USMLE Step 2 CK cardiology questions

When primary PCI cannot be performed within 120 minutes of first medical contact, fibrinolytic therapy should be given within 30 minutes of arrival if there are no contraindications, rather than delaying treatment for transfer. A 3-hour transport time far exceeds the 120-minute window, so the door-to-needle strategy minimizes total ischemic time and myocardial loss. After lytics, the patient should still be transferred to a PCI-capable center for rescue or early angiography. This patient has an inferior STEMI with no contraindications to thrombolysis.

• A. Echocardiography is not needed to diagnose STEMI and would only delay time-critical reperfusion therapy.
• B. A 3-hour transfer time exceeds the guideline-recommended 120-minute window for primary PCI, making immediate lytics preferred.
• C. Anticoagulation alone without reperfusion therapy does not restore coronary flow and delays definitive treatment.
• E. Nitroglycerin does not achieve reperfusion and delaying treatment worsens myocardial salvage.

Unstable angina is defined by ischemic symptoms at rest or with minimal exertion without a significant rise or fall in cardiac troponin, distinguishing it from NSTEMI, which requires a rise and/or fall in troponin with at least one value above the 99th percentile upper reference limit. This patient's troponin values remain below the diagnostic threshold and show no significant delta between serial draws, consistent with myocardial ischemia without infarction. The clinical picture (rest pain, dynamic T-wave changes) still warrants an ACS pathway with risk stratification and possible angiography. The absence of ST elevation also rules out STEMI.

• A. Prinzmetal angina is caused by coronary vasospasm, typically with transient ST elevation at rest, not the pattern seen here.
• C. STEMI requires ST-segment elevation on ECG, which is absent here.
• D. NSTEMI requires a rise and/or fall in troponin with a value exceeding the 99th percentile; this patient's troponin stayed below threshold and essentially unchanged.
• E. Takotsubo cardiomyopathy classically follows severe emotional or physical stress and shows apical ballooning on echocardiography, not suggested by this vignette.

Standard initial medical therapy for NSTEMI includes dual antiplatelet therapy with aspirin plus a P2Y12 inhibitor (ticagrelor, clopidogrel, or prasugrel), anticoagulation, and a high-intensity statin such as atorvastatin 80 mg or rosuvastatin 20-40 mg started early regardless of baseline LDL. Ticagrelor is preferred over clopidogrel in most ACS patients proceeding to invasive management due to more consistent and rapid platelet inhibition and mortality benefit shown in trials. High-intensity statins reduce plaque inflammation and recurrent events independent of lipid-lowering effects alone. Prasugrel should be avoided before angiography defines coronary anatomy because of bleeding risk if urgent CABG is needed.

• A. Dabigatran is not used for ACS anticoagulation, and a low-intensity statin does not meet guideline-recommended intensity.
• B. Warfarin is not indicated in ACS management, and low-intensity statins are insufficient in the acute setting.
• D. Fenofibrate has no role in acute ACS management; a P2Y12 inhibitor is needed instead.
• E. Ezetimibe alone is not appropriate acutely, and prasugrel is relatively contraindicated before the coronary anatomy is known.

Any history of hemorrhagic stroke at any time is an absolute contraindication to fibrinolytic therapy because of the markedly increased risk of recurrent or fatal intracranial hemorrhage. In this setting, primary PCI is the preferred reperfusion strategy even if it requires transfer and a longer delay, because fibrinolysis cannot be safely offered. Emergency transfer should be arranged promptly, and supportive therapy (antiplatelets, anticoagulation, analgesia) continued during transport. This overrides the usual 120-minute PCI-versus-lytics decision rule, since lytics are not an option at all.

• A. Alteplase is a fibrinolytic and is absolutely contraindicated given the history of hemorrhagic stroke.
• B. Streptokinase is a fibrinolytic and is absolutely contraindicated given the history of hemorrhagic stroke.
• D. Tenecteplase is a fibrinolytic and is absolutely contraindicated given the history of hemorrhagic stroke.
• E. Reteplase is a fibrinolytic and is absolutely contraindicated given the history of hemorrhagic stroke.

This patient has inferior STEMI with right ventricular infarction, indicated by ST elevation in V4R, elevated jugular venous pressure, and hypotension with clear lung fields (preload-dependent right ventricular failure). Nitrates and other preload-reducing agents (diuretics, morphine) are avoided because the hypotensive right ventricle depends on adequate preload to maintain cardiac output. The immediate treatment for nitrate-induced hypotension in this setting is intravenous fluid boluses to restore right ventricular filling pressure and cardiac output. Clear lungs support that volume loading is safe despite systemic hypotension.

• A. Morphine reduces preload and can worsen hypotension in right ventricular infarction; it is relatively contraindicated here.
• C. Repeating nitroglycerin would further reduce preload and worsen the hypotension already present.
• D. Furosemide reduces preload further and would worsen hypotension in right ventricular infarction.
• E. Dobutamine is not first-line for this preload-dependent hypotension; volume resuscitation should be tried first.

Left ventricular free wall rupture typically occurs 2-7 days after MI and presents with sudden chest pain, hemodynamic collapse, and pulseless electrical activity (an organized rhythm on the monitor without a palpable pulse) due to rapid hemopericardium and cardiac tamponade. Muffled heart sounds and jugular venous distension with a normal-appearing rhythm but no pulse (PEA) are classic for tamponade physiology. This complication is often fatal within minutes and requires emergency pericardiocentesis and surgical repair. Risk factors include first MI, female sex, advanced age, and delayed reperfusion.

• A. Dressler syndrome is a delayed autoimmune pericarditis occurring weeks after MI, not an acute catastrophic event on day 4.
• B. Pulmonary embolism can cause PEA arrest but would not typically cause muffled heart sounds and jugular distension from pericardial tamponade specifically.
• C. Stent thrombosis typically presents with recurrent ST-elevation and chest pain but not acute PEA arrest with tamponade signs.
• E. Papillary muscle rupture causes acute severe mitral regurgitation with pulmonary edema, not pulseless electrical activity with tamponade signs.

Papillary muscle rupture is a mechanical complication typically occurring 2-7 days after MI, most often following inferior/posterior infarction because the posteromedial papillary muscle has a single blood supply from the posterior descending artery. It presents with sudden-onset pulmonary edema and a new holosystolic murmur at the apex radiating to the axilla, reflecting acute severe mitral regurgitation into a non-compliant left atrium. Emergency transthoracic echocardiography confirms the diagnosis, and emergency surgical repair or replacement is usually required given hemodynamic instability. The lack of a murmur at the right sternal border argues against ventricular septal rupture.

• A. Recurrent infarction would show new ECG changes or troponin rise but would not explain the new apical murmur with radiation to the axilla.
• C. Acute pericarditis presents with a friction rub and positional chest pain, not acute pulmonary edema with a new regurgitant murmur.
• D. Pulmonary embolism can cause dyspnea and tachycardia but does not produce a new mitral regurgitant murmur.
• E. Ventricular septal rupture produces a harsh holosystolic murmur at the lower left sternal border, often with a step-up in oxygen saturation from right ventricle to pulmonary artery, not an apical murmur radiating to the axilla.

After acute coronary syndrome with stent placement, dual antiplatelet therapy (aspirin plus a P2Y12 inhibitor such as clopidogrel) is continued for at least 12 months to prevent stent thrombosis, after which aspirin is continued indefinitely. A beta-blocker and an ACE inhibitor (or ARB) are indicated for patients with reduced ejection fraction or large infarcts to reduce mortality and adverse remodeling. A high-intensity statin is given to all patients with established atherosclerotic disease regardless of baseline LDL. This combination reflects current ACC/AHA secondary prevention guidelines.

• B. Aspirin should not be discontinued; dual antiplatelet therapy with aspirin plus a P2Y12 inhibitor is standard after stenting.
• C. Verapamil is not preferred over a beta-blocker post-MI, and 3 months of dual antiplatelet therapy is shorter than the standard 12-month course after ACS.
• D. Warfarin is not indicated for routine post-MI antiplatelet therapy; it is reserved for specific indications like LV thrombus or atrial fibrillation.
• E. One month of aspirin is insufficient; dual antiplatelet therapy should continue for at least 12 months after stenting for ACS.

Dressler syndrome is an autoimmune-mediated pericarditis that typically develops 2 to 10 weeks after myocardial infarction, presenting with pleuritic chest pain, low-grade fever, a pericardial friction rub, and diffuse ST elevation with PR depression on ECG. It results from an immune response to myocardial antigens exposed during infarction. Echocardiography often shows a pericardial effusion, and treatment is with NSAIDs or aspirin, with colchicine often added. The delayed timing after MI and classic pericarditis findings distinguish it from early post-MI pericarditis or recurrent ischemia.

• A. Recurrent MI would present with ischemic chest pain unrelated to respiration or position, and ECG would show localized changes rather than diffuse ST elevation with PR depression.
• B. Endocarditis would present with persistent fever, bacteremia, and often a new regurgitant murmur, not a friction rub with diffuse ECG changes.
• C. Papillary muscle rupture causing mitral regurgitation presents with acute pulmonary edema and a new holosystolic murmur, not pleuritic pain with a friction rub.
• D. Free wall rupture occurs acutely, usually within days of MI, and presents with sudden hemodynamic collapse from tamponade, not a subacute pleuritic presentation 6 weeks later.

B-type natriuretic peptide (BNP) or NT-proBNP is the most useful initial test when heart failure is suspected because it is released in response to ventricular wall stretch and volume overload, and a markedly elevated level supports the diagnosis while a normal level makes heart failure unlikely. In this patient with classic signs of volume overload (JVD, crackles, edema), an elevated BNP confirms the clinical suspicion and should prompt echocardiography to determine ejection fraction and classify heart failure as HFrEF or HFpEF. BNP also has prognostic value and can be trended to assess response to therapy. Chest X-ray and troponin are complementary but less specific for establishing the heart failure diagnosis itself.

• A. Troponin may be mildly elevated in heart failure from myocardial strain but is used to evaluate for acute coronary syndrome, not to diagnose heart failure itself.
• B. Renal function is important for guiding diuretic and ACE inhibitor therapy but does not confirm the diagnosis of heart failure.
• C. Chest X-ray may show pulmonary congestion or cardiomegaly but is less sensitive and specific than BNP for confirming heart failure.
• E. D-dimer is used to evaluate for venous thromboembolism and has no role in diagnosing heart failure.

Acute decompensated heart failure with volume overload and hypoxia is treated initially with intravenous loop diuretics such as furosemide to promote rapid diuresis and relieve pulmonary congestion, along with supplemental oxygen to correct hypoxemia. IV diuretics act faster and more reliably than oral formulations in the setting of gut edema and decreased absorption. Vasodilators such as IV nitroglycerin may be added if blood pressure remains adequate and symptoms persist. Inotropes and mechanical support are reserved for patients with evidence of low cardiac output or cardiogenic shock, which this patient does not have given her preserved blood pressure.

• A. Dobutamine is reserved for patients with evidence of low cardiac output or cardiogenic shock, not for a hemodynamically stable patient with volume overload.
• C. Hemodialysis is reserved for diuretic-refractory volume overload or significant renal failure, not as an initial step in a patient without those findings.
• D. IV fluids would worsen volume overload in a patient who is already congested; the patient needs diuresis, not additional fluid.
• E. Oral metolazone has unreliable absorption in decompensated heart failure with gut edema and is typically added to IV loop diuretics for diuretic resistance, not used as initial monotherapy.

Heart failure with preserved ejection fraction (HFpEF) is diagnosed in patients with signs and symptoms of heart failure, an elevated natriuretic peptide, and an ejection fraction of 50% or greater, along with echocardiographic evidence of diastolic dysfunction such as left atrial enlargement, increased wall thickness, and an elevated E/e' ratio reflecting impaired relaxation and elevated filling pressures. Hypertension is the most common risk factor, leading to concentric hypertrophy and reduced ventricular compliance. This patient's preserved EF of 60% with these structural and functional abnormalities fits HFpEF rather than HFrEF, which requires an EF of 40% or less.

• A. COPD can cause dyspnea but would not explain the elevated NT-proBNP, S4 gallop, and echocardiographic diastolic dysfunction findings described.
• C. HFrEF is defined by an ejection fraction of 40% or less with evidence of systolic dysfunction, which does not match this patient's EF of 60%.
• D. Constrictive pericarditis typically presents with signs of right-sided heart failure, pericardial knock, and characteristic septal bounce on echocardiogram, not isolated diastolic dysfunction from hypertensive heart disease.
• E. Amyloidosis is suggested by features like low-voltage ECG despite increased wall thickness, extracardiac findings, and specific imaging patterns (e.g., global longitudinal strain with apical sparing), none of which are described here.

Digoxin inhibits the Na+/K+-ATPase pump, and potassium competes with digoxin for the same binding site on this pump. Hypokalemia, commonly caused by loop diuretics like furosemide, increases digoxin binding to the Na+/K+-ATPase, potentiating its effect even at a given serum digoxin concentration. This explains why toxicity can occur with excessive diuresis and resultant hypokalemia. Clinical features include GI symptoms, visual disturbances (xanthopsia), and arrhythmias such as bradycardia with ectopy; treatment includes potassium repletion and digoxin-specific antibody fragments if severe.

• B. Furosemide causes hypokalemia but is not directly cardiotoxic; its effect on digoxin toxicity is mediated through potassium loss.
• C. Renal impairment, not increased clearance, is the typical cause of reduced digoxin excretion and toxicity.
• D. Volume depletion does not cause a clinically relevant redistribution of digoxin into skeletal muscle that would explain toxicity.
• E. ACE inhibitors do not significantly alter digoxin pharmacokinetics or increase its levels.

This patient has a CHA2DS2-VASc score of at least 3 (age ≥65, hypertension, diabetes), warranting anticoagulation regardless of rate or rhythm control strategy. Because the onset of atrial fibrillation is uncertain and may exceed 48 hours, immediate cardioversion carries a risk of thromboembolism from a possible atrial thrombus, so rate control and anticoagulation should be initiated first, with cardioversion deferred until either 3 weeks of therapeutic anticoagulation or a transesophageal echocardiogram excludes left atrial thrombus. A beta-blocker controls the ventricular rate while anticoagulation reduces stroke risk. This stepwise approach follows ACC/AHA/HRS guidelines for new-onset atrial fibrillation of uncertain duration in a hemodynamically stable patient.

• A. Immediate cardioversion is inappropriate without adequate anticoagulation when the duration of atrial fibrillation is unknown and may exceed 48 hours.
• B. Aspirin alone is inadequate stroke prophylaxis for a CHA2DS2-VASc score of 3 or higher; a direct oral anticoagulant is indicated.
• C. Pharmacologic cardioversion today carries the same thromboembolic risk as electrical cardioversion if anticoagulation has not been established.
• D. TEE-guided cardioversion still requires anticoagulation before and after the procedure, not cardioversion without anticoagulation.

The short PR interval, widened QRS complex, and delta wave (slurred upstroke at the onset of the QRS) are the classic ECG triad of Wolff-Parkinson-White syndrome, caused by an accessory pathway (bundle of Kent) that bypasses the AV node and allows early ventricular pre-excitation. Patients may have episodes of paroxysmal supraventricular tachycardia from reentry involving the accessory pathway. In these patients, AV nodal blocking agents such as adenosine, verapamil, and digoxin should be avoided during atrial fibrillation or wide-complex tachycardia because blocking the AV node can preferentially promote conduction down the accessory pathway, leading to a dangerously rapid ventricular rate or degeneration into ventricular fibrillation. Definitive treatment is catheter ablation of the accessory pathway.

• A. Hypertrophic cardiomyopathy may show voltage criteria for left ventricular hypertrophy but does not produce a delta wave or short PR interval.
• B. Brugada syndrome shows a coved ST-segment elevation in the right precordial leads, not a short PR interval with delta wave.
• C. First-degree AV block is characterized by a prolonged, not shortened, PR interval.
• E. Left bundle branch block shows a widened QRS without a short PR interval or delta wave.

This patient's presentation is classic for torsades de pointes, a polymorphic ventricular tachycardia associated with QT prolongation, here likely precipitated by fluoroquinolone-induced QT prolongation combined with hypokalemia and hypomagnesemia. Intravenous magnesium sulfate is the first-line treatment for torsades de pointes even if the serum magnesium level is normal, as it stabilizes the cardiac membrane and reduces triggered activity regardless of magnesium level. Potassium should also be repleted to a goal above 4 mEq/L, and the offending QT-prolonging drug should be discontinued, but magnesium is the immediate pharmacologic treatment of choice in a patient who is not currently in cardiac arrest. Defibrillation is reserved for sustained torsades or degeneration into ventricular fibrillation.

• A. Unsynchronized defibrillation is reserved for sustained torsades de pointes causing hemodynamic collapse or degeneration to ventricular fibrillation, not a self-terminated episode.
• B. Lidocaine is not the preferred agent for torsades de pointes; magnesium is first-line therapy.
• D. Amiodarone prolongs the QT interval and could worsen torsades de pointes; it is not first-line therapy for this rhythm.
• E. Potassium repletion is important but does not have the rapid membrane-stabilizing effect of magnesium in active torsades de pointes.

In the ACLS algorithm for shock-refractory ventricular fibrillation or pulseless ventricular tachycardia, amiodarone is the first-line antiarrhythmic, given as a 300 mg IV bolus after the second or third defibrillation attempt fails, along with continued CPR and epinephrine every 3-5 minutes. Amiodarone improves the likelihood of return of spontaneous circulation and survival to hospital admission in refractory VF/VT. Lidocaine is an acceptable alternative only if amiodarone is unavailable. Synchronized cardioversion is used for stable tachyarrhythmias with a pulse, not pulseless rhythms, which require unsynchronized defibrillation.

• A. Lidocaine is a secondary alternative to amiodarone in the ACLS algorithm, not the first-line agent.
• B. Procainamide is used for stable wide-complex tachycardia with a pulse, not pulseless arrest.
• D. Magnesium is reserved for torsades de pointes or suspected hypomagnesemia, not standard refractory VF.
• E. Synchronized cardioversion requires a perfusing rhythm with a pulse; this patient is pulseless and requires defibrillation, not synchronized shock.

Sick sinus syndrome (sinus node dysfunction) classically presents in elderly patients with alternating bradycardia and paroxysmal supraventricular tachyarrhythmias such as atrial fibrillation, known as tachycardia-bradycardia syndrome, often producing syncope from prolonged sinus pauses at rhythm transitions. The ambulatory monitor findings of alternating bradycardia, tachyarrhythmia, and significant pauses are diagnostic. Treatment typically requires permanent pacemaker placement to allow safe use of rate- or rhythm-control medications for the tachyarrhythmia component. AV block and isolated vasovagal syncope do not explain the alternating tachyarrhythmia pattern seen here.

• A. Mobitz type I block shows progressive PR prolongation before a dropped beat, not alternating bradycardia and atrial fibrillation.
• C. Hypertrophic cardiomyopathy would show septal hypertrophy and outflow obstruction on echocardiogram, which is normal here.
• D. Atrial flutter with variable block would show a sawtooth flutter pattern, not alternating sinus bradycardia and atrial fibrillation.
• E. Vasovagal syncope is typically triggered by a situational or emotional stimulus and does not explain the documented arrhythmias on monitoring.

For hemodynamically stable paroxysmal supraventricular tachycardia (most commonly AV nodal reentrant tachycardia) that fails to respond to vagal maneuvers, adenosine is the first-line pharmacologic agent. It transiently blocks conduction through the AV node, terminating reentrant circuits that depend on the AV node, and has a very short half-life (under 10 seconds), limiting the duration of side effects such as flushing and chest tightness. If the initial 6 mg dose fails, a second dose of 12 mg can be given. Calcium channel blockers and beta-blockers are reasonable second-line options but are not first-line given slower onset and longer duration of action.

• A. Amiodarone is not first-line for acute termination of stable narrow-complex SVT.
• B. Esmolol is a second-line option for rate control but does not reliably terminate reentrant SVT as effectively as adenosine.
• C. Verapamil is an effective second-line agent but has a longer duration of action and more hypotensive effect than adenosine, making it second-line.
• E. Digoxin has a slow onset of action and is not used for acute termination of SVT.

This patient has severe aortic stenosis (valve area under 1.0 cm², mean gradient over 40 mmHg) with symptoms of exertional dyspnea, which is an indication for aortic valve replacement regardless of ejection fraction. Symptomatic severe AS carries a poor prognosis without intervention, and valve replacement (surgical or transcatheter, depending on surgical risk) relieves the fixed outflow obstruction and improves survival. Medical therapy with diuretics or nitrates may provide symptomatic relief but does not alter the natural history and risks precipitating hypotension due to the fixed obstruction. Balloon valvuloplasty alone is a temporizing measure, generally reserved for bridging unstable patients or pediatric/congenital AS, not definitive therapy in adults.

• A. Delaying valve replacement in symptomatic severe AS increases mortality risk; medical therapy alone is inadequate.
• B. Balloon valvuloplasty alone has high restenosis rates and is not definitive therapy for adults with severe symptomatic AS.
• D. Nitrates can cause dangerous hypotension in AS due to the fixed outflow obstruction and do not address the underlying lesion.
• E. Symptomatic severe AS requires intervention now, not repeat imaging in a year.

Transthoracic echocardiography with Doppler is the best initial and most informative test for evaluating a murmur suggestive of mitral regurgitation, as it allows direct visualization of valve morphology and quantification of severity through regurgitant volume, regurgitant fraction, effective regurgitant orifice area, and assessment of left ventricular and left atrial size and function. These parameters determine whether the regurgitation is severe and guide decisions about timing of surgical intervention. Electrocardiography and chest radiography may show secondary findings such as left atrial enlargement but cannot quantify valve severity. Cardiac catheterization is invasive and reserved for cases where echocardiography is inconclusive or concomitant coronary assessment is needed.

• B. Exercise stress ECG assesses functional capacity and ischemia, not structural valve severity.
• C. Chest radiograph may show cardiomegaly or pulmonary congestion but does not directly assess valve severity.
• D. Catheterization with ventriculography is invasive and reserved for cases where noninvasive imaging is inconclusive.
• E. ECG may show left atrial enlargement or atrial fibrillation but cannot quantify regurgitant severity.

This patient has a history consistent with prior rheumatic fever (migratory polyarthritis and rash in childhood) and now presents with findings classic for mitral stenosis: a loud S1, an opening snap shortly after S2, and a low-pitched diastolic rumble at the apex best heard in the left lateral decubitus position. Rheumatic heart disease is the most common cause of mitral stenosis worldwide, resulting from chronic inflammatory scarring and fusion of the mitral valve leaflets. The irregular heart rhythm likely reflects atrial fibrillation from left atrial enlargement, a common complication of long-standing mitral stenosis. Tricuspid stenosis is rare and would produce a similar murmur at the left lower sternal border rather than the apex.

• A. Atrial myxoma can mimic mitral stenosis but typically presents with constitutional symptoms and a variable murmur that changes with position, without a clear rheumatic history.
• C. Aortic regurgitation produces a diastolic decrescendo murmur at the left sternal border, not a low-pitched apical rumble with an opening snap.
• D. Mitral valve prolapse produces a midsystolic click and late systolic murmur, not a diastolic rumble with an opening snap.
• E. Tricuspid stenosis is rare and the murmur would be heard best at the left lower sternal border, not the apex.

This patient has findings classic for chronic aortic regurgitation: a wide pulse pressure (148/54 mmHg) producing bounding pulses, head bobbing (de Musset sign), rapid capillary refill (Quincke sign), and a displaced hyperdynamic apical impulse from left ventricular volume overload. The early diastolic decrescendo murmur at the left sternal border, accentuated by leaning forward, is characteristic of aortic regurgitation, and bicuspid aortic valve is a common underlying cause. Chronic volume overload leads to eccentric left ventricular hypertrophy and dilation, explaining the displaced apical impulse. Mitral stenosis and pulmonic regurgitation do not produce this combination of wide pulse pressure and peripheral signs.

• A. Mitral stenosis produces a diastolic rumble with an opening snap, not a wide pulse pressure with bounding pulses.
• B. Pulmonic regurgitation murmur is heard best at the left upper sternal border and does not typically cause bounding peripheral pulses.
• D. Patent ductus arteriosus produces a continuous machinery murmur, not an isolated early diastolic decrescendo murmur.
• E. Hypertrophic cardiomyopathy produces a systolic murmur that increases with Valsalva, not a diastolic murmur with wide pulse pressure.

This patient already meets two major modified Duke criteria (typical organism in two separate blood cultures and evidence consistent with endocarditis), so the next step is imaging to evaluate for a vegetation, which would confirm the diagnosis. Transthoracic echocardiography (TTE) is the recommended initial imaging test in suspected infective endocarditis because it is noninvasive, widely available, and has reasonable sensitivity, especially for right-sided lesions such as the tricuspid valve suggested by this patient's murmur. Transesophageal echocardiography is reserved for when TTE is nondiagnostic, when prosthetic valves or suspected complications are present, or when image quality is poor. Starting with the less invasive test is appropriate before escalating.

• A. TEE is more sensitive but is reserved for cases where TTE is inconclusive or when prosthetic material or complications are suspected, not as the first test.
• B. Procalcitonin is nonspecific and not part of the Duke diagnostic criteria for infective endocarditis.
• D. Cardiac MRI is not a standard tool for detecting valvular vegetations in suspected infective endocarditis.
• E. Chest CT angiography is used to evaluate septic pulmonary emboli but does not establish the Duke imaging criterion for endocarditis.

Empiric therapy for suspected native valve infective endocarditis in a patient without risk factors for resistant or atypical organisms should cover the most common causative pathogens: staphylococci, streptococci, and enterococci. Vancomycin provides coverage for methicillin-resistant Staphylococcus aureus and most streptococci and enterococci, while ceftriaxone adds coverage for streptococci and most enterococci and provides activity against HACEK organisms. This combination is a standard empiric regimen while blood culture and susceptibility results are pending, after which therapy is narrowed based on the identified organism.

• A. Azithromycin alone does not adequately cover staphylococci or enterococci, the leading causes of native valve endocarditis.
• B. Doxycycline alone is insufficient empiric coverage for the usual bacterial causes of native valve endocarditis.
• C. Oral antibiotics are inadequate for the high bactericidal blood levels needed to treat endocarditis, which requires intravenous therapy.
• E. Metronidazole targets anaerobes, which are not typical pathogens in infective endocarditis, and this combination lacks reliable staphylococcal and streptococcal coverage.

In Black patients with hypertension who do not have diabetes, chronic kidney disease, or heart failure, ACC/AHA guidelines recommend initiating therapy with a thiazide diuretic or a calcium channel blocker, as these classes have demonstrated superior blood pressure control and cardiovascular outcomes in this population compared with ACE inhibitors or ARBs used alone. This reflects differences in the pathophysiology of hypertension, which in many Black patients involves greater volume sensitivity and lower renin activity. ACE inhibitors and ARBs remain first-line in patients with diabetes or chronic kidney disease due to their renoprotective effects, which do not apply here.

• A. ACE inhibitors are preferred first-line in patients with diabetes, chronic kidney disease, or heart failure, none of which this patient has, and have shown less robust monotherapy response in Black patients without these comorbidities.
• C. Clonidine is a centrally acting agent reserved for resistant hypertension, not first-line therapy.
• D. Beta-blockers are not first-line for uncomplicated hypertension and are reserved for specific indications such as coronary disease or heart failure.
• E. ARBs share the same limitation as ACE inhibitors for first-line monotherapy in Black patients without diabetes or CKD.

This patient has hypertensive emergency, defined as severe hypertension with acute end-organ damage, here manifested as hypertensive retinopathy with papilledema. Treatment requires a controlled reduction in blood pressure using a titratable intravenous agent such as labetalol, nicardipine, or nitroprusside, targeting a reduction in mean arterial pressure of no more than 10-20% in the first hour and a further gradual reduction over the following 23 hours. Rapid or excessive blood pressure reduction can cause cerebral, coronary, or renal hypoperfusion due to impaired autoregulation in chronically hypertensive patients. Oral or sublingual agents with unpredictable onset and duration, such as nifedipine, are avoided in hypertensive emergencies.

• A. Furosemide is not first-line for hypertensive emergency and a 50% reduction in 1 hour is far too rapid and risks organ hypoperfusion.
• B. This patient has end-organ damage requiring immediate treatment, not outpatient management with oral agents.
• C. Sublingual nifedipine causes an unpredictable, rapid drop in blood pressure that risks cerebral or coronary hypoperfusion and is contraindicated in hypertensive emergencies.
• E. Observation without treatment is inappropriate given evidence of acute end-organ damage (papilledema, flame hemorrhages).

Resistant hypertension with unexplained hypokalemia raises strong suspicion for primary hyperaldosteronism, and the recommended initial screening test is the plasma aldosterone-to-renin ratio (ARR). An elevated ratio, typically above 20-30 with an aldosterone level above 15 ng/dL, suggests autonomous aldosterone production with suppressed renin and warrants confirmatory testing such as an oral sodium loading test or saline infusion test. Antihypertensives that significantly affect the renin-aldosterone axis, such as spironolactone, should ideally be withheld before testing, although ACE inhibitors and calcium channel blockers are more commonly continued with interpretation adjusted accordingly. Renal vein renin sampling and other localization studies are reserved for after biochemical confirmation to differentiate unilateral from bilateral adrenal disease.

• A. The captopril challenge test is a confirmatory test used after an elevated screening ARR, not the initial screening test.
• C. Urinary free cortisol screens for Cushing syndrome, which can cause hypokalemia but is not suggested by this presentation without cushingoid features.
• D. Plasma free metanephrines screen for pheochromocytoma, which usually presents with episodic hypertension, palpitations, and diaphoresis rather than isolated resistant hypertension with hypokalemia.
• E. Renal vein renin sampling is a localization procedure used after biochemical confirmation of primary hyperaldosteronism, not an initial screening test.

ACE inhibitors such as lisinopril block the breakdown of bradykinin, which accumulates in the respiratory tract and causes a dry cough in up to 10-20% of patients. The cough typically develops within weeks of starting therapy and resolves within days to weeks of discontinuation. Switching to an angiotensin receptor blocker, which does not affect bradykinin metabolism, is the appropriate next step if the cough is bothersome. Angioedema and hyperkalemia are other bradykinin- and aldosterone-related adverse effects of ACE inhibitors but do not explain this patient's presentation.

• A. Hydrochlorothiazide can cause hypokalemia and hyperglycemia but not a dry cough.
• B. Amlodipine, a calcium channel blocker, causes peripheral edema and flushing, not cough.
• C. Losartan, an ARB, does not increase bradykinin levels and rarely causes cough.
• D. Metoprolol can cause bradycardia and fatigue but not a bradykinin-mediated cough.

This patient's episodic triad of headache, palpitations, and diaphoresis with paroxysmal severe hypertension is classic for pheochromocytoma. Plasma free metanephrines have high sensitivity for catecholamine-secreting tumors because metanephrines are produced continuously by tumor metabolism, independent of episodic catecholamine release. A positive biochemical test should be followed by CT or MRI of the adrenal glands to localize the tumor, but biochemical confirmation must come first to avoid unnecessary imaging and to guide interpretation of incidental adrenal findings. 24-hour urinary fractionated metanephrines are an acceptable alternative but plasma free metanephrines are now preferred as the best initial test given this classic presentation.

• A. Aldosterone-to-renin ratio is used to screen for primary hyperaldosteronism, which causes sustained rather than episodic hypertension with hypokalemia.
• B. Urinary cortisol is used to evaluate Cushing syndrome, not pheochromocytoma.
• C. Renal artery imaging evaluates for renovascular hypertension, which typically causes sustained rather than paroxysmal hypertension.
• E. Imaging should follow, not precede, biochemical confirmation of catecholamine excess.

Hypertrophic cardiomyopathy produces a systolic murmur from dynamic left ventricular outflow tract obstruction that worsens with maneuvers that decrease preload, such as Valsalva and standing, because reduced ventricular volume brings the hypertrophied septum closer to the mitral valve apparatus. The murmur decreases with maneuvers that increase preload or afterload, such as squatting or sustained handgrip. This condition is a leading cause of sudden cardiac death in young athletes, often due to ventricular arrhythmia during exertion. An S4 gallop reflects decreased left ventricular compliance from hypertrophy, and echocardiography confirming asymmetric septal hypertrophy establishes the diagnosis.

• A. Ventricular septal defect produces a holosystolic murmur that does not vary significantly with Valsalva maneuver.
• B. Aortic stenosis murmurs decrease with Valsalva and increase with squatting, the opposite pattern.
• C. Pulmonary stenosis produces a murmur at the left upper sternal border that does not show this preload-dependent dynamic pattern.
• E. Mitral valve prolapse murmurs occur with a click and typically become louder with standing but do not classically present with an S4 or exertional sudden death risk in this pattern.

Beta-blockers such as metoprolol are first-line therapy for symptomatic hypertrophic cardiomyopathy because they reduce heart rate and myocardial contractility, which prolongs diastolic filling time and decreases the dynamic left ventricular outflow tract gradient. Patients should also avoid volume depletion, diuretics, and vasodilators, which worsen outflow obstruction by reducing ventricular preload or afterload. Nondihydropyridine calcium channel blockers like verapamil are alternatives if beta-blockers are not tolerated. Agents that increase contractility or decrease preload are contraindicated because they worsen the dynamic obstruction.

• A. Digoxin increases contractility and would worsen outflow tract obstruction.
• B. Nifedipine is a dihydropyridine calcium channel blocker that causes vasodilation and can worsen obstruction; nondihydropyridines like verapamil are preferred alternatives, not nifedipine.
• C. Furosemide reduces preload, which can worsen the dynamic outflow obstruction and reduce cardiac output.
• E. Nitroglycerin reduces preload through venodilation, which worsens outflow tract obstruction in hypertrophic cardiomyopathy.

Chronic heavy alcohol use causes dilated cardiomyopathy through a direct toxic effect of ethanol and its metabolites on myocardial fibers, impairing contractile protein function and promoting myocyte apoptosis over years of exposure. This leads to global ventricular dilation and systolic dysfunction without regional wall motion abnormalities, distinguishing it from ischemic cardiomyopathy. Alcoholic cardiomyopathy is often partially reversible with abstinence, especially if caught before severe fibrosis develops. Other major causes of dilated cardiomyopathy include viral myocarditis (often coxsackievirus) and peripartum cardiomyopathy, which involve different mechanisms.

• A. Autoimmune lymphocytic myocarditis is a cause of dilated cardiomyopathy but is not supported by this patient's history of heavy alcohol use.
• B. Viral myocyte invasion causes dilated cardiomyopathy through myocarditis but this patient's presentation is explained by chronic alcohol toxicity, not an infectious trigger.
• D. Regional wall motion abnormalities and a history of ischemic risk factors would be expected with coronary atherosclerosis, which are absent here.
• E. Amyloid deposition causes restrictive, not dilated, cardiomyopathy with increased wall thickness.

Restrictive cardiomyopathy is characterized by increased ventricular wall thickness due to infiltrative or fibrotic disease, biatrial enlargement, and a restrictive diastolic filling pattern with normal pericardial thickness. Cardiac MRI showing diffuse late gadolinium enhancement suggests an infiltrative process such as cardiac amyloidosis. In contrast, constrictive pericarditis typically shows a thickened or calcified pericardium with normal or only mildly increased myocardial wall thickness, since the primary pathology is pericardial rather than myocardial. Differentiating the two is essential because constrictive pericarditis is potentially curable with pericardiectomy, while restrictive cardiomyopathy is managed medically or with treatment of the underlying infiltrative disease.

• A. Hypertrophic cardiomyopathy typically shows asymmetric septal hypertrophy rather than diffuse wall thickening with biatrial enlargement and infiltrative MRI findings.
• B. Constrictive pericarditis would show a thickened or calcified pericardium rather than increased myocardial wall thickness.
• D. Dilated cardiomyopathy presents with ventricular dilation and reduced wall thickness, not increased wall thickness.
• E. Tuberculous pericarditis is a cause of constrictive pericarditis and would show pericardial thickening, not myocardial infiltration.

Acute pericarditis presents with sharp pleuritic chest pain that improves with sitting forward and worsens with lying supine, often following a viral prodrome. The ECG classically shows diffuse ST-segment elevation with concave morphology and PR-segment depression, along with reciprocal PR elevation in lead aVR, reflecting subepicardial and atrial inflammation rather than a single coronary territory. A pericardial friction rub supports the diagnosis, and a normal troponin argues against significant myocardial necrosis. Viral infection is the most common cause of acute pericarditis in immunocompetent patients in developed countries.

• A. Myocardial infarction typically shows ST elevation localized to a vascular territory with reciprocal depression and elevated troponin, not diffuse changes with a normal troponin.
• B. Stable angina presents with exertional chest pain that resolves with rest and does not cause a friction rub or diffuse ECG changes.
• D. Pulmonary embolism presents with pleuritic chest pain and dyspnea but does not cause diffuse ST elevation with PR depression.
• E. Aortic dissection presents with tearing chest pain radiating to the back and pulse or blood pressure asymmetry, not positional pleuritic pain with diffuse ECG changes.

First-line therapy for acute idiopathic or viral pericarditis is a combination of a nonsteroidal anti-inflammatory drug, such as ibuprofen, plus colchicine. NSAIDs reduce pericardial inflammation and relieve pain, while colchicine, which disrupts microtubule-dependent inflammatory cell function, decreases symptom duration and significantly reduces the risk of recurrence compared with NSAID monotherapy. Treatment is typically continued for one to two weeks with NSAIDs and three months with colchicine, guided by symptom resolution and inflammatory marker normalization. Corticosteroids are reserved as second-line therapy for cases refractory to NSAIDs and colchicine or when NSAIDs are contraindicated, because early steroid use is associated with higher recurrence rates.

• A. Colchicine alone is less effective than combination therapy for initial symptom control; it is typically added to an NSAID.
• B. Diuretics and beta-blockers do not address the inflammatory mechanism of pericarditis and are not standard therapy.
• D. First-line corticosteroid monotherapy increases the risk of recurrent pericarditis and is reserved for refractory cases.
• E. Aspirin alone can be used in NSAID-sensitive situations such as post-MI pericarditis but combination with colchicine is preferred over monotherapy to reduce recurrence.

This patient has clinical and echocardiographic findings of cardiac tamponade: hypotension, elevated jugular venous pressure, muffled heart sounds (Beck triad), pulsus paradoxus, and right ventricular diastolic collapse on echocardiography. Tamponade is a mechanical problem caused by fluid restricting ventricular filling, and the definitive treatment is prompt drainage of the pericardial fluid by pericardiocentesis. Delaying drainage for further imaging or medical therapy risks hemodynamic collapse. Diuretics and vasopressors do not address the underlying restriction and can worsen hemodynamics by reducing preload.

• A. Vasopressors are a temporizing measure only and do not treat the underlying cause.
• C. Anti-inflammatory therapy is used for pericarditis, not to relieve the mechanical compression of tamponade.
• D. Diuresis reduces preload further and can precipitate hemodynamic collapse in tamponade.
• E. CT would delay definitive treatment and is not needed when echocardiography has already confirmed tamponade.

Prior mediastinal radiation is a classic risk factor for constrictive pericarditis, which presents with signs of right-sided venous congestion (ascites, edema, jugular venous distension) that paradoxically increases with inspiration (Kussmaul sign) because the rigid pericardium prevents the right atrium from accommodating increased venous return. The early diastolic sound described is a pericardial knock, caused by sudden cessation of ventricular filling against the stiff pericardium. Clear lungs despite systemic congestion reflect isolated impairment of diastolic filling rather than left-sided failure. Imaging showing pericardial thickening or calcification supports the diagnosis.

• B. Dilated cardiomyopathy typically causes left-sided congestion with pulmonary edema, which is absent here.
• C. Tricuspid regurgitation produces a holosystolic murmur, not an early diastolic knock, and is not associated with radiation exposure.
• D. Right ventricular infarction presents acutely with hypotension and jugular venous distension, not a 4-month progressive course.
• E. Restrictive cardiomyopathy presents similarly but is not linked to prior mediastinal radiation and would not produce a pericardial knock.

The USPSTF recommends one-time screening for abdominal aortic aneurysm with abdominal ultrasound in men aged 65-75 years who have ever smoked. This patient fits that profile exactly. Ultrasound is noninvasive, inexpensive, and highly sensitive and specific for detecting infrarenal aortic dilation, making it the preferred screening modality. Routine repeat screening is not recommended for a normal-caliber aorta on initial screening, and waiting for symptoms defeats the purpose of screening since most AAAs are asymptomatic until rupture.

• A. Screening is meant to detect asymptomatic aneurysms before rupture; waiting for symptoms defeats this purpose.
• B. CT angiography is reserved for surveillance or preoperative planning, not initial screening, due to cost and radiation exposure.
• C. Routine annual screening is not recommended; a normal one-time ultrasound does not require repeat screening.
• D. Men aged 65-75 years with a smoking history meet USPSTF criteria for screening.

This patient has hemodynamic instability (hypotension, tachycardia, altered mentation) with a known large AAA and a new pulsatile, tender abdominal mass, findings diagnostic of a ruptured abdominal aortic aneurysm. Rupture is a surgical emergency, and any delay for additional imaging in an unstable patient increases mortality. The patient should go directly to emergent surgery (open repair or endovascular repair as available) without delaying for confirmatory imaging. Resuscitation with blood products should occur simultaneously but should not delay operative intervention.

• A. Ultrasound would not change management and delays the needed emergent surgical intervention.
• B. CT imaging delays definitive treatment and is inappropriate in a hemodynamically unstable patient with a clinically evident rupture.
• D. Lowering blood pressure further would worsen hypotension and end-organ perfusion in a patient who is already in hemorrhagic shock.
• E. Observation is inappropriate and would result in exsanguination and death.

This presentation, tearing chest pain radiating to the back, a blood pressure differential between arms, a new diastolic murmur suggesting aortic regurgitation, and a widened mediastinum, is classic for acute aortic dissection. In a hemodynamically stable patient, CT angiography of the chest is the test of choice because it rapidly identifies the intimal flap, determines the extent of dissection, and distinguishes type A from type B disease with high sensitivity and specificity. Transesophageal echocardiography is an alternative when the patient is too unstable to undergo CT, but CT angiography remains preferred for stable patients.

• A. Transthoracic echocardiography has limited sensitivity for detecting dissection, especially of the descending aorta.
• C. Stress testing is contraindicated in suspected acute aortic syndrome and risks precipitating rupture.
• D. A D-dimer may support the diagnosis but cannot confirm it or define the anatomy needed for management.
• E. Coronary angiography is not the diagnostic test of choice and risks worsening the dissection via catheter manipulation.

This dissection involves the ascending aorta (Stanford type A), regardless of whether it also extends into the descending aorta. Type A dissections carry a high risk of rapidly fatal complications such as aortic rupture, cardiac tamponade, and acute aortic regurgitation, and require emergent open surgical repair. Medical management with beta-blockers to control heart rate and blood pressure is appropriate initial therapy for type B (descending-only) dissections without complications, but it is not definitive therapy when the ascending aorta is involved. Delaying surgery for medical management alone in type A dissection significantly increases mortality.

• A. This patient's dissection, though pain-free at present, is unstable and life-threatening and cannot be discharged.
• B. Medical therapy alone is inadequate for type A dissection and surgery should not be delayed.
• D. Endovascular repair of the descending aorta is the approach for uncomplicated type B dissection, not for ascending (type A) involvement.
• E. Anticoagulation is contraindicated in aortic dissection as it would worsen bleeding into the false lumen or mediastinum.

This patient's history of exertional calf pain relieved by rest (claudication), diminished pulses, and trophic skin changes is classic for peripheral artery disease. The ankle-brachial index, the ratio of systolic blood pressure at the ankle to that in the arm, is the recommended first-line noninvasive test to confirm the diagnosis; a value of 0.90 or less is diagnostic of PAD. It is inexpensive, quick, and has good sensitivity and specificity, making it the appropriate initial confirmatory test before considering further anatomic imaging for revascularization planning.

• A. A cardiac stress test evaluates for coronary ischemia and is not used to diagnose peripheral artery disease.
• B. Digital subtraction angiography is invasive and used for planning revascularization, not as an initial diagnostic study.
• C. MR angiography provides detailed anatomic imaging but is reserved for planning intervention, not as the initial diagnostic test.
• E. Venous duplex evaluates venous, not arterial, pathology and would not explain this arterial claudication picture.

Cilostazol, a phosphodiesterase-3 inhibitor with antiplatelet and vasodilatory properties, is the first-line pharmacologic agent specifically indicated to improve walking distance and reduce claudication symptoms in patients with peripheral artery disease who remain symptomatic despite exercise therapy and risk factor modification. It is used in addition to, not instead of, antiplatelet therapy, statin therapy, and smoking cessation, all of which reduce cardiovascular risk but do not directly improve claudication distance the way cilostazol does. Cilostazol is contraindicated in patients with heart failure due to its phosphodiesterase inhibition.

• A. Warfarin has no proven benefit for claudication and increases bleeding risk without improving walking distance.
• C. Calcium channel blockers are used for hypertension but have no specific role in improving claudication symptoms.
• D. Diuretics have no role in peripheral artery disease management and do not address claudication.
• E. Clopidogrel is an alternative antiplatelet agent but switching from aspirin does not specifically improve walking distance.

This patient has acute limb ischemia (motor and sensory deficits, absent pulses, pallor, coolness) from presumed cardioembolism due to atrial fibrillation. A threatened limb with neurologic deficit (sensory loss, motor weakness) requires immediate revascularization; imaging should not delay definitive treatment. Immediate anticoagulation with intravenous heparin prevents clot propagation, and emergent surgical or catheter-based embolectomy is required to restore perfusion before irreversible muscle and nerve damage occurs. Delaying for imaging (CT angiography, ABI, duplex ultrasound) in a limb with sensory and motor deficits risks limb loss.

• A. Venous duplex evaluates for DVT, which does not explain absent arterial pulses and pallor.
• B. ABI is useful for chronic peripheral arterial disease, not for diagnosing or managing acute threatened limb ischemia.
• C. Thrombolysis alone is too slow and insufficient for a limb with motor deficit; emergent surgical intervention is needed.
• D. Imaging should not delay revascularization when motor/sensory deficits indicate a threatened limb.

This patient falls into the intermediate-risk category (7.5–19.9% 10-year ASCVD risk) by the pooled cohort equations. ACC/AHA guidelines recommend a clinician-patient discussion of risk-enhancing factors in this group, and coronary artery calcium (CAC) scoring can help refine the decision when the choice to start a statin remains uncertain: a CAC score of 0 may allow deferring statin therapy, while a CAC score of 1-99 generally favors statin therapy, especially in patients over 55 years old, and a CAC score of 100 or higher (or above the 75th percentile) strongly favors statin initiation. Simply reassuring her or starting a fixed-intensity statin without further risk stratification does not follow guideline-based shared decision-making for intermediate-risk patients.

• A. LDL below 190 mg/dL does not exclude the need for risk-based statin therapy in intermediate-risk patients.
• B. High-intensity statin is reserved for very high-risk or LDL ≥190 mg/dL patients, not for this intermediate-risk scenario.
• C. Moderate-intensity statin can be reasonable but risk-enhancing factor discussion and CAC scoring should guide the decision first in borderline/intermediate risk.
• E. Fibrates are not first-line for ASCVD risk reduction and triglycerides of 100 mg/dL are normal.

This patient has diabetes mellitus with a 10-year ASCVD risk of 18%, placing him in the high-risk category for whom ACC/AHA guidelines recommend high-intensity statin therapy to achieve at least a 50% reduction in LDL cholesterol. Rosuvastatin 40 mg daily is a high-intensity statin dose, appropriate given his elevated LDL (165 mg/dL) and diabetes with high calculated risk. Moderate- or low-intensity statins (atorvastatin 10 mg, simvastatin 10 mg, pravastatin 20 mg) would not achieve the needed LDL reduction in this high-risk patient, and ezetimibe alone is not first-line monotherapy for primary ASCVD prevention.

• A. Pravastatin 20 mg is a low- to moderate-intensity statin, insufficient to achieve the needed LDL reduction.
• B. Atorvastatin 10 mg is only moderate-intensity, which under-treats this high-risk diabetic patient.
• C. Ezetimibe alone is not appropriate first-line therapy; statins remain first-line and ezetimibe is typically added if LDL goals are not met on maximal statin therapy.
• E. Simvastatin 10 mg is a low-intensity statin, insufficient for this high-risk patient.

This patient has statin-associated muscle symptoms with significantly elevated creatine kinase (greater than 4 times the upper limit of normal), consistent with statin-induced myopathy. The appropriate step is to discontinue the statin, ensure adequate hydration to support renal clearance of myoglobin, and monitor symptoms and CK until they resolve. Once CK normalizes and symptoms resolve, a different statin (often at a lower dose or with a different pharmacokinetic profile) or alternate-day dosing can often be tried, since most patients can tolerate a rechallenge. Continuing the same statin risks progression to rhabdomyolysis and acute kidney injury.

• B. Continuing the statin despite significant CK elevation is unsafe; CoQ10 has not been proven effective for statin myopathy.
• C. Permanent avoidance of all statins is not necessary; most patients tolerate a different statin or lower dose after symptoms resolve.
• D. Continuing the statin at this CK level risks progression to rhabdomyolysis and kidney injury.
• E. Fibrates are not indicated here and can further increase myopathy risk, especially gemfibrozil in combination with statins.

Initial management of stable angina with a hemodynamically non-significant lesion (less than 70% stenosis in a major vessel, no left main disease, preserved LV function) is medical therapy rather than revascularization. This includes sublingual nitroglycerin for acute anginal episodes, a beta-blocker as first-line anti-anginal therapy to reduce myocardial oxygen demand, aspirin for secondary prevention of cardiovascular events, and a statin to reduce atherosclerotic progression and cardiovascular risk. Revascularization (PCI or CABG) is reserved for lesions causing significant ischemia, left main or multivessel disease, or symptoms refractory to optimal medical therapy.

• B. Antiplatelet therapy with aspirin and statin therapy are essential components of secondary prevention in coronary artery disease, not optional.
• C. Omitting antiplatelet and lipid-lowering therapy leaves the patient at increased risk for cardiovascular events; these are standard of care.
• D. Beta-blockers, not calcium channel blockers, are first-line anti-anginal therapy in stable angina without contraindications.
• E. A 60% stenosis without left main or multivessel disease and preserved LV function does not meet criteria for immediate revascularization; medical therapy is first-line.

This patient has good functional capacity, demonstrated by the ability to climb two flights of stairs (an activity requiring more than 4 metabolic equivalents) without symptoms, and he is undergoing a surgery of intermediate risk. According to ACC/AHA perioperative guidelines, patients with good functional capacity (≥4 METs) do not require further cardiac stress testing before noncardiac surgery, regardless of the number of clinical risk factors, because their perioperative risk is already acceptably low. Further testing (echocardiography, stress testing, angiography, calcium scoring) would only delay surgery without providing additional risk stratification benefit when functional capacity is adequate.

• B. Coronary artery calcium scoring is not part of standard perioperative risk assessment algorithms.
• C. Echocardiography is not indicated when functional capacity is good and there are no signs or symptoms of heart failure or valvular disease.
• D. Preoperative stress testing is unnecessary in patients with good functional capacity (≥4 METs) regardless of risk factors.
• E. Coronary angiography is invasive and not indicated without symptoms or evidence of ischemia prompting further workup.