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 Horners 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)
- Kussmauls 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, Chapmans sign and Cabreras 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 Kawasakis 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 patients 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 betablocker 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 wave
Type 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 elevation
These 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 patients
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 regurgitation
2. 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 abscess
4. Peripheral embolism of vegetation
5. 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 aorta

Type 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 aorta
Type 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
Eisenmengers 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?

Prinzmetals 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 hemorrhage
2. Ischemic stroke within 3 months
3. Known cerebrovascular abnormality such as aneurysm or arteriovenous malformation
4. Known malignant intracranial tumor
5. 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 past
2. Intracranial abnormality not listed as absolute contraindication (i.e. benign intracranial tumor).
3. Ischemic stroke > 3 months prior
4. Bleeding within 2-4 weeks (excluded menses)

5. Traumatic or prolonged cardiopulmonary resuscitation (CPR)

6. Major surgery within 3 weeks
7. Pregnancy
8. Current use of anticoagulants
9. Non-compressible vascular puncture
10. Dementia
Note 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 betablockers 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 together

2. Evidence of endocardial involvement

Echocardiographic 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 valve

New 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
Oslers nodes
Roth spots
Positive rheumatoid factor

Microbiologic 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 nonselective 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) Obesity
2) COPD
3) Pericardial effusion
4) Severe hypothyroidism
5) Subcutaneous emphysema
6) Massive myocardial damage/infarction
7) 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 endocarditis
3. 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 LV

5. When acute VSD develops after myocardial infarction

If Eisenmengers 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. Fibrates
The 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 acids
Fish 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 failure
Class II: Symptoms of heart failure with moderate exertion such as ambulating 2 blocks or 2 flights of stairs
Class III: Symptoms of heart failure with minimal exertion such as ambulating 1 block or 1 flight of stairs, but no
symptoms at rest
Class IV: Symptoms of heart failure at rest
Note 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, pericarditis
Ischemia, intravenous line (central line advanced too far into the right atrium)
Rheumatic valvular heart disease (specifically mitral valve stenosis)
Alcohol, anemia
Thyroid (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 depression
3. Signs or symptoms of congestive heart failure (rales on examination, hypoxia with pulmonary edema on chest xray)
4. Hemodynamic instability
5. Sustained ventricular tachycardia or ventricular fibrillation
6. Recent coronary intervention within 6 months

7. Prior coronary artery bypass grafting

8. High TIMI risk score
9. Reduced left ventricular systolic function (EF < 40%)
10. Recurrent angina at rest or with low level activity
11. High risk findings from non-invasive testing
The 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 actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae
These 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 echocardiography
2. 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 probability
4. 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 noncardiac source
7. 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 hypertrophy
2. Ventricular septal defect
3. 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)

Kussmauls 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 NTproBNP 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. Syncope
2. Interventricular septal thickness of 30 mm or greater
3. Documented ventricular tachycardia and/or cardiac arrest
4. Family history of sudden cardiac death
5. 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
afterload
When 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, Pagets disease and Fabrys 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 (Marfans 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 Abascals 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 proliferatoractivated 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)

Ischemic cardiomyopathy

Rheumatic heart disease (RHD)

Dilated cardiomyopathy
Endocarditis
Hypertrophic cardiomyopathy
Collagen vascular disease
Left atrial dilation
Papillary muscle dysfunction
Mitral annular calcification (MAC)
Spontaneous chordal rupture
Trauma

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 murmurs

Intensity

Description

Grade I/VI
Barely audible
Grade II/VI
Audible, but soft
Grade III/VI
Easily audible
Grade IV/VI
Easily audible and associated with a thrill
Grade V/VI
Easily audible, associated with a thrill, and still heard with the
stethoscope only lightly on the chest
Easily audible, associated with a thrill, and still heard with the
Grade VI/VI 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 dissection
3. Trauma
4. 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 disease
2. Aging of the heart
3. Ischemic heart disease
4. Hypertrophic cardiomyopathy

5. 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 diastole

Occurs in late diastole

Occurs during passive LV filling

Occurs during active LV filling

May be normal at times

Almost always abnormal

Requires a very compliant LV

Requires a non-compliant LV

Can be a sign of systolic CHF

Can 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 blockers
2. Beta-blockers
3. Spironolactone
4. Combination of hydralazine/nitrates when ACE inhibitors or angiotensin receptor blockers are not able to be tolerate
Note: 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
2.
Idiopathic
3.
4.
5.
Chemotherapeutic
agents
6.
7.
8.
9. Peripartum

B,
(about

influenza,
50%

(most
commonly
Selenium
Thyroid
Tachycardia

HIV,
of

daunorubicin

and

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. Viral

enteroviruses)
cases)
Familial/genetic
Alcohol
doxarubacin)
deficiency
disease
mediated

3. Radiation therapy (frequently in the late 1970s and early 1980s when high doses were given for non-Hodgkin's
lymphoma. Constrictive pericarditis can present decades later)
4. Trauma
5. 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, lifethreatening arrhythmias, mitral regurgitation and sudden cardiac death.
The causes of heart failure in HOCM include:
1.
Diastolic
2.
Mitral
3.
4. End-stage HOCM results in systolic dysfunction burnt-out HOCM

dysfunction
regurgitation
Arrhythmia

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
2.
3.
4. Smooth muscle cell cap formation

cell
Lipoprotein
Inflammatory

injury
deposition
reaction

Endothelial 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
Mitral
valve
prolapse
Aortic
Myocardial
bridging
Aortic
Arrhythmogenic
right
ventricular
Ischemic
heart
disease
Undiagnosed
congenital
Genetic channelopathies (i.e. prolonged QT syndrome)

dysplasia
heart

cardiomyopathy
(controversial)
rupture
(controversial)
stenosis
(ARVD)
(atherosclerosis)
disease

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 fixedsplit 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, crescendodecrescendo, 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 Carvallos sign?

Carvallos 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
procedures
3.
Massive
myocardial
infarction
without
other
therapeutic
options
4. Severe cardiac decompensation (regardless of cause) such as progression of a non-ischemic cardiomyopathy
5.
Bridge
to
transplantation
6. 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
Severe
sinus
Sinus
pauses/sinus
Sinoatrial
nodal
exit
- Chronotropic incompetence (failure of heart rate to increase during exercise)

to

sinus

rhythm)
bradycardia
arrest
block

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 (betablockers), 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
>
65
2.
Aspirin
use
in
the
prior
7
days
3. ST changes of at least 0.5 mm on the initial ECG (ST elevation or depression)
4.
Elevated
serum
cardiac
biomarkers
5.
Two
or
more
potential
anginal
symptoms
in
the
last
24
hours
6.
Previously
diagnosed
coronary
artery
disease
with
at
least
50%
stenosis
7. Three or more traditional risk factors for CAD
The risk at 14 days of all-cause mortality, acute coronary syndrome or severe ischemia requiring coronary
revascularization is below:
1
2

point
points

=
=

4.7%
8.3%

3
4
5
6 or 7 points = 40.9%

points
points
points

=
=
=

13.2%
19.9%
26.2%

Note that the TIMI score is different that TIMI grade coronary flow
TIMI 0 flow indicates no antegrade coronary flow past the obstruction (complete occlusion)
TIMI
1
flow
is
minimal
antegrade
flow
past
the
coronary
obstruction
TIMI 2 flow is partial antegrade flow past the obstruction with complete filling of the distal coronary vessel
TIMI 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.
2.
3.
4.
5.
AV
6.
AV
7. Other less common SVTs

nodal

Sinus
Atrial
Atrial
Atrial
reentrant
reentrant

tachycardia
tachycardia

tachycardia
tachycardia
fibrillation
flutter
(AVNRT)
(AVRT)

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 lifethreatening 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
2.
3.
4.
Takotsubo
5.
6.
7.
8.
Trauma
9. Congenital coronary anomalies

Aortic
cardiomyopathy
Radiation
Coronary
Cocaine
or

(stress-induced

cardiac

spasm
dissection
Vasculitis
cardiomyopathy)
therapy
embolus
use
contusion

Conditions 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,
Chapmans
sign
and
Cabreras
sign)
2.
Left
ventricular
hypertrophy
with
repolarization
abnormalities
3.
Pericarditis
4. 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
2.
Acute
mitral
regurgitation
3. Left ventricular free wall rupture

from

septal
papillary

muscle

defect
rupture

What is Dresslers syndrome?

Dresslers 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 4565% 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 Murmurs

Intensity

Description

Grade 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 Costas
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, betablockers 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
instability
2. A patient is not a candidates for PCI and has continued symptoms with a significant area of myocardium at risk
3.
At
the
time
of
ventricular
septal
defect
or
mitral
valve
repair
4. When left main coronary disease or 3-vessel coronary disease is present with cardiogenic shock or ventricular
arrhythmias (ventricular tachycardia or fibrillation
CABG 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 symptoms
1.
Discordant
exercise
ECG
and
imaging
results
(equivocal
stress
test)
2.
Prior
normal
stress
test
with
continued
symptoms
concerning
for
angina
3. ECG interpretable, able to exercise, intermediate pretest probability for coronary disease
4. ECG uninterpretable or unable to exercise with low or intermediate pretest probability for coronary disease
5. Evaluation of patency coronary artery bypass grafts
Acute symptoms
1. Normal ECG and cardiac markers with low or intermediate pretest probability for coronary disease
2. ECG uninterpretable (old left bundle branch or paced rhythm) with low or intermediate pretest probability for
coronary
disease
3. Non-diagnostic ECG or equivocal cardiac biomarkers with low to intermediate pretest probability
Other scenarios
1. New onset heart failure with reduced ejection fraction, no prior coronary disease and no anginal symptoms
2. Coronary evaluation prior to non-coronary cardiac surgery (i.e. valve replacement) in a patient with intermediate
pretest
probability
for
coronary
disease
3. 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.