how is it used?A newer assay measuring NT-terminal proBNP (NT-proBNP) is more sensitive to detect heart failure and used in many institutions. The levels of BNP and NT-proBNP are essentially the same in normal individuals, but in the presence of heart failure the NT-proBNP is approximately four times higher than the corresponding BNP level, thus reducing the likelihood of a result in the ambiguous range (i.e. BNP level of 300 which is high, but not quite definite heart failure which would be > 400).NT-proBNP levels are also higher in patients with atrial fibrillation and acute coronary syndrome. The level of NT-proBNP may be helpful not only to evaluate heart failure, but also to detect acute coronary syndromes in patients with

chest pain presenting to the emergency department where it has been found to be elevated (although further investigation is underway).

What are the three common and two less common types of cardiomyopathies?The term “cardiomyopathy” refers to “cardio” (heart), “myo” (muscle), “pathy” (disease of). The term is used somewhat loosely which can create confusion. In general, when someone refers to a cardiomyopathy they mean the three common types below. Some people will use cardiomyopathy in reference to an “ischemic cardiomyopathy” which implies that ahterosclerotic coronary disease has resulted in left ventricular systolic dysfunction. This is technically improper use of the term cardiomyopathy, however it is much easier to say/write than “chronic systolic congestive heart failure from ischemic heart disease”.  Likewise, the term “non-ischemic cardiomyopathy” is frequently used when the left ventricular systolic function is low from a non-ischemic cause (dilated cardiomyopathy).The three common cardiomyopathies are:1. Dilated cardiomyopathy: This results in left ventricular systolic dysfunction and clinical manifestations of congestive heart failure. Etiologies include viral, alcoholic, idiopathic, familial and other rare causes.2. Hypertrophic cardiomyopathy: Also known as hypertrophic obstructive cardiomyopathy (HOCM), this results in abnormal hypertrophic changes most commonly in the interventricular septum  with pathologic “myocardial disarray”. HOCM is familial in about 50% of cases and transmitted in an autosomal dominant fashion. HOCM can result in clinic heart failure, life-threatening arrhythmias, mitral regurgitation and sudden cardiac death. 3. Restrictive cardiomyopathy: This results in heart failure related to severe diastolic dysfunction. Causes include amyloid heart disease, infiltrative disorders, and familial.The two least common and least researched types of cardiomyopathy are:1. Left ventricular non-compaction: Also known as spongy myocardium or hypertrabeculation syndrome), left ventricular non-compaction is a pathologic cardiac condition in which the myocytes exhibit a “spongy” appearance. This is considered a genetic cardiomyopathy and is somewhat rare. The left ventricular myocardium exhibits pronounced trabeculae with intracavitary recesses (similar to diverticulum). This can lead to systolic dysfunction and arrhythmia.2. Arrhythmogenic right ventricular dysplasia (ARVD): This occurs when fatty tissue replaces that of the right ventricular myocardium and as the name implies, frequent causes arrhythmia. Most commonly ventricular tachycardia occurs. Sudden cardiac death is the main concern in ARVD. The classic ECG finding of “Epsilon waves” from early afterdepolarizations of the ventricles is actually rare.

What are the two therapies what may reduces statin mediate myalgias?The two therapies that have been researched to reduce myalgias in patients taking statin therapy (HMG CoA reductase inhibitors) are coenzyme Q10 and vitamin D.Two very small trials of coenzyme Q10 were conflicting as to the efficacy of this therapy to relieve statin induced myalgias. Likewise, some studies, but not all, have shown that replacing vitamin D in patients who are deficient can relieve similar myalgias. Better strategies include switching therapy to statins with less intrinsic muscle toxicity (fluvastatin and pravastatin) or alternate day dosing. Some have even had success with once weekly dosing of rosuvastatin.

What is pulsus paradoxus? Describe the physiologic mechanism.Pulsus paradoxus is the term used to describe an exaggerated blood pressure variation with the respiratory cycle. This can be found in cardiac tamponade or during COPD/asthma exacerbations.To understand the physiologic mechanism of pulsus paradoxus, the normal changes intrathoracic pressures during the respiratory cycle must be described first. Normal intrapericardial pressures range from -5 to 5 mmHg. With inspiration there is a net decrease in intrathoracic pressures (as the thoracic cavity volume expands). This allows blood to easily flow into the right heart. Conversely, left heart filling decreases during inspiration as the intrapericardial volume is fixed (meaning if the right heart is full, the left heart is less full and vise versa). During expiration, the intrathoracic pressures increase (as the thoracic cavity volume decreases). This results in less right heart filling and augments filling of the left heart chambers. These changes with the respiratory cycle only result in small changes in measured systolic blood pressure of no more than 10 mmHg.Any condition that results in increasing pressure variation with the respiratory cycle with exaggerate the measurable blood pressure difference to > 12 mmHg, which is considered an abnormal pulsus paradoxus. When fluid accumulates in the pericardial space and the intrapericardial pressures increase, the right heart is compressed increasing the right heart pressures. This results in the right heart relying more heavily on the decreased intrathoracic pressures during inspiration to fill, exaggerating the pressure change which is measurable.To measure the pulsus paradoxus, place a blood pressure cuff on the patients arm and very very slowly deflate the cuff while listening for brachial pulsations. Note the pressure that you first hear pulsations during expiration (which will be the highest). Repeat the process and record the pressure where pulsations are heard during inspiration (which will be the lowest). The difference between these two numbers is the pulsus paradoxus

.

What blood test can help distinguish between restrictive cardiomyopathy and constrictive pericarditis?Measuring the BNP level (b-type natriuretic peptide) can help distinguish these two entities which have historically been quite difficult to diagnosis.In constrictive pericarditis the BNP level is normal to very minimally elevated while in restrictive cardiomyopathy the BNP level is significantly elevated. This was initially described by Leya et. al. in 2005. BNP is released in response to myocardial wall stretch. In constrictive pericarditis, the scarred pericardium probits wall stretch and thus the levels are low. In restrictive cardiomyopathy, the walls indeed do stretch from the increased cardiac pressures resulting in high serum levels of BNP.

What is the most common cause of mitral stenosis?The most common cause of mitral valve stenosis is rheumatic valvular disease. Other less common causes include severe mitral annular calcification, cor triatriatum, congenital subvalvular ring, left atrial myxoma, prosthetic mitral valve dysfunction, inflammatory disorders (Lupus or rheumatoid arthritis) or a large mitral valve vegetation. Pulmonic vein stenosis has similar hemodynamics to mitral stenosis and can occur after atrial fibrillation ablation (although less common now with newer techniques). 

What is a bisferiens pulse (pulsus bisferiens)?Most frequently caused by hemodynamically significant aortic regurgitation, pulsus bisferiens is detected by examining the carotid upstroke. Two pulsations are detected in systole. The first is from the pressure increase related to left ventricular ejection. The second systolic pulsation is reflected from the periphery and only palpable in high left ventricular out states such as severe aortic regurgitation. The Valsalva maneuver or inhalation of amyl nitrate can precipitate pulsus bisferiens in some cases.Pulsus bisferiens can also be seen in hypertrophic obstructive cardiomyopathy (HOCM), patent ductus arteriosus, arteriovenous fistulas and normal hearts in a hyperdynamic state.

What are the indications for an implantable cardioverter defibrillator (ICD) in patients with hypertrophic obstructive cardiomyopathy (HOCM)?Hypertrophic obstructive cardiomyopathy (HOCM) patients have a high risk of sudden cardiac death, however an implantable cardioverter defibrillator (ICD) is not recommend in all patients with HOCM. If any of the criteria below are present, then an ICD should be implanted:1. Syncope2. Interventricular septal thickness of 30 mm or greater3. Documented ventricular tachycardia and/or cardiac arrest4. Family history of sudden cardiac death5. Left ventricular systolic dysfunction in the setting of wall thinning (a.k.a. “burnt out” left ventricle)

Which beta-blockers are FDA approved for systolic heart failure?There are only three beta-blockers FDA approved for the treatment of chronic systolic congestive heart failure. They are metoprolol succinate (Toprol XL), carvedilol (Coreg) and bisoprolol. Note that metoprolol tartrate (Lopressor) is NOT FDA approved for patients with chronic systolic heart failure.

Which segment of which leaflet is most commonly involved in mitral valve prolapse?Mitral valve prolapse is a connective tissue disorder which results in the valve leaflets becoming redundant causing prolapse into the left atrium during systole. This can lead to mitral valve regurgitation. The most common segment involved in mitral valve prolapse is termed the P2 segment. The mitral valve structure is complex. The anterior and posterior leaflets have been anatomically separated into 3 segments each (A1, A2, A3 and P1, P2, P3).

What creates the second heart sound (S2) and describe its characteristics?The second heart sound is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2 and the sound produced by the closure of the pulmonic valve is termed P2. The A2 sound is normally much louder than the P2 due to higher pressures in the left side of the heart, thus A2

radiates to all cardiac listening posts (loudest at the right upper sternal border) and P2 is usually only heard at the left upper sternal border. The A2 sound is thus the main component of S2.Like the S1 heart sound, the S2 sound is described regarding splitting and intensity. S2 is physiologically split in about 90% of people. The S2 heart sound can exhibit persistent (widened) splitting, fixed splitting, paradoxical (reversed) splitting, or the absence of splitting. The S2 heart sound intensity decreases with worsening aortic valve stenosis due in immobile leaflets. In severe aortic stenosis, the A2 component may not be audible at all.

How is the measurement of b-type natriuretic peptide (BNP) used clinically?The initial primary use of measuring b-type natriuretic peptide (BNP) is to determine the etiology of dyspnea in patients presenting to the emergency department. If the BNP level is significantly elevated (greater than 400 pg/mL), heart failure is the likely diagnosis. Note that the degree of BNP elevation does not correlate with the severity of symptoms.BNP levels are elevated in patients with atrial fibrillation and acute coronary syndromes as well, however it is not used to diagnose these conditions.BNP levels play an important prognostic role in other cardiac conditions. Patients with high BNP levels during acute coronary syndromes or in the setting of severe valvular heart disease (aortic stenosis and/or mitral regurgitation) have a worse prognosis. Also, BNP levels are low in patients with heart failure from constrictive pericarditis which differentiates it from restrictive cardiomyopathy where the BNP levels are high.A newer assay measuring NT-terminal pro-BNP (NT-proBNP) is more sensitive to detect heart failure and used in many institutions. The levels of BNP and NT-proBNP are essentially the same in normal individuals, but in the presence of heart failure the NT-proBNP is approximately four times higher than the corresponding BNP level, thus reducing the likelihood of a result in the ambiguous range (i.e. BNP level of 300 which is high, but not quite definite heart failure which would be > 400).

What causes the fourth heart sound?The fourth heart sound (S4), also known as the "atrial gallop", occurs just before S1 when the atria contract to force blood into the LV.  If the LV is non-compliant and atrial contraction forces blood through the AV valves, an S4 is produced by the blood striking the LV. 

Therefore any condition that creates a non-compliant LV will produce a S4, while any condition that creates an overly compliant LV will produce a S3(as described above).A S4 heart sound can be an important sign of diastolic heart failure or active ischemia and is rarely a normal finding. Diastolic heart failure frequently results from severe left ventricular hypertrophy (LVH) resulting in impaired relaxation (compliance) of the LV. In this setting, a S4 is often heard. Also, if a person is actively having myocardial ischemia, adequate ATP can't be synthesized to allow for the release of myosin from actin, thus the myocardium is not able to relax and a S4 will be present.Like S3, the S4 sound is low pitched and best heard at the apex with the patient in the left lateral decubitus position.

What is a “cannon A wave” in the jugular venous pulse?

A “cannon A wave” occurs when the right atrium contracts against a closed tricuspid valve causing a large pulsation to occur in the jugular venous pulsation. This occurs at times of electrical “AV dissociation”, meaning with the P wave on the ECG overlaps with the QRS complex and thus atrial systole occurs simultaneously with ventricular systole. This can result in significant stretch of the atrium causing ANP (Atrial Natriuretic Peptide) to be released causing polyuria.

What is a V wave in the jugular venous pulse and when is it accentuated?A V wave in the jugular venous pulse represents venous filling of the right atrium when the tricuspid valve is closed. In severe tricuspid valve regurgitation, there is dramatic accentuation of the jugular V wave (sometimes difficult to distinguish from elevated jugular venous pressure from right heart failure). Similarly, when examining a left atrial (or pulmonary capillary wedge) pressure tracing, the V wave is accentuated in severe mitral regurgitation.

What causes an accentuated V wave in the left atrial pressure or pulmonary capillary wedge pressure tracing?The V wave in the left atrial pressure (LAP) or pulmonary capillary wedge pressure (PCWP) tracing represents left atrial filling against a closed mitral valve. If severe mitral valve regurgitation is present, the V wave will be significantly accentuated. This can be helpful if a patient with an acute inferior MI presents with pulmonary edema and shock to diagnose acute severe mitral regurgitation.

What is the diagnosis if the right ventricular oxygen saturation is significantly higher than the right atrial oxygen saturation during a right heart catheterization?During right heart catheterization, oxygen saturations are frequently measured from different cardiac chambers in order to identify left to right shunts. If a ventricular septal defect is present, the oxygen saturation will be markedly higher in the right ventricle due to shunting of well oxygenated blood from the left ventricle to the right ventricle. This diagnostic technique can be helpful when a patient presents after an acute MI with pulmonary edema and shock to diagnose an acute ventricular septal defect.

What is the treatment for an acute ventricular septal defect after a myocardial infarction?Emergency surgical repair is warranted in the setting of an acute ventricular septal defect. Without surgical intervention, the mortality rate is > 90%. Fortunately, with the early revascularization techniques now employed (PCI), VSD formation is less common. An intraaortic balloon pump (IABP) can be used to improve hemodynamics reduce afterloadWhen infarction of the interventricular septum occurs, this area can thin with the remodeling process and on occasion, a complete defect between the right and left ventricles can develop. This results in left to right shunting of blood and can be life-threatening when acute. A holosystolic murmur at the left lower sternal border occurs. Right heart catheterization will show an “oxygen step-up” between the right atrium and right ventricle (since oxygenated blood will be present in the right ventricle).The ventricles are good at adapting to hemodynamic stress when gradually introduced, as in worsening aortic regurgitation, however when acute, ventricular failure and shock occurs as is present with acute VSD formation.

How do you distinguish a pericardial knock from an S3 heart sound?A pericardial knock can be present in patients with constrictive pericarditis as the early filling of the left ventricle is limited from the constrictive process. This pericardial knock occurs earlier than an S3 heart sound which is the distinguishing factor (since the S3 heart sound occurs from stretch of a very compliant left ventricle which takes a short time longer).

What is the most common cause of aortic valve stenosis in patients over the age of 70? Under the age of 70?The most common cause of aortic valve stenosis in patients over the age of 70 is senile calcific degeneration of the valve leaflets. The most common cause in patients under the age of 70 is calcification of a congenitally bicuspid aortic valve.

Other causes of aortic stenosis include congental aortic stenosis, rheumatic valvular heart disease, systemic lupus erythematosus, familial hypercholesterolemia, ochronosis, Paget’s disease and Fabry’s disease. These are all relatively rare.

Which three physical exam findings in patients with aortic stenosis can help determine the severity?The three physical exam findings that help determine the severity of aortic stenosis are the timing of the peak of the murmur in systole, the intensity of the S2 heart sound and the presence of “pulsus parvus et tardus.”In mild aortic stenosis, the murmur peaks in early systole, however as the disease progresses the peak moves to later in systole since longer time is required to complete LV systole and aortic valve closure is delayed. The intensity of the murmur typically increases as disease progresses, however when heart failure develops and cardiac output declines, the murmur becomes softer. Thus the intensity of the murmur is not a good indicator of disease severity.As disease progresses and the aortic valve leaflets lose their mobility, the intensity of S2 decreases. When the S2 sound is no longer audible, it can be concluded that the AS is relatively severe.Perhaps the best bedside method to estimate the severity of AS is derived from evaluation of the carotid arteries. The phenomenon known as "pulsus parvus et tardus" refers to a weak (parvus) and delayed (tardus) carotid upstroke. To asses for "parvus", it is often helpful to palpate your own carotid artery (assuming you do not have significant AS) while concurrently palpating the patient's carotid artery. It is important to note that in some elderly individuals the carotids may be stiff due to calcification, which may falsely normalize the carotid upstroke. To assess for "tardus", auscultate the patient's S2 heart sound while palpating their carotid upstroke. The S2 and carotid upstroke should occur almost simultaneously. If the carotid upstroke comes significantly after the S2 heart sound, "tardus" is present indicating severe AS.

What is the most common cause of severe aortic valve regurgitation?The most common cause of severe aortic valve regurgitation is dilation of the aortic root. A dilated aortic root can occur from a number of different causes including idiopathic (most common), systemic hypertension, connective tissue diseases (Marfan’s syndrome, Ehlers Danlos syndrome) and syphilitic aortitis.

What is the Wilkins echocardiographic score for mitral stenosis? What are the components and how are they graded?The Wilkins echocardiographic score, also known as the Abascal’s echocardiographic score, is used to determine the suitability of the mitral valve structure for percutaneous mitral balloon valvuloplasty, a minimally invasive procedure using a balloon to open the stenotic mitral valve. Poor valve morphology can lead to severe mitral regurgitation after intervention and thus the Wilkins score attempts to identify those at risk people. The Wilkins score is described below:

What are the causes of acute severe mitral regurgitation?Acute severe mitral regurgitation is a life-threatening disorder. The causes are listed below:1. Papillary muscle rupture after acute myocardial infarction: This usually occurs as a complication on an inferior MI (right coronary artery supply) since the posteromedial papillary muscle receives its sole blood supply from this vessel. The anterolateral papillary muscle has dual blood supply from the left anterior descending and circumflex coronary arteries.2. Mitral valve endocarditis: Most commonly related to Staph aureus, but other organisms can cause valve destruction as well.3. Spontaneous chordal rupture: This is more common in mitral valve prolapse (most often posterior leaflet) and rheumatic mitral valve disease (most often anterior leaflet).4. Trauma.

5. Complication from percutaneous mitral balloon valvuloplasty. 

What is the mechanism of action of fenofibrate and gemfibrozil?The drugs fenofibrate and gemfibrozil are considered fibric acid derivatives. They can reduce serum triglycerides by as much as 50% in some studies. The mechanism of action is complex. Fibrates activate peroxisome proliferator-activated receptor alpha which in turn activates lipoprotein lipase. This increases lipolysis and the elimination of triglycerides from the plasma. Despite the triglyceride reduction, there is little data to support a mortality benefit from fibrates.

What is the difference between functional and organic mitral regurgitation?The etiologies of mitral regurgitation (MR) are diverse since the mitral valve apparatus is complex. MR can occur when the mitral valve apparatus is itself diseased (organic MR) or in the absence of any abnormality of the mitral valve apparatus (functional MR). The causes of functional and organic MR are listed in the table below.

Organic MR Functional MR

Myxomatous changes (MVP)Rheumatic heart disease (RHD)EndocarditisCollagen vascular diseasePapillary muscle dysfunctionMitral annular calcification (MAC)Spontaneous chordal ruptureTrauma

Ischemic cardiomyopathyDilated cardiomyopathyHypertrophic cardiomyopathyLeft atrial dilation

Functional MR occurs when the left atrium or left ventricle dilates causing the mitral valve annulus to also dilate thus preventing the mitral valve leaflets from properly coapting. There are many causes of left atrial and left ventricular dilation and the treatment of this type of MR is directed at the primary cause. For example, if a patient develops systolic heart failure with a dilated left ventricle resulting in functional MR, treatment would be directed at the improvement of the heart failure.Organic MR results from actual disease of the mitral valve apparatus. The mitral valve leaflets, annulus, papillary muscles and chordae tendinae must interact properly for the mitral valve to function properly. Thus, disruption of any of these structures can result in organic MR.

What two percutaneous procedures have been experimented with to help treat patients with severe mitral regurgitation without surgery?Alfieri stitch and mitral clip: The Alfieri stitch is a surgical technique during which a suture was placed between the A2 and P2 segments of the mitral valve. This resulted in two mitral valve orifices. It was shown to significantly reduce the degree of mitral regurgitation, however may result in some degree of mitral stenosis. This is best suited for functional mitral regurgitation from annular dilation. Inserting a clip percutaneously between the A2 and P2 mitral valve leaflet segments has been done successfully, although research to support its use is lacking.Coronary sinus: A percutaneous procedure has been developed during which a ring is placed in the coronary sinus (which runs along the external part of the mitral annulus) and the right is tightened to allow the mitral valve leaflets to coapt better in systole.

Which heart valve problem can cause hemoptysis (coughing up of blood)?Mitral valve stenosis is known to cause hemoptysis in severe cases. This is due to the sudden rupture of a bronchial vein from the increased pressure being transmitted back from the left atrium. This phenomenon is termed “pulmonary apoplexy”

How would you describe the intensity of a systolic murmur that is easily audible, associated with a thrill, however the stethoscope must remain on the chest to hear the murmur?This would be described as a grade IV/VI murmur or 4/6. This describes the intensity, but remember the timing, pitch, location and radiation must be described as well to be complete.Systolic murmurs are graded on a scale of 1-6 while diastolic murmurs are graded on a scale of 1-4 (see below). Often, grade 1 murmurs are not discernable to inexperienced clinicians, while grade 6 murmurs are heard even

without the stethoscope on the chest and may actually be visible. The intensity of a murmur is primarily determined by the volume/velocity of blood flowing through a defect and the distance between the stethoscope and the lesion. For example, a very thin patient with severe aortic stenosis with a high pressure gradient across the valve (thus high velocity of blood flow) will have a loud murmur. Conversely, the exact same valvular lesion in a morbidly obese person or a person with severe COPD and a widened anterior-posterior chest diameter may be inaudible.

Grading systolic murmursIntensity Description

Grade I/VIGrade II/VIGrade III/VIGrade IV/VIGrade V/VI

                     

Grade VI/VI

Barely audibleAudible, but softEasily audibleEasily audible and associated with a thrillEasily audible, associated with a thrill, and still heard with the stethoscope only lightly on the chestEasily audible, associated with a thrill, and still heard with the stethoscope off of the chest

What is the main hemodynamic contraindication to surgical repairing severe mitral valve regurgitation?If severe left ventricular systolic dysfunction is present then the mitral valve should not surgically be repaired. In this situation, repairing/replacing the mitral valve will significantly increase the afterload which the dysfunctional left ventricle will not be able to tolerate. When severe mitral regurgitation is present, the blood can be ejected in two directions from the left ventricle (the normal route through the aortic valve or abnormally backward through the regurgitant mitral valve). Closing one of these routes will put an extra workload on the left ventricle. If the left ventricle is not able to handle this, cardiogenic shock and death will ensue. Specifically, the American Heart Association guidelines recommend medical therapy alone for patients with left ventricular ejection fraction < 30% and/or end systolic dimension > 55 mm when mitral valve repair is not likely.

What are the two neurohormonal mechanisms in play in patients with systolic heart failure?Activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) occur in patients with systolic heart failure. Then mainstay of therapy for this disorder is directed at these two systems. Beta-blockers inhibit the sympathetic nervous system activity and ACE inhibitors/angiotensin receptor blockers as well as spironolactone inhibit the RAAS.

What are the causes of acute aortic valve regurgitation?1. Aortic valve endocarditis (commonly Staph aureus)2. Ascending aortic dissection3. Trauma4. Iatrogenic (as a complication of cardiac catheterization or aortic valvuloplasty)5. Rupture of a congenitally fenestrated aortic valve cusp

What are the indications to surgically repair the tricuspid valve?The ACC/AHA Guidelines give the following indications to surgically repair the tricuspid valve:1. Repair of the tricuspid valve in severe tricuspid regurgitation when mitral valve surgery is planned (class I, level of

evidence B).2. Tricuspid valve replacement or annuloplasty ring is reasonable to severe primary tricuspid regurgitation when right

heart failure symptoms are present (class IIa, level of evidence C).3. Tricuspid valve replacement is reasonable for severe tricuspid regurgitation due to organic valve disease that is

not amenable to annuloplasty ring (class IIa, level of evidence C).4. Tricuspid annuloplasty ring may be considered for moderate tricuspid regurgitation in patients undergoing mitral

valve surgery when there is pulmonary hypertension or tricuspid annular dilatation (class IIb, level of evidence C).

What are the complications of pacemaker implantation?The complications of pacemaker implantation include:1. Infection of the pacemaker pocket (treated with IV antibiotics).2. Infection of the pacemaker leads (requires explantation of the device).3. Lead dislodgement/fracture (requires repositioning or replacement of lead).4. Pericardial effusion/tamponade from right ventricular perforation.5. Congestive heart failure (from induced ventricular dyssynchrony from RV pacing).

Which papillary muscle is most likely to rupture during an acute myocardial infarction and why?The posteromedial papillary muscle is the most likely to rupture during an acute myocardial infarction causing severe acute mitral valve regurgitation which can be life threatening if not immediately surgically repaired.There are two papillary muscles that comprise part of the complex anatomy of the mitral valve. The anterolateral papillary muscle receives dual blood supply from the left anterior descending coronary artery and the left circumflex coronary artery in most individuals while the posteromedial papillary muscle receives its sole blood supply from the right coronary artery. Complete infarction of the posteromedial papillary muscle can occur during an inferior MI (from thrombosis of the right coronary artery) while only partial or no damage will be done to the anterolateral papillary muscle during an anterior (left anterior descending) or lateral (circumflex) infarction since there is dual blood supply to this papillary muscle. Thus, the posteromedial papillary muscle is the most likely to rupture.

Amyl nitrate would have what effect on the murmur of mitral regurgitation?Amyl nitrate can be given via inhalation to reduce afterload for diagnostic purposes in the cardiac catheterization laboratory (to invoke a LV outflow tract gradient in hypertrophic obstructive cardiomyopathy patients) or as a diagnostic tool during cardiac physical examination. Due to the advancement of echocardiography, it is not commonly used any longer.Amyl nitrate decreases afterload and would decrease the murmur of mitral regurgitation. When the afterload is decreased, there is less resistance to blood flow from the left ventricle through the aortic valve and thus less blood regurgitates through the mitral valve, decreasing the intensity of the murmur.

What are the causes of diastolic congestive heart failure with a preserved left ventricular ejection fraction?1. Hypertensive heart disease2. Aging of the heart3. Ischemic heart disease4. Hypertrophic cardiomyopathy5. Restrictive/infiltrative cardiomyopathies

What percentage of patients with peripartum cardiomyopathy have a recurrence during subsequent pregnancies?The risk of subsequent heart failure during a pregnancy following one that resulted in peripartum cardiomyopathy depends predominantly on whether the left ventricular systolic function normalized or remained depressed. In general, the data to answer this question is limited.If the left ventricular systolic function returned to normal after the prior pregnancy, then the risk is low (one case series reporting about 21% developing symptomatic heart failure.If the left ventricular systolic function did not return to normal after the prior pregnancy, then the mortality rate was 19% in one small case series with a large majority developing heart failure symptoms.The current recommendation is to avoid pregnancy if the left ventricular systolic function remains depressed, however it is safe to attempt future pregnancies if the systolic function returned to normal.

What are the status classifications for patients waiting for heart transplantation?Status IA: The most critically ill patients. Must be hospitalized and requiring mechanical or pharmacological support to sustain life (intraaortic balloon counterpulsation, left ventricular assist device, high doses of intravenous inotropic therapy). New York Heart Association functional class IV.Status 1B: Less critically ill, but still seriously impaired. These patients may have outpatient daily inotrope infusion. New York Heart Association functional class III or IV.Status 2: The least urgent patients. These patients rarely receive transplantation since organs are in short supply and given to status 1A or status 1B patients first. New York Heart Association functional class II or III.

What are the indications for surgery in patients with severe mitral valve regurgitation?1. Symptoms related to heart failure that can be attributed to the mitral regurgitation and left ventricular ejection fraction > 30% (Class I)2. Symptoms related to heart failure that can be attributed to the mitral regurgitation and left ventricular ejection fraction < 30%. Mitral repair not replacement likely. (Class IIa)3. Asymptomatic severe mitral regurgitation if the left ventricular ejection fraction is < 60% and/or the end systolic dimension is > 40 mm. (Class I).4. Asymptomatic severe mitral regurgitation with the left ventricular ejection fraction > 60% and end systolic dimension < 40 mm if atrial fibrillation or pulmonary hypertension is present (Class IIa).5. Severe mitral valve regurgitation (usually from mitral valve prolapse) if repair rather than replacement is likely, even in the lack of symptoms and normal left ventricular ejection fraction (Class IIa).

What causes a widened split S2 heart sound?The second heart sound is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2 and the sound produced by the closure of the pulmonic valve is termed P2. When these sounds are distinguishable from each other a split S2 can be heard. The patterns of splitting of the S2 heart sound include physiologic splitting, paradoxical splitting, widened splitting and fixed splitting.

Persistent (widened) splitting occurs when both A2 and P2 are audible (split) during the entire respiratory cycle, however the splitting becomes greater with inspiration (due to increased venous return) and less prominent with expiration. This differs from a fixed split S2 which exhibits the same amount of splitting throughout the entire respiratory cycle.

Any condition that causes a non-fixed delay in the closure of the pulmonic valve or early closure of the aortic valve will result in a wide split S2. Thus, a persistently split S2 occurs in the setting of a RBBB or severe mitral regurgitation. A RBBB causes a delay in the closure of the pulmonic valve and this a delay in P2 without any effect on A2. In severe mitral regurgitation (MR), the A2 occurs early secondary to a large proportion of the left ventricular stroke volume entering the left atrium, thus causing the left ventricular pressure to decrease faster. The P2 is not affected in severe MR. 

What is tolvaptan and when is it indicated for heart failure treatment?Tolvaptan is a vasopressin receptor antagonist. Vasopressin (a.k.a. ADH or antidiuretic hormone) helps to regulate water retention by absorbing water in the collecting ducts of the nephron. Blocking this receptor will allow water to be excreted more readily. Many heart failure patients present with some degree hyponatremia from water retention. Tolvaptan has been shown in more than one clinical trial to raise sodium levels, however mortality and rehospitalization was not improved and thus the role for this therapy is not well defined.

What is the treatment for digoxin toxicity and when should Digibind (Fab) be given?Digoxin administration should be discontinued immediately. Arrhythmia should be treated according to ACLS (Advanced Cardiac Life Support) protocols. Intravenous fluids given for hypotension. If hemodynamic compromise is present or serious arrhythmia manifests from digoxin toxicity, then the mainstay of treatment is digoxin specific antibody (Fab). Below are the indications to give Fab:1. Life threatening arrhythmia including ventricular arrhythmias (ventricular tachycardia/ventricular fibrillation),

asystole, complete or high grade AV block or other symptomatic bradycardia.2. Evidence of end-organ dysfunction (renal failure, shock liver, altered mental status).3. Significant hyperkalemia (serum potassium > 5.5 mmol/L).

When is spironolactone indicated in patient with heart failure?Spironolactone is indicated (class IIa, level of evidence B) in systolic heart failure with recent or current New York Heart Association functional class IV symptoms, preserved renal function and a normal potassium concentration.Spironolactone was investigated in the RALES trial and a mortality benefit was shown in New York Heart Association functional class III and IV patients. Significant hyperkalemia did contribute to sudden cardiac death.

What medical therapy for heart failure is recommended when an ACE inhibitor or angiotensin receptor blocker is not able to be used?The combination of a direct arterial vasodilator (hydralazine) and a long acting nitrate (isosorbide mononitrate or isosorbide dinitrate) is recommended in patients who are not able to tolerate an ACE inhibitor and angiotensin receptor blocker (class IIa, level of evidence B). The most common reasons that a person would not be able to tolerate these medications would be renal insufficiency, hypotension or angioedema.The hemodynamic effects of using the combination of hydralazine and nitrates are similar to using an ACE inhibitor or angiotensin receptor blocker (ARB). ACE inhibitors/ARBs reduce afterload by blocking angiotensin II (which is vasoconstrictor) and reduce preload by blocking aldosterone (which normally promotes sodium and water retention). Hydralazine reduces afterload by directly dilating the arteries and long acting nitrates reduce preload by their vasodilator effects. The major difference between using an ACE inhibitor/ARB versus a combination of

hydralazine/nitrates is the former blocks the neurohormonal mechanism that is overactive in heart failure patients that leads to negative myocardial remodeling and the latter does not.

What is the American College of Cardiology/American Heart Association heart failure classification?The ACC/AHA classification of heart failure has four stages.Stage A includes those at risk for heart failure, but who have not yet developed structural heart changes (diabetics, those with coronary disease, but no prior infarct).Stage B includes individuals with structural heart disease, however no symptoms of heart failure have ever developed.Stage C includes patients who have developed clinical heart failure.Stage D are patients with refractory heart failure requiring advanced intervention (biventricular pacemakers, left ventricular assist device, or transplantation).Note that the ACC/AHA classification is much different from the New York Heart Association (NYHA) functional class in that there is no moving backwards between stages. Once symptoms develop, stage C heart failure is present and stage B will never again be achieved. The NYHA classification, in contrast, can move between class I and class IV relative quickly as these are all designated based on symptoms alone.

What are the indications for biventricular pacing?Biventricular pacing is an excellent option for certain patients with advanced heart failure. Also known as “cardiac resynchronization therapy”, biventricular pacing has been shown to improve heart failure symptoms in a majority cases. The normal cardiac conduction system delivers the electrical impulse to both the right and left ventricles simultaneously, however in the presence of a left bundle branch block (LBBB) or right bundle branch block (RBBB), the electrical impulse will reach one ventricle first then slowly transmit to the other causing “cardiac dyssynchrony”. Remember that a LBBB and RBBB by definition prolong the QRS duration.The indications for biventricular pacing are below:1. Left ventricular ejection fraction < 35%, a QRS duration of > 120 ms and New York Heart Association (NYHA) functional class III or IV with optimal medical therapy.2. Left ventricular ejection fraction < 35% and frequent reliance on right ventricular pacing (which significantly prolongs the QRS duration).3. Left ventricular ejection fraction < 35% and NYHA functional class I or II who are undergoing pacemaker or implanted cardioverter defibrillator (ICD) insertion and may rely on frequent cardiac pacing.*Note: Meta-analysis has shown a mortality benefit for those patients with a QRS duration of > 150 ms who receive biventricular pacing and not those with a QRS duration < 150 ms.*Note: Many patients who are candidates for biventricular pacing also receive an implanted cardioverter defibrillator (ICD) at the same time.

How does atrial fibrillation effect the ability of a biventricular pacemaker to function properly?When atrial fibrillation is present, the QRS complex occurs at random intervals and the biventricular pacing device does not know when to initiate atrial pacing and may not be able to initiate biventricular pacing (if the native QRS complex comes earlier than expected). This results in less beneficial effects on cardiac output and thus symptoms.Therefore, it is recommended that any patient with permanent atrial fibrillation undergoing biventricular pacing also have AV nodal ablation performed, thus eliminating the unpredictability of the onset of the QRS complex allowing for near 100% biventricular pacing.

What is the most common cause of right heart failure? What are the physical exam findings in left and right heart failure?The most common cause of right heart failure is left heart failure. As the left ventricle fails, the pressures increase and transmit to the left atrium, the pulmonary veins, the pulmonary arterial system and eventually into the right heart. This can cause right heart failure. There are multiple causes of left heart failure as described in our heart failure section.Other causes of right heart failure include severe lung disease (resulting in severe pulmonary hypertension), pulmonic/tricuspid valve disease, primary pulmonary hypertension, chronic pulmonary embolism, sleep related breathing disorders (obstructive sleep apnea)  or right ventricular infarction.

What are the cardiovascular complications of obstructive sleep apnea?The four cardiovascular complications of obstructive sleep apnea (OSA) are:

1. Hypertension: OSA is well known to cause hypertension. In severe cases the hypertension can be refractory to medical management unless the sleep apnea is controlled. The mechanism is theorized to be related to enhanced sympathetic tone. Some degree of hypertension in sleep apnea patients is likely related to obesity.2. Right heart failure: OSA causes pulmonary hypertension from chronic hypoxemia. This can leads to right heart failure.3. Ischemic heart disease: OSA is known to cause coronary artery disease and increase the risk of acute coronary syndromes likely due to enhanced sympathetic tone and hypertension.4. Arrhythmia:   - Atrial fibrillation and atrial flutter are very strongly associated with OSA. Some studies estimate 82% of patients with atrial fibrillation/flutter have sleep apnea (likely an overestimate).   - Bradycardia and asystole are common during sleeping hours in patients with obstructive sleep apnea, however the clinical importance of this is not clear. Bradycardia can occur during waking hours as well however less commonly. One study reported that almost 60% of patients that needed a permanent pacemaker (for sick sinus syndrome or AV block) had obstructive sleep apnea.   - Premature ventricular and atrial contractions are markedly more common in patients with OSA. These can be symptomatic.5. Left heart failure: Some studies suggest that OSA may be the cause of LV systolic dysfunction and left heart failure in some patients when severe.

What are the indications for ICD implantation in systolic heart failure patients?An implantable cardioverter defibrillator (ICD) is a permanent device in which a lead (wire) inserts into the right ventricle and monitors the heart rhythm. It is implanted similar to a pacemaker and the generator lays in the upper chest area. Therapies are delivered in the form of anti-tachycardia pacing (ATP) or shocks to convert to sinus rhythm from sustained ventricular tachycardia or ventricular fibrillation, both of which are life-threatening rhythms.For primary prevention of sudden cardiac death, ICDs are indicated:1. Patients with a prior myocardial infarction and a left ventricular ejection fraction of < 30% (MI must have been at least 40 days prior in order to allow time for recovery of LV systolic function)2. Patients with systolic heart failure (New York Heart Association functional class II or III) and an ejection fraction < 35%. Optimal medical therapy must be present and at least 3 months must have elapsed in case the systolic function recovers to an ejection fraction > 35% in both non-ischemic cardiomyopathy patients and ischemic cardiomyopathy patients who underwent bypass surgery.For secondary prevention of sudden cardiac death, ICDs are indicated:1. Patients with documented cardiac arrest from sustained ventricular tachycardia or ventricular fibrillation or documented hemodynamically stable sustained ventricular tachycardia even if the left ventricular ejection fraction is > 35%, as long as no reversible cause is identified. The above must not be within 48 hours of an acute coronary syndrome.

What is the mainstay of treatment for the different types of shock (cardiogenic, hypovolemic, distributive)?Shock is defined as hypotension that is severe and results in end-organ hypoperfusion. It is a life threatening condition and appropriate therapy is crucial in a timely fashion.Cardiogenic shock: This occurs when the primary problem is low cardiac output from heart failure. Causes include acute myocardial infarction, acute valvular regurgitation (aortic or mitral), and dilated cardiomyopathies. Treatment includes correcting the primary cause and intravenous inotropic therapy. Intraaortic balloon counterpulsation is frequently beneficial. Refractory cases may require emergent left ventricular assist device placement.Hypovolemic shock: This occurs from severe intravascular volume depletion as occurs in dehydration or acute hemorrhage. The treatment is aggressive IV fluid hydration, blood transfusion and correction primary cause.Distributive shock: This occurs with something causes intense systemic vasodilation (septic shock or neurogenic shock). Treatment is directed at the source. Pressors such as norepinephrine are frequently used to maintain blood pressure until the primary problem resolves.

What is the electrophysiologic mechanism of atrioventricular reentrant tachycardia (AVNRT)?AVNRT is the most common narrow-complex tachycardia in healthy individuals and only second to atrial fibrillation/flutter in the general population. AVNRT occurs when there is “dual AV nodal physiology”. This means there is one pathway that conducts slowly within the AV node and another that conducts fast. A premature atrial or ventricular contraction can alter the normal conduction cycle to produce a reentrant circuit within these two pathways resulting in SVT.

What is the definition of a non-ST segment elevation myocardial infarction?Anginal symptoms at rest that result in myocardial necrosis as identified by elevated cardiac biomarkers (see Cardiac Biomarkers) with no ST segment elevation on the 12-lead electrocardiogram.

When are beta-blockers contraindicated in heart failure?Beta-blockers are contraindicated specifically in systolic heart failure when pulmonary edema is present, when there are signs of cardiogenic shock, severe bradycardia, hypotension or wheezing related to asthma.Beta-blockers should be initiated in patients hospitalized for acute systolic congestive heart failure prior to hospital discharge. It is reasonable to withhold beta-blockers in patients who were previously taking them in the outpatient setting for chronic systolic heart failure when they are admitted with a heart failure exacerbation.

Compare and contrast the third heart sound and the fourth heart sound (give at least 5 differences and two similarities). 

S3 - "ventricular gallop" S4 - "atrial gallop"Occurs in early diastoleOccurs during passive LV fillingMay be normal at timesRequires a very compliant LVCan be a sign of systolic CHF

Occurs in late diastoleOccurs during active LV fillingAlmost always abnormalRequires a non-compliant LVCan be a sign of diastolic CHF

Which medications offer a mortality benefit in patients with chronic systolic congestive heart failure?1. ACE inhibitors or angiotensin receptor blockers2. Beta-blockers3. Spironolactone4. Combination of hydralazine/nitrates when ACE inhibitors or angiotensin receptor blockers are not able to be tolerateNote: Digoxin and loop diuretics have no mortality data to support their use, although dramatic symptomatic improvement can be seen with these therapies.

When are beta-blockers contraindicate during an acute myocardial infarction?Beta-blockers are contraindicated during an acute myocardial infarction when there are signs of pending cardiogenic shock. These include systolic blood pressure < 110 mmHg and pulmonary edema. Typical contraindications include severe bradycardia, heart block more advanced than 1st degree (unless a pacemaker is in place) and for use during a MI from cocaine use.

What is another name for “slow ventricular tachycardia” and what is the clinical implication?Slow ventricular tachycardia is also known as an “idioventricular rhythm” and it is a common post-MI heart rhythm. An idioventricular rhythm is hemodynamically stable and does not cause any problems and thus no specific treatment is needed. This rhythm meets all of the Brugada Criteria for ventricular tachycardia except the heart rate is < 100 beats per minute thus the term “slow ventricular tachycardia” is commonly used.

What is the treatment for frequent premature ventricular contractions (PVCs) after a myocardial infarction?No treatment is necessary. Lidocaine was tried after myocardial infarctions to suppress PVCs. While the drug was successful, there was no clinical or mortality benefit from this therapy. This is not the same as ventricular tachycardia which frequently requires urgent therapy to terminate.

What are the causes of dilated cardiomyopathy?1. Viral (Coxsackie B, influenza, HIV, enteroviruses)2. Idiopathic (about 50% of cases)3. Familial/genetic4. Alcohol5. Chemotherapeutic agents (most commonly daunorubicin and doxarubacin)6. Selenium deficiency7. Thyroid disease8. Tachycardia mediated9. Peripartum

What are the causes of constrictive pericarditis?Constrictive pericarditis can be caused by any entity that can trigger pericarditis. These include:1. Tuberculosis (most common cause worldwide)2. Viral3. Radiation therapy (frequently in the late 1970’s and early 1980’s when high doses were given for non-Hodgkin's lymphoma. Constrictive pericarditis can present decades later)4. Trauma5. Post-cardiac surgery

What are the causes of congestive heart failure in patients with hypertrophic obstructive cardiomyopathy?Also known as hypertrophic obstructive cardiomyopathy (HOCM), this disease results in abnormal hypertrophic changes most commonly in the interventricular septum with pathologic “myocardial disarray”. HOCM is familial in about 50% of cases and transmitted in an autosomal dominant fashion. HOCM can result in clinic heart failure, life-threatening arrhythmias, mitral regurgitation and sudden cardiac death. The causes of heart failure in HOCM include:1. Diastolic dysfunction2. Mitral regurgitation3. Arrhythmia4. End-stage HOCM results in systolic dysfunction “burnt-out HOCM”

What are the indications for surgery in patients with aortic valve regurgitation?Indications for aortic valve replacement according to the American Heart Association Guidelines are as follows:1. Severe aortic regurgitation with symptomatic heart failure (class I).2. Severe aortic regurgitation with equivocal symptoms who performed poorly on a treadmill exercise test (class I).3. Severe aortic regurgitation with no symptoms left ventricular ejection fraction < 50% (class I).4. Severe aortic regurgitation with no symptoms, a normal left ventricular ejection fraction, but left ventricular end systolic dimension of > 55 mm or end diastolic dimension of 75 mm (class IIa).5. Severe aortic regurgitation with no symptoms, a normal left ventricular ejection fraction, but left ventricular end systolic dimension between 50-55 mm or end diastolic dimension between 70-75 mm (class IIb).

What are the two mechanical therapies (non-medication) for hypertrophic obstructive cardiomyopathy (HOCM) and what are their indications?The two mechanical therapies to treat HOCM are surgical myomectomy and catheter based alcohol septal ablation.The indications for mechanical therapy for HOCM are simply persistent symptoms despite optimal medical therapy (New York Heart Association functional class III and IV) or recurrent syncope despite medical therapy.

Surgical myectomy (a.k.a. septal myectomy) is simply performed when the surgeon removes the hypertrophied part of the interventricular septum relieving the outflow tract obstruction. Complications include a ventricular septal defect (if too much tissue is removed), LV dysfunction (if other myocardial segments are damaged during surgery), or the development of complete heart block (due to injury of the AV node).Alcohol (Ethanol) septal ablation is a catheter based, minimally invasive intervention during which the septal perforator coronary arteries are identified and alcohol is infused. This causes thrombosis and infarction of the interventricular septum. This causes the infarcted tissue to thin thus relieving the outflow tract obstruction. Complications can be serious and include complete heart block, ventricular arrhythmias, sudden cardiac death, coronary dissection/perforation resulting in pericardial effusion, and LV systolic dysfunction.The above two procedures have never been compared head-to-head in any clinical trials. Observational data suggest that alcohol septal ablation has more variable results with some patients achieving excellent results while others had no benefit. Both procedures have similar mortality rates. Cardiovascular complications (complete heart block) are lower with surgical myectomy, but non-surgical complications (infection) were higher. Both procedures similarly improve symptoms of heart failure. Alcohol septal ablation was more likely to result in the need for a second procedure.

What is the treatment for constrictive pericarditis?There is no medical therapy that works well to treat constrictive pericarditis. The mainstay of therapy is surgical pericardiectomy which is a tedious surgery to perform.

What is the pathological finding of hypertrophic obstructive cardiomyopathy (HOCM)?In patients with HOCM, the myocardial muscle cells are abnormally thickened related to mutations in the genes encoding contractile proteins in the sarcomere. The myocytes are not able to align properly and the typical description pathologically of heart specimens is that of “myocardial disarray”. Over time, the myocytes are replaced with fibrous tissue which can lead to systolic heart failure or “burnt-out HOCM”.

How is hypertrophic obstructive cardiomyopathy (HOCM) treated medically?There are no large randomized clinical trials available to evaluate different drug therapy in symptomatic patients with HOCM. Since most symptoms from HOCM are related to left ventricular outflow tract obstruction which occurs during systole, medical therapy is aimed at lowering the heart rate to allow better diastolic filling and using negative inotropic agents to decrease the force of contractility.Non-dihydropyridine calcium channel blockers such as verapamil are commonly used. These drugs slow the heart rate and decrease the inotropic force of LV contraction relieving the symptoms of HCOM.Beta-blockers act similar to the above in mechanism in HOCM patients.Disopyramide is the historical treatment for HOCM. This drug has significant negative inotropic effects, however is considered an antiarrhythmic drug. It is currently recommended only for persistent symptoms if non-dihydropyridine calcium channel blockers and beta-blockers fail. Patients on disopyramide should also take one of the above concomitantly since disopyramide enhances AV nodal conduction and should atrial fibrillation/flutter develop, it will very rapidly conduct to the ventricles. Disopyramide can prolong the QT interval resulting in polymorphic ventricular tachycardia in some patients. There are significant anticholinergic side effects including xerostomia (dry mouth), urinary retention, visual disturbances and decreased perspiration.

What are the four main steps in the development of the atherosclerotic plaque?The pathophysiologic process by which atherosclerosis occurs is complex and somewhat controversial. The working theory includes four steps:1. Endothelial cell injury2. Lipoprotein deposition3. Inflammatory reaction4. Smooth muscle cell cap formationEndothelial cell injury: This is likely the initial factor that begins the process of atherosclerotic plaque formation. Since the endothelium are constantly exposed to the circulation, any toxin present can result in damage (as occurs during tobacco use, diabetes and dyslipidemia). The continuous physical force exerted upon the endothelium also plays a role as commonly the greatest atherosclerotic plaque occurs at arterial bifurcations (i.e. the bifurcation of the left main coronary artery and the left anterior descending). Hypertension increases the physical force present.Lipoprotein deposition: When the endothelium is injured or disrupted, lipoprotein molecules can gain entry where they are then modified by oxidation (via free radicals or oxidizing enzymes) or glycation (diabetics). This modified lipoprotein (modified LDL) is inflammatory and able to be ingested by macrophages creating “foam cells” causing a “fatty streak” in the arterial wall.Inflammatory reaction: The modified LDL is antigenic and attracts inflammatory cells into the arterial wall. Also, after endothelial injury, inflammatory mediators are released further increasing leukocyte recruitment.

Smooth muscle cell cap formation: Smooth muscle cells migrate to the surface of the plaque creating a “fibrous cap”. When this cap is thick, the plaque is stable, however thin capped atherosclerotic plaques are thought to be more prone to rupture or erosion causing thrombosis.

How is hypertrophic obstructive cardiomyopathy (HOCM) genetically transmitted?HOCM is an autosomal dominant genetic disorder in about 60% of cases. The remainder are related to spontaneous mutations. Several different genes are involved that can result in HOCM. Most of these encode for sarcomere proteins in the contractile apparatus of the myocardial cells. The most common gene affected is the cardiac myosin binding protein C followed by mutations in the cardiac beta-myosin heavy chain.

What is the most common cause of death in young athletes?The most common cause of sudden cardiac death in young athletes is hypertrophic obstructive cardiomyopathy (HOCM) which accounts for approximately one-third of cases. The second leading cause is an anomalous origin of a coronary artery causing ischemia. Other causes are listed below:Myocarditis/dilated cardiomyopathyMitral valve prolapse (controversial)Aortic ruptureMyocardial bridging (controversial)Aortic stenosisArrhythmogenic right ventricular dysplasia (ARVD)Ischemic heart disease (atherosclerosis)Undiagnosed congenital heart diseaseGenetic channelopathies (i.e. prolonged QT syndrome)

A systolic ejection click is frequently a finding of what specific heart valve problem?A systolic ejection click frequently indicates a bicuspid aortic valve. This sound is heard just after the 1st heart sound (S1). Usually, the opening of the aortic valve is not audible, however with a bicuspid aortic valve the leaflets “dome” suddenly prior to opening which creates a systolic ejection click. The click may be difficult to hear in the presence of significant aortic stenosis.

What causes a III/VI crescendo-decrescendo murmur heard at the right upper sternal border that peaks early in systole and does not change with handgrip?This is a describes the murmur of mild aortic stenosis (AS).The classic murmur of aortic stenosis is a high pitched, crescendo-decrescendo ("diamond shaped"), midsystolic murmur located at the aortic listening post and radiating toward the neck. The radiation of the AS murmur is often mistaken for a carotid bruit. The AS murmur is also well known to radiate to the cardiac apex on occasion, making it difficult to distinguish if mitral regurgitation is also present. This radiation of the AS murmur to the apex is known as "Gallavardin dissociation". It requires dynamic auscultation or echocardiography to determine if coexisting mitral regurgitation is the cause of the apical murmur in a patient with AS.    The intensity of the murmur of AS is not a good indicator as to the severity of disease. As AS worsens, the left ventricle begins to fail and the ejection fraction declines to the point where sufficient force to create turbulent flow is no longer produced, resulting in a decrease in the intensity of the murmur.    While the intensity of the murmur may not be an accurate determinant of the severity of AS, the shape of the murmur can be very helpful. As AS worsens, it takes longer for blood to eject through the valve, so the peak of the crescendo-decrescendo murmur moves to later in systole. Thus mild AS would have an early peaking murmur while the murmur of severe AS peaks later in systole. 

This arrhythmia is characterized by three different morphology P waves in on 12-lead ECG with a ventricular rate < 100 beats per minute.Wandering atrial pacemaker (WAP) is a rhythm that occurs when three different P wave morphologies are seen on a 12-lead ECG. This is a benign rhythm and no treatment is indicated. If the heart rate exceeds 100 beats per minute, then the rhythm is called multifocal atrial tachycardia (MAT).

Describe the murmur of an atrial septal defect (ASD)?The murmur produced by an ASD is due to increased flow through the pulmonic valve, thus it is remarkably similar to that of pulmonic stenosis. The difference lies in the intensity and splitting pattern of the S2 heart sound. The intensity of S2 should remain unchanged and may infact be accentuated if pulmonary hypertension develops. The S2 is fixed-split in a person with an ASD. This differs from the widened split S2 seen in severe pulmonic stenosis. Also, the murmur of an ASD does not increase in intensity with inspiration like that of pulmonic stenosis.

How can you distinguish the murmur of aortic stenosis from that of hypertrophic obstructive cardiomyopathy (HOCM)?The murmur of HOCM is important to detect due to its clinical implications. The murmur is high-pitched, crescendo-decrescendo, midsystolic murmur heard best at the left lower sternal border.  The murmur of HOCM does not radiate to the carotids like that of AS.  The important auscultatory features of HOCM that distinguish it from AS relate to dynamic auscultation.The murmur of HOCM becomes quite loud with Valsalva. This maneuver effectively acts to decrease left ventricular filling which results in worsened left ventricular outflow tract obstruction in patients with HOCM making the murmur louder. Standing from the squatting position has a similar effect (this results in sudden pooling of blood in the legs decreasing venous return). In patients with aortic valvular stenosis, the murmur will get softer with Valsalva/standing since less blood is being ejected through the aortic valve. Rapid squatting from a standing position forces increased venous return and would have the opposite effect of Valsalva/rapid standing.

When can sustained ventricular tachycardia be treated medically and when does it require emergent direct current cardioversion?Ventricular tachycardia can be a fatal arrhythmia, however at times it can be tolerated quite well hemodynamically. This usually occurs in the ventricular rate is > 150 beats per minute. The reasons to emergently cardiovert a patient with ventricular tachycardia would be:

- Altered consciousness- Severe hypotension- Chest pains- Signs of shock- If the ventricular tachycardia is hemodynamically stable without the above signs/symptoms, then amiodarone can be given intravenously. Lidocaine is acceptable as well.

Which antiarrhythmic drugs prolong the QT interval?Quinidine, disopyramide, procainamide, sotalol, dofetilide, ibutilide and amiodarone can potentially prolong the QT interval.The antiarrhythmic drugs that do not prolong the QT interval include propafenone, flecainide, lidocaine and mexiletine. 

Which is the most effective statin to raise the HDL?Rosuvastatin is the most effective HMG-CoA reductase inhibitor to increase HDL levels.HMG-CoA reductase inhibitors are also known as “statins” and work by inhibiting the synthesis of cholesterol in the liver by the enzyme HMG-CoA reductase. These drugs which include pravastatin, fluvastatin, atorvastatin, simvastatin and rosuvastatin are the mainstay of therapy for elevated LDL cholesterol and secondary prevention of acute coronary syndrome and strokes.They also raise the HDL levels.

How does the murmur of mild aortic regurgitation differ from that of severe aortic regurgitation (AR)?Mild aortic regurgitation causes a long, soft early diastolic decrescendo murmur. As the regurgitation becomes more severe, the pressure between the aorta and left ventricle equalizes more quickly and the murmur becomes significantly shorter, although the intensity can increase slightly.The murmur of aortic regurgitation is a soft, high-pitched, early diastolic decrescendo murmur usually heard best at the 3rd intercostal space on the left (Erb's point) at end expiration with the patient sitting up and leaning forward. If the AR is due to aortic root disease, the murmur will be best heard at the right upper sternal border and not at Erb's point.In patients with AR, an early diastolic rumble may also be heard at the apex due to the regurgitant jet striking the anterior leaflet of the mitral valve causing it to vibrate. This murmur is termed the Austin-Flint murmur.In addition to the above two murmurs, a systolic ejection murmur may be present in people with severe AR at the right upper sternal border simply due to the large stroke volume passing through the aortic valve with each systolic contraction of the LV.

What causes a continuous murmur throughout systole and diastole?The two most common causes of a continuous murmur are a patent ductus arteriosus and severe aortic valve regurgitation.A patent ductus arteriosus causes a continuous murmur since there is a constant pressure gradient in both systole and diastole forcing blood from the aorta into the pulmonary artery. The normal aortic systolic/diastolic pressure is 120/80 mmHg and the normal pulmonary arterial pressure is 25/5 mmHg. Thus in systole there is an average of a 95 mmHg gradient causing a left to right shunt and during diastole there is a 75 mmHg gradient causing a similar shunt.Severe aortic regurgitation causes an early diastolic murmur which can be short, however when heart rates are faster and diastole is shortened, it can sound holodiastolic. There is a systolic flow murmur present as well due to the high volume of blood ejected across the aortic valve (normal LV forward volume from blood that filled via the left atrium PLUS the regurgitant volume). This effectively creates the effect of a continuous murmur throughout systole and diastole.

What is Carvallo’s sign?Carvallo’s sign occurs when the murmur of tricuspid valve regurgitation gets louder with deep inspiration. This, as well as the location of the murmur, helps to distinguish tricuspid regurgitation from mitral regurgitation. Deep inspiration lowers intrathoracic pressures causing increased venous return to the right heart. Since there is more volume in the right heart, the regurgitant volume in the presence of tricuspid regurgitation increases, thus increasing the intensity of the murmur.

A post-PVC beat would have what effect on the murmur of aortic stenosis (AS)? What about the murmur of hypertrophic obstructive cardiomyopathy (HOCM)?A post-PVC beat allows more time for the left ventricle to fill. The more blood in the left ventricle, the more will be ejected. This results in increasing the intensity of the murmur of AS.In contrast, if there is more blood in the LV, the hypertrophied interventricular septum is pushed out of the left ventricular outflow tract relieving the obstruction to some degree, decreasing the intensity of HOCM.

What are the indications for a left ventricular assist device (LVAD)?A left ventricular assist device is a surgically implanted cardiac assist mechanism which essentially acts like a heart. One cannula sits in the left ventricle which pulls blood out of the body into its chamber where it pumps blood to the second cannula inserted into the aorta.1. Post-operative cardiogenic shock (not able to be weaned from cardiopulmonary bypass)2. Back-up in patients undergoing high risk surgical procedures3. Massive myocardial infarction without other therapeutic options4. Severe cardiac decompensation (regardless of cause) such as progression of a non-ischemic cardiomyopathy5. Bridge to transplantation6. Chronic heart failure with a poor prognosis that are not a transplant candidate (LVAD implantation in this situation is termed “destination therapy” since their final destination is not transplant, but they will have the LVAD until death).

What alteration in the heart sounds is heard in a patient having an acute coronary syndrome? What is the physiologic mechanism?An acute coronary syndrome causes an S4 heart sound.Remember the LV relaxation is an active process which requires ATP (adenosine triphosphate). If ischemia is present, the synthesis of ATP is limited and the LV is not able to relax well. This results in a S4 heart sound.The fourth heart sound (S4), also known as the "atrial gallop", occurs just before S1 when the atria contract to force blood into the LV.  If the LV is non-compliant and atrial contraction forces blood through the atrioventricular valves (mitral/tricuspid), a S4 is produced by the blood striking the LV. 

What are the two most common indications for a permanent pacemaker implantation?Sick sinus syndrome (SSS) occurs from sinoatrial node dysfunction is the most common indication for permanent pacemaker implantation. This may manifest in multiple different ways including:- Tachycardia-bradycardia syndrome (i.e. pauses after converting to sinus rhythm)- Severe sinus bradycardia- Sinus pauses/sinus arrest- Sinoatrial nodal exit block- Chronotropic incompetence (failure of heart rate to increase during exercise)The second most common indication for a permanent pacemaker is atrioventricular (AV) nodal disease such as second degree type II AV block or third degree heart block.The AV blocks occur when there is fibrosis/dysfunction of the atrioventricular node or His-Purkinje system. The AV node itself is subject to autonomic input. If the parasympathetic tone is high of if sympathetic tone is inhibited (beta-blockers), then a 1st degree AV block (prolonged PR interval) or second degree type I AV block may manifest. This is reversible if the autonomic tone is returned to normal.In contrast, if there is disease of the His-Purkinje system, the rhythm may be second degree type II or third degree heart block, which is not reversible and indicates the need for permanent pacemaker implantation.

What are the diagnostic criteria for ventricular tachycardia?The Brugada criteria/algorithm is below:1. Do you see concordance present in the precordial leads (leads V1-V6)?Also sometime explained as the absence of an RS complex, concordance is diagnostic of VT. A simple way to think of this would be to ask the question, are all of the QRS complexes completely upright or completely downward in the precordial leads? If the answer is yes, then VT is the diagnosis.2. Is the R to S interval > 100 ms in any one precordial lead?If present, then VT is the diagnosis. Simply use calipers to measure the distance between the R wave to S wave in each precordial lead and see if it exceeds 100 ms.3. Do you see atrioventricular (AV) dissociation?If present, the diagnosis is ventricular tachycardia.

AV dissociation occurs when P wave (represents atrial depolarization) are seen at different rates than the QRS complex. This is present in only a small percentage of ventricular tachycardia ECG tracings, however is diagnostic of VT. Frequently, this is difficult to see due to the fast rate of the QRS complex. Below is an ECG strip of a ptient with ventricular tachycardia. See the P-P inteval when in sinus rhythm then march out the P waves within the wide QRS complex to find the AV dissociation that is present confirming the diagnosis of ventricular tachycardia:

4. Examine the morphology of the QRS complex to see if it meets the below specific criteria for VT as below.VT is frequently either in a right bundle branch block pattern (upright in V1) or a left bundle branch block pattern (downward in V1).If upward in lead V1 (RBBB pattern), then VT is present in the following situations:

A monophasic R or biphasic qR complex in V1. If an RSR’ pattern (“bunny-ear”) is present in V1 with the R peak being higher in amplitude than the R’ peak, the VT is

present (see image below). A rS complex in lead V6 favors VT

If downward in lead V1 (LBBB pattern), then VT is present in the following situations: The presence of any Q or QS wave in lead V6 favors VT A wide R wave in lead V1 or V2 of 40 ms or more favors VT (see below image) Slurred or notched downstroke of the S wave in V1 or V2 favors VT Duration of onset of QRS complex to peak of QS or S wave > 60 ms favors VT

A fusion beat (a.k.a. Dressler beat) occurs during ventricular tachycardia and is also known as a fusion beat. This occurs when sinus node activity (P wave) begins to conduct through the normal conduction pathway during an episode of ventricular tachycardia. The abnormal ventricular impulse then conducts retrograde across the AV node and the resulting QRS is a “fusion beat” of the normal QRS morphology and that of the ventricular morphology from the ventricular tachycardia.A “capture beat” is similar to a fusion beat, except the QRS morphology looks completely like the normal QRS complex since sinus node impulse conducts to the ventricles before the retrograde ventricular activation occurs.

What is the treatment for left ventricular free wall rupture?This is a fatal complication of myocardial infarction and occurs when thinning of the left ventricular free wall occurs as a part of remodeling. A complete defect results in blood from the left ventricle filling the pericardium. This usually

occurs rapidly resulting in cardiac tamponade, pulseless electrical activity (PEA) and death. Treatment is emergent surgical repair.Right heart catheterization will show increased right heart pressures and decreased left heart pressures with inspiration. Also, the diastolic pressures are elevated and equal. Normally, the pericardium can expand as the heart fills, however with cardiac tamponade from a large pericardial effusion or constrictive pericarditis, this is not able to occur. As a person inspires, venous return is increased to the right heart and the interventricular septum bulges to the left impairing left ventricular filling, reducing left heart cardiac output and thus decreasing systemic pressure (increasing the “pulsus paradoxus”). As a person exhales, right ventricular filling decreases and the left heart fills causing the interventricular septum to bulge to the right impairing right ventricular filling. The diastolic pressures are elevated and equal since every cardiac chamber pressure influences the other considering the heart is not able to expand as mentioned above.

What causes a split S1 heart sound and/or a widened split S1 heart sound?The first heart sound results from the closing of the mitral and tricuspid valves. The sound produced by the closure of the mitral valve is termed M1 and the sound produced by closure of the tricuspid valve is termed T1. The M1 sound is much louder than the T1 sound due to higher pressures in the left side of the heart, thus M1 radiates to all cardiac listening posts (loudest at the apex) and T1 is usually only heard at the left lower sternal border. The M1 sound is thus the main component of S1.In about 40-70% of normal individuals, as well as in certain cardiac conditions, a "split S1" sound can be appreciated. This occurs when the mitral valve closes significantly before the tricuspid valve allowing both valves to make an audible, separate sound. Inspiration delays the closure of the tricuspid valve in a normal person (due to increased venous return), thus enhancing the splitting of the S1 sound. Also, a split S1 sound is common in the setting of a right bundle branch block (RBBB) or ventricular tachycardia/PVCs with a RBBB morphology. A RBBB causes the electrical impulse to reach the left ventricle before the right ventricle. Dyssynchrony then occurs resulting in the left ventricle contracting before the right ventricle, thus the pressures in the left ventricle rises before that of the right ventricle. This delays the closure of the tricuspid valve resulting in a split S1 sound. A left bundle branch block (LBBB) has the opposite effect on S1. In this setting, the electrical impulse reaches the right ventricle before the left ventricle, thus the pressure in the right ventricle rises before that of the left ventricle. This forces the tricuspid valve closed earlier resulting in complete overlap of M1 and T1 and thus no audible split S1 sound.

The M1 sound occurs slightly before T1. Since the mitral and tricuspid valves normally close almost simultaneously, only one single heart sound is usually heard. However, in about 40-70% of normal individuals, as well as in certain cardiac conditions, a "split S1" sound can be appreciated. This occurs when the mitral valve closes significantlybefore the tricuspid valve allowing both valves to make an audible, separate sound. Inspiration delays the closure of the

tricuspid valve in a normal person (due to increased venous return), thus enhancing the splitting of the S1 sound. Also, a split S1 sound is common in the setting of a right bundle branch block (RBBB) or ventricular tachycardia/PVCs with a RBBB morphology. A RBBB causes the electrical impulse to reach the left ventricle before the right ventricle. Dysynchrony then occurs resulting in the left ventricle contracting before the right ventricle, thus the pressures in the left ventricle rises before that of the right ventricle.

What is the TIMI risk score?The TIMI risk score stands for “Thrombolysis In Myocardial Infarction” and is a scoring system to determine the likelihood that of death and the presence of an acute coronary syndrome in patients presenting with potential anginal symptoms. Each component of the score gives 1 point and is listed below:1. Age > 652. Aspirin use in the prior 7 days3. ST changes of at least 0.5 mm on the initial ECG (ST elevation or depression)4. Elevated serum cardiac biomarkers5. Two or more potential anginal symptoms in the last 24 hours6. Previously diagnosed coronary artery disease with at least 50% stenosis7. Three or more traditional risk factors for CADThe risk at 14 days of all-cause mortality, acute coronary syndrome or severe ischemia requiring coronary revascularization is below:1 point = 4.7%2 points = 8.3%3 points = 13.2%4 points = 19.9%5 points = 26.2%6 or 7 points = 40.9%Note that the TIMI score is different that TIMI grade coronary flowTIMI 0 flow indicates no antegrade coronary flow past the obstruction (complete occlusion)TIMI 1 flow is minimal antegrade flow past the coronary obstructionTIMI 2 flow is partial antegrade flow past the obstruction with complete filling of the distal coronary vesselTIMI 3 flow is normal flow filling the distal coronary artery

Which antiarrhythmic drug can cause drug induced lupus erythematosus?Procainamide can cause drug induced systemic lupus erythematosus (SLE). Anti-histone antibodies are present in about 95% of cases. Other medications known to cause drug induced SLE include hydralazine (used to treat hypertension) and isoniazid (used to treat tuberculosis).

What maneuvers can increase the intensity of the murmur of mitral valve regurgitation?Handgrip exercises and transient arterial occlusion increase the murmur of mitral regurgitation.Handgrip exercises, performed by having the patient squeeze both hands intensely for at least one minute, increases afterload. When the afterload is increased, there is more resistance to blood flow from the left ventricle through the aortic valve and thus more blood regurgitates through the mitral valve.Transient arterial occlusion (TAO) is performed by inflating blood pressure cuffs on both arms to increase the afterload. This has the same effect on the murmur of mitral regurgitation as handgrip exercises and may be the preferred method if a patient is not able to adequately perform a strong handgrip.

What is the most common narrow complex tachycardic arrhythmia besides atrial fibrillation or atrial flutter?The most common cause of a narrow complex tachycardia is AVNRT or atrioventricular reentrant tachycardia.The term “SVT” can be confusion at times. In general, this term is used to describe a narrow complex tachycardia not including atrial fibrillation/flutter. The term SVT frequently refers to AVNRT, however technically it means any tachycardic rhythm that originates from above the ventricles (above the AV node). This would include:1. Sinus tachycardia2. Atrial tachycardia3. Atrial fibrillation4. Atrial flutter5. AV nodal reentrant tachycardia (AVNRT)6. AV reentrant tachycardia (AVRT)7. Other less common SVTs

This arrhythmia is characterized by three different morphology P waves one 12-lead ECG with a ventricular rate > 100 beats per minute.Multifocal atrial tachycardia (MAT) is a rhythm that frequently occurs in the setting of severe lung disease. MAT is characterized by three different P wave morphologies within one 10 second 12-lead ECG at a heart rate > 100 beats per minutes. This indicates multiple irritable foci generating atrial electrical activity. This rhythm is benign and once the underlying lung disease is treated, it should resolve. If rate control is needed, the historical treatment (without much evidence to support it) has been verapamil. There is no thromboembolism risk in MAT such is seen in atrial fibrillation/flutter since the atrium are contractile in MAT. If the heart rate is < 100 beats per minute, then the rhythm is called wandering atrial pacemaker (WAP).

What is the mainstay of treatment for multifocal atrial tachycardia (MAT)?The treatment for MAT is directed at the underlying disorder causing the rhythm, usually severe lung disease. If the heart rate needs to be controlled in MAT, verapamil is the preferred pharmacologic therapy.Multifocal atrial tachycardia (MAT) is a rhythm that frequently occurs in the setting of severe lung disease. MAT is characterized by three different P wave morphologies within one 10 second 12-lead ECG at a heart rate > 100 beats per minutes. This indicates multiple irritable foci generating atrial electrical activity.

What is the difference between the CHADS 2 score and the CHADS 2 Vasc score to predict the risk of stroke in patient with atrial fibrillation/flutter?The CHADs 2 score and the CHADs 2 Vasc score guide us in regards to using full anticoagulation to prevent stroke in patients with atrial fibrillation/flutter. If two or more points are present, then full anticoagulation should be undertaken. The presence of one point can be individualized to the patient. If none are present, aspirin alone is adequate.The CHADs 2 Vasc score is a more recent measure to predict annual stroke risk. It includes female gender, different age brackets (age 65-74 gets 1 point and over 75 gets 2 points) and the presence of vascular disease (prior MI, peripheral arterial disease or aortic plaque/aneurysm).The CHADs 2 score gives one point for age > 65 and does not distinguish any further for age > 75. There are no points awarded for female gender or vascular disease.Both scoring systems give 2 points for TIA/stroke/prior thromboembolism.

Which antiarrhythmic drugs are considered safe in the setting of LV systolic dysfunction?The only two drugs considered safe in the setting of left ventricular systolic dysfunction (ejection fraction < 35%) are amiodarone and dofetilide.There is evidence of increased mortality using sotalol, flecainide and propafenone in the setting of systolic heart failure.

What is a glycoprotein IIb/IIIa inhibitor?These drugs include abciximab, eptifibatide, and tirofiban. They very strongly inhibit platelet function by blocking the binding of fibrinogen to the activated glycoprotein IIb/IIIa receptor complex. Any of these agents may be used in addition to aspirin, a thienopyridine and anticoagulation (except with bivalirudin) at the time of PCI in high risk patients with STEMI. They are also used during unstable angina/non-ST elevation MI when PCI is planned. Using glycoprotein IIb/IIIa inhibitors prior to PCI does not have strong data to support its use at the present time.

What is the difference in the electrophysiologic mechanism of atrial fibrillation and atrial flutter?A majority of cases of atrial fibrillation originate within the pulmonary veins. In atrial fibrillation, the atrial rate is between 400 and 600 beats per minute. Not all of these are conducted to the ventricles due to block in the AV node, but frequently the ventricular rate is 150 beats per minute in the absence of AV blocking medications (beta-blockers or non-dihydropyridine calcium channel blockers).Ablation of atrial fibrillation, also known as “pulmonary vein isolation” or PVI, electrically disconnects the erratic electrical activity in the pulmonary veins (which are creating action potentials at a rate of 400-600 beats per minute) from the rest of the heart thus effectively eliminating the atrial fibrillation. Ablation for atrial fibrillation is complex, requires multiple catheters and is performed via venous access then puncturing the interatrial septum to obtain entry to the left atrium where the pulmonary veins empty.Atrial flutter most commonly occurs in a reentrant circuit around the tricuspid valve. Ablation for this rhythm is easy since it requires only venous access to get the the right heart. Success rate is high and complication risk is low.

What are the three main concerns with long-term amiodarone use?The three main complications of long-term amiodarone use are pulmonary toxicity, thyroid disease and liver toxicity. Rarely ocular problems and a bluish discoloration of the skin can occur.Pulmonary toxicity is slowly progressive in the setting of amiodarone use, may be subtle initially and is the most common cause of death related to amiodarone therapy. It can take months to years of amiodarone therapy to develop and occurs in about 1-5% of patients taking 200 mg daily and as many as 15% taking > 400 mg daily. It can manifest as chronic interstitial pneumonitis or mmc pulmonary fibrosis. Routing pulmonary function testing is not recommended as it has not been shown to be accurate  enough to predict/prevent amiodarone lung toxicity. Amiodarone lung toxicity is a diagnosis of exclusion and treatment includes simply withdrawing amiodarone. Steroids can be used in severe cases. A majority of patients improve significantly once amiodarone is stopped.Thyroid toxicity in the setting of amiodarone therapy can be either hyperthyroidism or hypothyroidism. One way to remember that amiodarone affects the thyroid is to recall how important iodine is to thyroid function. AmIODarone (as the name indicates), has a large amount of iodine. About 3-5% of patients on amiodarone develop hyperthyroidism and about 5% develop hypothyroidism. Amiodarone induced hypothyroidism can be easily treated with thyroid replacement therapy however hyperthyroidism must be considered further. If amiodarone is being used to treat life-threatening arrhythmia, then it is continued and the hyperthyroidism is treated medically. If the amiodarone is being used to treat a more benign rhythm disturbance, then alternative therapy should be used.Hepatotoxicity with amiodarone is seen in about 25% of patients in the form of aminotransferase (AST and ALT) elevation. Amiodarone should be stopped if there is more than a 2-fold increase in these levels. Liver failure and cirrhosis can occur and it is thought that cumulative dose/long term therapy increases this risk.

What is the treatment of polymorphic ventricular tachycardia (VT)?Polymorphic ventricular tachycardia (a.k.a. Torsades de Pointes) is best treated with intravenous magnesium. Patients with a prolonged QT interval have a higher risk of developing polymorphic VT. Remove offending drugs that prolong the QT interval and correct potassium or calcium imbalances as well.

What are the two main drugs indicated to treat sustained ventricular tachycardia? Which two drugs can be used, but are not commonly utilized?The two drugs indicated for the treatment of sustained ventricular tachycardia are lidocaine and amiodarone. Procainamide and sotalol are also rarely used.Amiodarone is the prefered therapy since it also can treat supraventricular tachycardia with aberrancy. Ischemic ventricular tachycardia as occurs during an acute coronary syndrome responds best to lidocaine. Surprisingly, procainamide can terminate almost 50% of sustained ventricular tachycardia episodes while lidocaine and amiodarone efficacy is somewhat lower.

Treating the precipitating factor for the ventricular tachycardia is important as well including PCI in acute coronary syndromes, electrolyte abnormalities and heart failure. Some rare forms of ventricular tachycardia respond to adenosine and verapamil. Mexiletine is an oral formulation of a class 1C antiarrhythmic drug (like lidocaine) which can be used in the outpatient setting.

What is the difference in the electrophysiologic mechanism of second degree type I AV block and second degree type II AV block?2:1 AV block (a form of second degree AV nodal block) occurs when every other P wave is not conducted through the AV node to get to the ventricles. 2:1 AV block may be either second degree type I AV nodal block (Wenckebach) or second degree type II AV nodal block. This distinction is crucial since the former is usually benign while the later requires implantation of a permanent pacemaker.A general rule to remember is that if the PR interval of the conducted beat is prolonged AND the QRS complex is narrow, then it is most likely second degree type I AV nodal block (Wenckebach). Alternatively, if the PR interval is normal and the QRS duration is prolonged (such as a left or right bundle branch block pattern), then it is most likely second degree type II AV block and a pacemaker is probably warranted.Second degree type I AV nodal block is an issue in the AV node itself which is subject to sympathetic and parasympathetic tone.Second degree type II AV block is "infranodal" conduction disease of the His/Purkinje system, therefore altering AV nodal conduction would have no effect.AV blocking medications (remember “ABCD” for adenosine/amiodarone, beta-blockers, calcium channel blockers and digoxin) can cause second degree type I AV block while they will not cause second degree type II AV block since the infranodal conduction system is not subject to these agents (similarly not affected by sympathetic/parasympathetic tone).In order to distinguish between the two potential rhythms when an ECG reveals 2:1 AV nodal block, a couple different maneuvers can be employed:1. Carotid sinus massage or adenosine (slows the sinus rate allowing the AV node more time to recover, thus reducing the block from 2:1 to 3:2 and unmasking any progressing prolonging PR intervals that would indicate second degree type I AV nodal block)2. Atropine administration (enhances AV nodal conduction and could eliminate second degree type I AV nodal block since it is due to slowed AV nodal conduction)3. Exercise ECG testing (enhances AV nodal conduction and could eliminate second degree type I AV nodal block since it is due to slowed AV nodal conduction)

What is the medical therapy for a patient with Wolff-Parkinson-White syndrome (WPW) and atrial fibrillation?The combination of WPW and atrial fibrillation can potentially be fatal, especially if AV blocking agents are given (remember “ABCD” for adenosine/amiodarone, beta-blockers, calcium channel blockers and digoxin). The medical treatment is procainamide, although electrical cardioversion (especially if hemodynamically unstable) is reasonable.Patients with WPW have an “accessory pathway” or a “bypass tract”. This connects the electrical system of the atria directly to the ventricles allowing conduction to avoid passing through the AV node. In normal individuals, when the sinus node creates an action potential it must pass through the AV node to get to the ventricles. When an accessory pathway is present, the sinus node action potential can pass through the bypass tract before the AV node resulting in the ventricles becoming depolarized quickly. This is termed “pre-excitation” and results in a shortened PR interval on the ECG.In patients with WPW and atrial fibrillation, the erratic atrial action potentials (occurring at 400-600 beats per minute) can conduct through the accessory pathway very quickly (faster than through the AV node). Therefore, WPW patients who develop atrial fibrillation have higher ventricular rates than those without WPW. If an AV blocking agent is given, fewer atrial action potentials will pass through the AV node and more will pass through the accessory pathway, paradoxically increasing the ventricular rate potentially causing ventricular fibrillation which is a fatal, hemodynamically unstable rhythm. Procainamide or electrical cardioversion is recommended in these situations.

This sign is when a patient clenches a fist in the center of their chest to describe the pain related to angina pectoris.Levine sign is when a patient clenches a fist in the center of the their chest to describe the pain related to angina pectoris, usually using the right fist since the pain of angina frequently affects the left arm.

What are the causes of myocardial infarction not related to the typical atherosclerotic process?Many disorders can mimic an acute coronary syndrome in both the symptomatic presentation and the ECG findings. Remember the true definition of an acute coronary syndrome implies an unstable atherosclerotic coronary plaque and thrombosis. Other disorders that can cause anginal symptoms and ischemic ST elevation on the ECG, but are not from atherosclerotic plaque rupture or erosion include:

1.Coronary spasm2. Aortic dissection3. Vasculitis4. Takotsubo cardiomyopathy (stress-induced cardiomyopathy)5. Radiation therapy6. Coronary embolus7. Cocaine use8. Trauma or cardiac contusion9. Congenital coronary anomaliesConditions that cause ECG findings similar to acute coronary syndromes include:1. Left bundle branch block (usually not from acute myocardial infarction, but at times can be - see Sgarbossa criteria, Chapman’s sign and Cabrera’s sign)2. Left ventricular hypertrophy with repolarization abnormalities3. Pericarditis4. Early repolarization

What is the mechanism of action of ezetimibe and when is it indicated?Ezetimibe (Zetia) is a drug that lowers serum cholesterol by decreasing cholesterol absorption. It acts by inhibiting the Niemann-Pick C1-Like 1 protein (NPC1L1 protein) which is important in the cellular transport of cholesterol from the small intestine. LDL levels are significantly reduced, however clinical trials have largely failed to prove a mortality benefit. The IMPROVE-IT trial will report in mid-2013 and will be pivotal to answer this question.

What is the definition of acute coronary syndrome?An acute coronary syndrome occurs when atherosclerotic coronary plaque becomes unstable leading to a series of events eventually resulting in partial or total thrombotic occlusion of a coronary artery. Acute coronary syndromes are categorized into unstable angina, non-ST segment elevation myocardial infarctions and ST segment elevation myocardial infarction. The terms “transmural”, “non-transmural”, “Q wave MI” and “non-Q wave MI” are no longer recommended. The differences between the types of acute coronary syndromes are below:Unstable angina pectoris: Three different presentations of unstable angina exist.1. Exertional angina of new onset. Even if relieved with rest and requiring a consistent amount of exertion to procedure symptoms, when angina first occurs it is considered unstable.2. Exertional angina that was previously stable and now occurs with less physical exertion.3. Anginal symptoms at rest without physical exertion.Non-ST segment elevation myocardial infarction: Anginal symptoms at rest that result in myocardial necrosis as identified by elevated cardiac biomarkers (see Cardiac Biomarkers) with no ST segment elevation on the 12-lead electrocardiogram.ST segment elevation myocardial infarction: Anginal symptoms at rest that result in myocardial necrosis as identified by elevated cardiac biomarkers (see Cardiac Biomarkers) with ST segment elevation on the 12-lead electrocardiogram.

What are the indications to use thrombolytic therapy to treat an acute myocardial infarction?When there is no primary PCI available, there is ST elevation on the ECG and transfer to a primary PCI facility is not able to be done in a timely fashion (transfer in less than 60 minutes), fibrinolytic therapy is indicated.The decision regarding primary PCI versus fibrinolytic therapy is important. Many major medical facilities have PCI capabilities since this is the treatment of choice for ST elevation myocardial infarction (STEMI). However, smaller hospitals or those located in rural areas may not. Those facilities frequently have capabilities to quickly transfer STEMI patients to a primary PCI facility.

When are beta blockers not indicated during an acute coronary syndrome?It is important NOT to give beta-blockers if there are signs of cardiogenic shock such as hypotension or pulmonary edema on chest x-ray. Bradycardia with a heart rate < 60 beats per minute or high grade AV blocks are also a contraindications. In asthmatics with significant wheezing and elevated heart rates during an acute coronary syndrome, beta-blockers should be avoided and non-dihydropyridine calcium channel blockers (diltiazem, verapamil) can be used instead.

What are the mechanical complications of myocardial infarction?1. Ventricular septal defect2. Acute mitral regurgitation from papillary muscle rupture3. Left ventricular free wall rupture

What is Dressler’s syndrome?

Dressler’s syndrome (a.k.a. post-myocardial infarction syndrome) is an autoimmune phenomenon that can occur after myocardial infarction and manifests 2-3 weeks later as pericarditis and a pericardial effusion. The diagnosis is clinical and based on ECG changes of pericarditis. Treatment includes aspirin and colchicine to decrease inflammation. Anticoagulation should be avoided in order to prevent hemorrhage into the pericardium and cardiac tamponade.

What is the mechanism of stroke after an anterior myocardial infarction?After myocardial infarctions (especially anteriorly), the myocardial stunning that occurs can result in blood pooling toward the akinetic segment (frequently the cardiac apex) resulting in thrombus formation. Embolization of this thrombus can cause a stroke. There is no good data in regards to prevention of left ventricular thrombi, however the ACC/AHA guidelines give a class I, level of evidence B recommendation to warfarin therapy for 3 months when there is a cardiac source of embolus suspected after a myocardial infarction.

What is the ECG finding of an acute mid LAD occlusion (be specific)?ST segment elevation in leads V3 and V4. Leads V1 and V2 are not affected since the definition of the mid-LAD is the portion after the first major septal branch and these leads reflect the interventricular septum. Leads V5 and V6 (lateral leads) may or may not be involved depending on the involvement of major diagonal branches which can supply this territory.

Which coronary artery can an ascending aortic dissection affect?During ascending aortic dissection, the right coronary ostium may be involved causing an inferior STEMI. This is relatively uncommon, however must be recognized quickly as surgical intervention is crucial for survival.

What is the average patency duration of a saphenous vein bypass graft?Saphenous vein grafts have an 80-90% patency rate at 1 year, 70-85% patency rate between 1 and 5 years and 45-65% patency rate at 10 years. Thus, essentially half of all saphenous vein grafts occlude at 10 years. In addition, about half of all patent vein grafts at 10 years have significant atherosclerotic changes.

What is the average patency duration of a LIMA bypass graft?Left internal mammary artery (LIMA) grafts have an 85% patency rate at 10 years. This is compared to about 50% for saphenous vein grafts in the same time period.

What is the leading cause of death during an acute myocardial infarction?Ventricular fibrillation causes sudden cardiac death and is the leading cause of death during acute coronary syndromes.

What is the treatment for acute severe mitral regurgitation from a rupture papillary muscle after a myocardial infarction?Emergent surgical repair or replacement of the mitral valve is indicated. Mortality approaches 100% if not surgically fixed. As a bridge to surgery, intraaortic balloon counterpulsation can be helpful hemodynamically to reduce afterload and lessen the mitral regurgitation.Acute severe mitral regurgitation is a life-threatening disorder. Papillary muscle rupture after acute myocardial infarction can occur as a complication of an inferior MI (right coronary artery supply) since the posteromedial papillary muscle is the most likely to rupture.There are two papillary muscles that comprise part of the complex anatomy of the mitral valve. The anterolateral papillary muscle receives dual blood supply from the left anterior descending coronary artery and the left circumflex coronary artery in most individuals while the posteromedial papillary muscle receives its sole blood supply from the right coronary artery. Complete infarction of the posteromedial papillary muscle can occur during an inferior MI while only partial or no damage will be done to the anterolateral papillary muscle during an anterior (left anterior descending) or lateral (circumflex) infarction since there is dual blood supply to this papillary muscle. Thus, the posteromedial papillary muscle is the most likely to rupture.Recall that right heart catheterization will show prominent “V waves” in the pulmonary capillary wedge pressure tracing in the setting of severe mitral valve regurgitation.

How would you describe the intensity of a very loud diastolic murmur?This would be described as a IV/IV murmur or 4/4 intensity murmur. This describes the intensity, but remember the timing, pitch, location and radiation must be described as well to be complete.Diastolic murmurs are graded on a scale of 1-4 while systolic murmurs are graded on a scale of 1-6. Often, grade 1 systolic/diastolic murmurs are not discernable to inexperienced clinicians, while grade 4 diastolic or grade 6 systolic

murmurs are heard even without the stethoscope on the chest and may actually be visible. The intensity of a murmur is primarily determined by the volume/velocity of blood flowing through a defect and the distance between the stethoscope and the lesion. For example, a very thin patient with severe aortic stenosis with a high pressure gradient across the valve (thus high velocity of blood flow) will have a loud murmur. Conversely, the exact same valvular lesion in a morbidly obese person or a person with severe COPD and a widened anterior-posterior chest diameter may be inaudible.

Grading Diastolic MurmursIntensity DescriptionGrade I Barely audible

Grade II Audible, but soft

Grade III Easily audible

Grade IV Loud

Which is the most effective statin medication in regards to LDL reduction?Rosuvastatin has shown the greatest LDL reduction with atorvastatin close behind.HMG-CoA reductase inhibitors are also known as “statins” and work by inhibiting the synthesis of cholesterol in the liver by the enzyme HMG-CoA reductase. These drugs which include pravastatin, fluvastatin, atorvastatin, simvastatin and rosuvastatin are the mainstay of therapy for elevated LDL cholesterol and secondary prevention of acute coronary syndrome and strokes.

What conditions commonly mimic the symptoms/findings of an acute myocardial infarction?Many disorders can mimic STEMI in both the symptomatic presentation and the ECG findings. Remember STEMI is an acute coronary syndrome which implies an unstable atherosclerotic plaque and thrombosis. Other disorders that can cause anginal type symptoms and ischemic ST elevation on the ECG, but are not from atherosclerotic plaque rupture include: Coronary spasm, aortic dissection, vasculitis, Takotsubo cardiomyopathy (stress-induced cardiomyopathy), radiation therapy, coronary embolus, non-cardiac chest pain with chronic ECG changes (LBBB or LVH), myocarditis, cocaine use, trauma or cardiac contusion, and congenital coronary anomalies.Conditions than mimic the symptoms of angina but are not related to ischemia either by coronary thrombosis or demand ischemia are musculoskeletal pain, aortic dissection, pulmonary embolism, esophageal spasm, Da Costa’s syndrome, syndrome X, gastroesophageal reflux disease and gallbladder disease.

What are the indications for ACE inhibitors during an acute myocardial infarction?Either an ACE inhibitor or angiotensin receptor blocker should be given to all STEMI patients upon hospital discharge. Caution must be used in the acute setting in order to avoid hypotension which can worsen myocardial ischemia. Guidelines give the use of these drugs a class I indication when there is left ventricular systolic dysfunction or if the patient is diabetic. When left ventricular function returns to normal and the patient is not diabetic, the benefits are less clear. Usually ARBs are only given if ACE inhibitors are not tolerate due to cough or other side-effects.

How is the S1 and S2 heart sound best auscultated?Both the S1 and the S2 heart sounds are best heard using the diaphragm of the stethoscope since they are high pitched. The S1 heart sound is best heard at the tricuspid listening post (left lower sternal border) since the T1 component of the S1 heart sound is the softest. The S2 heart sound is best heard at the pulmonic listening post since the P2 component of the S2 heart sound is the softest.

What is the appropriate treatment for frequent PVCs during or after an acute coronary syndrome?No specific treatment is required for premature ventricular contractions after an acute coronary syndrome, although if symptoms occur beta-blockers can be helpful.The prophylactic administration of lidocaine to suppress premature ventricular contractions or prevent ventricular tachycardia or ventricular fibrillation is not recommended. The CAST trial demonstrated increased mortality using encainide, flecainide and moricizine to suppress premature ventricular contractions after an acute coronary syndrome.

What is the appropriate treatment for an accelerated idioventricular rhythm during or after an acute myocardial infarction?There is no treatment necessary for an accelerated idioventricular rhythm during or after an acute myocardial infarction. An accelerated idioventricular rhythm is a common post-STEMI rhythm and is also termed “slow ventricular

tachycardia” since it meets morphology criteria for VT, however has a heart rate < 100. This is a benign, hemodynamically stable rhythm.

What is the mechanism of action of ranolazine?The exact mechanism is somewhat controversial, however it likely inhibits sodium channels eventually reducing intracardiac calcium causing reduced oxygen consumption. Initially, ranolazine was thought to shift the main energy substrate of myocytes from lipid metabolism to glucose metabolism, however this has not been definitively proven at normal doses.The drug ranolazine is a novel agent to treat angina. Ranolazine does not change any hemodynamic parameters (blood pressure, heart rate, vascular tone). Ranolazine is considered for patients with angina that fail nitrates, beta-blockers and calcium channel blockers. Side effects are relatively uncommon, however ranolazine can prolong the QT interval increasing the risk of polymorphic ventricular tachycardia (Torsades de Pointes).

What are the indications for coronary artery bypass grafting?Coronary artery bypass grafting (CABG) as a means of coronary revascularization is indicated when:1. PCI fails and there is persistent symptoms or hemodynamic instability2. A patient is not a candidates for PCI and has continued symptoms with a significant area of myocardium at risk3. At the time of ventricular septal defect or mitral valve repair4. When left main coronary disease or 3-vessel coronary disease is present with cardiogenic shock or ventricular arrhythmias (ventricular tachycardia or fibrillationCABG is NOT indicated when there is a small area of myocardium in jeopardy and the patient is stable.

What is the Duke Treadmill Score? How does it predict survival?The Duke Treadmill Score (DTS) is a point system to predict 5-year mortality based on treadmill ECG stress testing in patients without known coronary artery disease. The Duke Treadmill Score is calculated as below:DTS = Exercise time (minutes) - (5 x ST deviation in mm) - (4 x angina index)The exercise time is based on using the standard Bruce protocol.ST deviation refers to maximum ST change (elevation or depression) in any lead except lead aVR.The angina index gives 0 points if no angina occurs, 1 point if non-limiting angina occurs and 2 points is angina occurs which limits exercise.Patients are categorized as low, intermediate or high risk.Low risk (score > 5) indicates a 5-year survival of 97%.Intermediate risk (score between 4 and - 11) indicates 5-year survival of 90%.High risk (score < - 11) indicates 5-year survival of 65%.In high risk patients, 74% had 3-vessel or left main occlusive coronary disease on angiography.

What are the indications for coronary CT angiography?Appropriateness criteria exist to help guide clinicians as to the indications for coronary CT angiography to evaluate for coronary artery disease or other coronary anomalies. The scoring system is 1-9 with scores of 1-3 being inappropriate indications, 4-6 uncertain indications and 7-9 appropriate indications. Note that a high pretest probability of coronary disease with symptoms warrants invasive coronary angiography and is not an indication for coronary CT angiography. The appropriate indications for coronary CT angiography that received a score of 7-9 are:Non-acute symptoms1. Discordant exercise ECG and imaging results (equivocal stress test)2. Prior normal stress test with continued symptoms concerning for angina3. ECG interpretable, able to exercise, intermediate pretest probability for coronary disease4. ECG uninterpretable or unable to exercise with low or intermediate pretest probability for coronary disease5. Evaluation of patency coronary artery bypass graftsAcute symptoms1. Normal ECG and cardiac markers with low or intermediate pretest probability for coronary disease2. ECG uninterpretable (old left bundle branch or paced rhythm) with low or intermediate pretest probability for coronary disease3. Non-diagnostic ECG or equivocal cardiac biomarkers with low to intermediate pretest probabilityOther scenarios1. New onset heart failure with reduced ejection fraction, no prior coronary disease and no anginal symptoms2. Coronary evaluation prior to non-coronary cardiac surgery (i.e. valve replacement) in a patient with intermediate pretest probability for coronary disease3. Evaluation of coronary anomalies and complex congenital heart disease

What are the indications for eplerenone during an acute myocardial infarction?The aldosterone antagonist eplerenone was evaluated in the EPHESUS trial leading to the recommendation for their with an ACE inhibitor prior to hospital discharge after UA/NSTEMI if there is left ventricular systolic dysfunction (EF < 40%) and either diabetes or symptomatic heart failure present and no contraindication (serum creatinine > 2.5 and or potassium > 5.0). A class effect is likely present and thus spironolactone is frequently used instead of eplerenone due to cost concerns, although there is no direct data to support this practice.

Which cardiac biomarker would be ideal to detect re-infarction in patients 4-10 days post initial myocardial infarction?Creatine kinase (a.k.a. creatine phosphokinase or CPK) is a muscle enzyme which exists as isoenzymes. The MB type is specific to myocardial cells while MM and BB are specific to skeletal muscle and brain tissue respectively. The CK level will increase approximately 3-4 hours after a myocardial infarction and stays elevated for 3-4 days. This makes it useful for the detection of re-infarction in the 4-10 day time window after the initial insult since troponin remains elevated for 10 days making it less useful for this purpose.

Name the thrombolytic medications and their differences.Fibrinolytic therapy is used in the treatment of ST segment elevation myocardial infarction (STEMI), acute stroke and other less common indications such as pulmonary embolism and acute deep venous thrombosis. The most commonly used agents are tPA (tissue plasminogen activator), alteplase, reteplase, streptokinase, tenecteplase, urokinase.Streptokinase is immunogenic (isolated from streptococci bacteria) and once exposed, a repeat exposure can cause severe allergic reactions including anaphylaxis and thus is not recommended.Tenecteplase is administered as a single bolus due to its long half-life which is convenient.Urokinase was initially isolated from human urine, is expensive and not commonly used. It is not immunogenic like streptokinase.The other fibrinolytic (thrombolytic) agents require a bolus followed by an infusion.

What does the term “atherosclerosis” mean (definition and origin of the term)?Atherosclerosis is the pathologic process by which cholesterol and calcium plaque accumulates within the arterial wall. The term “athero” means porridge and “sclerosis” means scarring which is how atherosclerosis was first described on autopsy.Atherosclerotic plaque within the coronary arteries is responsible for coronary artery disease and acute coronary syndromes. When occurring in the cerebrovascular system, stroke can occur. Atherosclerosis also contributes to peripheral arterial disease, aortic aneurysms, renal artery disease and mesenteric ischemia.

What is the major side effect of fenofibrate?Fibrates must be used with caution in patients on HMG-CoA reductase inhibitors due to potential myalgias and rhabdomyolysis. Pravastatin or fluvastatin are the safest to use in combination with fibrates due to their elimination via the CYP3A4 system. While rosuvastatin also uses this system, doses should not exceed 10 mg daily while taking fibrates concomitantly.

What maneuvers can be done to alter the timing of the click in mitral valve prolapse?Mitral valve prolapse produces a mid-systolic click usually followed by a uniform, high-pitched murmur.  The murmur is actually due to mitral regurgitation that accompanies the MVP, thus it is heard best at the cardiac apex. MVP responds to dynamic auscultation.After sudden standing, preload is decreased and the click moves earlier in systole. With sudden squatting, preload increases and the click moves later in systole.

Which statin is the safest to use in the setting of liver disease?Pravastatin is the safest HMG CoA reductase inhibitor (statin) in the setting of liver disease.

How should someone describe an episode of ventricular tachycardia?By type (monomorphic or polymorphic), by duration (sustained versus non-sustained) and by heart rate. For example, monomorphic VT non-sustained at a heart rate of 220 beats per minute or sustained polymorphic ventricular tachycardia at a heart rate of 250 beats per minute.

What proportion of acute coronary syndromes are silent? What percent do not have classic symptoms? What patient populations most commonly have minimal or atypical symptoms from acute coronary syndromes?Approximately 25% of all acute coronary syndromes occur without reported symptoms. Some estimates are as high as 64%.Approximately 50% of acute coronary syndromes do not have classic symptoms.Women, diabetics and the elderly are more likely to have minimal or atypical symptoms.