American Board of Internal Medicine Certification (ABIM Board Certification) Cardiovascular Disease Syllabus

What is the recommended first-line treatment for symptomatic congestion in acute decompensated heart failure?

IV loop diuretics (e.g., furosemide), typically at >=2.5x the home oral dose, given as bolus or continuous infusion. Add vasodilators (nitroglycerin) for hypertensive pulmonary edema if BP allows.

Describe the four clinical hemodynamic profiles used to classify acute heart failure (Stevenson/Forrester).

Based on congestion (wet/dry) and perfusion (warm/cold): Warm-dry (A, compensated), Warm-wet (B, congested but perfused - diurese/vasodilate), Cold-wet (C, congested and hypoperfused - inotropes +/- diuretics), Cold-dry (L, hypoperfused, not congested - cautious fluids/inotropes).

What defines cardiogenic shock hemodynamically?

Sustained hypotension (SBP <90 mmHg for >=30 min or need for vasopressors), with evidence of end-organ hypoperfusion, cardiac index <2.2 L/min/m2, and elevated PCWP >15 mmHg, in the setting of adequate or elevated filling pressures.

What is the most common cause of cardiogenic shock, and what is the cornerstone of treatment?

Acute MI with LV pump failure is the most common cause. Cornerstone is emergent revascularization (PCI) of the culprit lesion (per SHOCK trial), plus hemodynamic support with inotropes/vasopressors and mechanical support (IABP, Impella, ECMO) as needed.

What is the diagnostic finding and triggers for Takotsubo (stress) cardiomyopathy?

Apical ballooning (akinesis of mid/apical LV with basal hyperkinesis) on imaging, often after intense emotional or physical stress, mimicking ACS with chest pain and ST changes but non-obstructive coronaries. Usually reversible over weeks.

What is the classic echocardiographic and physiologic finding distinguishing hypertrophic obstructive cardiomyopathy (HOCM)?

Asymmetric septal hypertrophy with systolic anterior motion (SAM) of the mitral valve and dynamic LV outflow tract obstruction. The murmur INCREASES with maneuvers that decrease preload/afterload (Valsalva, standing) and DECREASES with squatting/handgrip.

How do you distinguish restrictive cardiomyopathy from constrictive pericarditis?

Constriction: pericardial thickening/calcification, ventricular interdependence (respiratory variation in mitral/tricuspid inflow), septal bounce, equalization of diastolic pressures - treated surgically. Restriction: biatrial enlargement, high BNP, no respiratory variation; often from infiltration (amyloid). Cardiac MRI and invasive hemodynamics help differentiate.

What is the CHA2DS2-VASc score and its use in atrial fibrillation?

Stroke risk score: Congestive HF (1), Hypertension (1), Age >=75 (2), Diabetes (1), Stroke/TIA/thromboembolism (2), Vascular disease (1), Age 65-74 (1), Sex category female (1). Anticoagulation is recommended for men with score >=2 and women >=3; consider for score of 1.

In atrial fibrillation, which anticoagulants are preferred and when must warfarin be used instead of DOACs?

DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) are preferred over warfarin for non-valvular AF. Warfarin is required for AF with moderate-to-severe mitral stenosis or a mechanical prosthetic valve, where DOACs are contraindicated.

What does the AFFIRM/RACE trial evidence say about rate vs rhythm control in atrial fibrillation, and what does EAST-AFNET 4 add?

Older trials (AFFIRM) showed no mortality difference between rate and rhythm control. EAST-AFNET 4 showed early rhythm control (within 1 year of diagnosis) reduces cardiovascular outcomes. Anticoagulation must continue regardless of rhythm strategy based on CHA2DS2-VASc.

What is the characteristic ECG appearance of typical atrial flutter and its preferred curative treatment?

Sawtooth flutter waves, classically negative in inferior leads (II, III, aVF), with atrial rate ~300 bpm and often 2:1 AV conduction (ventricular rate ~150). Cavotricuspid isthmus ablation is highly effective and curative for typical (counterclockwise) flutter.

How do you acutely manage a stable patient with AVNRT (regular narrow-complex SVT)?

First vagal maneuvers (Valsalva, modified Valsalva, carotid sinus massage). If unsuccessful, IV adenosine (6 mg then 12 mg). Alternatives: IV diltiazem/verapamil or beta-blockers. If hemodynamically unstable, synchronized cardioversion.

In Wolff-Parkinson-White syndrome with atrial fibrillation, which AV nodal blocking agents must be AVOIDED and why?

Avoid AV nodal blockers (adenosine, beta-blockers, calcium channel blockers, digoxin) - they can accelerate conduction down the accessory pathway, causing rapid ventricular response and VF. Use procainamide or ibutilide, or synchronized cardioversion if unstable.

What ECG finding is diagnostic of WPW in sinus rhythm?

A short PR interval (<120 ms) and a delta wave (slurred upstroke of the QRS) with a widened QRS, reflecting pre-excitation through an accessory pathway.

What criteria favor ventricular tachycardia over SVT with aberrancy in a wide-complex tachycardia?

AV dissociation, capture/fusion beats, very wide QRS (>140 ms in RBBB pattern), extreme axis (northwest), concordance across precordial leads, and a history of structural heart disease/prior MI. When in doubt, treat wide-complex tachycardia as VT.

What are the indications for a primary prevention ICD in nonischemic and ischemic cardiomyopathy?

Ischemic: LVEF <=30% (or <=35% with NYHA II-III), >=40 days post-MI on GDMT. Nonischemic: LVEF <=35%, NYHA II-III, on >=3 months GDMT. Survival expectation >1 year. Secondary prevention: ICD after survived cardiac arrest or sustained VT with structural disease.

What is the acute management of sustained ventricular tachycardia in a pulseless patient vs a stable patient?

Pulseless VT/VF: immediate defibrillation (unsynchronized) and CPR per ACLS, with epinephrine and amiodarone. Stable monomorphic VT: IV antiarrhythmics (amiodarone, procainamide, or lidocaine) or synchronized cardioversion. Unstable with pulse: synchronized cardioversion.

What is the management of polymorphic VT (torsades de pointes) associated with a long QT?

IV magnesium sulfate is first-line. Correct electrolytes (K, Mg), stop QT-prolonging drugs, and increase heart rate via overdrive pacing or isoproterenol to shorten the QT. Defibrillate if pulseless/unstable.

Differentiate the triggers for the major congenital long QT syndrome subtypes.

LQT1 (KCNQ1, IKs): events with exercise, especially swimming. LQT2 (KCNH2/hERG, IKr): events with emotional stress or auditory stimuli (alarm). LQT3 (SCN5A, late sodium current): events during sleep/rest/bradycardia. Beta-blockers are mainstay (most effective in LQT1).

What is the characteristic ECG pattern of Brugada syndrome, and how are events prevented?

Coved-type ST-segment elevation (>=2 mm) with T-wave inversion in right precordial leads (V1-V2) - type 1 Brugada pattern. Risk of polymorphic VT/sudden death, often during sleep or fever. ICD for symptomatic/high-risk patients; avoid sodium channel blockers and treat fevers aggressively.

What inherited arrhythmia is triggered by catecholamines/exercise and shows bidirectional VT, and how is it managed?

Catecholaminergic polymorphic VT (CPVT), commonly from RYR2 mutations. Exercise/stress provokes bidirectional or polymorphic VT with a structurally normal heart. Treated with beta-blockers (nadolol), flecainide, exercise restriction, and ICD if needed.

What are the indications for permanent pacing in bradyarrhythmias?

Symptomatic sinus node dysfunction; symptomatic or high-grade AV block; complete (third-degree) AV block; Mobitz type II second-degree AV block; symptomatic Mobitz I; and AF with symptomatic bradycardia/pauses. Pace for the conduction disease, not asymptomatic reversible causes.

How do you distinguish Mobitz type I (Wenckebach) from Mobitz type II second-degree AV block, and which is more dangerous?

Mobitz I: progressive PR prolongation until a dropped beat (block in AV node, usually benign). Mobitz II: constant PR with sudden dropped beats (block in His-Purkinje system, often wide QRS), high risk of progression to complete block - requires pacing.

What echocardiographic criteria define severe aortic stenosis?

Aortic valve area <1.0 cm2 (or <0.6 cm2/m2 indexed), mean transvalvular gradient >=40 mmHg, and peak aortic jet velocity >=4 m/s. 'Low-flow low-gradient' severe AS may have low gradients despite small valve area; dobutamine echo helps clarify.

When is aortic valve replacement (AVR) indicated in aortic stenosis?

Symptomatic severe AS (angina, syncope, dyspnea/HF); asymptomatic severe AS with LVEF <50%; severe AS undergoing other cardiac surgery; and select asymptomatic very severe AS or abnormal exercise testing. Choice of TAVR vs SAVR depends on surgical risk and anatomy.

What are the key features and management of acute vs chronic aortic regurgitation?

Acute AR (e.g., endocarditis, dissection): sudden severe pulmonary edema, tachycardia, NO time for LV dilation, soft S1 - surgical emergency. Chronic AR: gradual LV dilation, wide pulse pressure, water-hammer pulse, decrescendo diastolic murmur; surgery for symptoms, LVEF <=55%, or LV end-systolic dimension >50 mm.

What distinguishes the murmurs and management of mitral stenosis vs mitral regurgitation?

MS: opening snap with low-pitched diastolic rumble at apex; usually rheumatic; treat with rate control, anticoagulation if AF, and percutaneous balloon valvuloplasty for symptomatic moderate-severe pliable valves. MR: holosystolic murmur radiating to axilla; surgery/repair for severe symptomatic MR or LVEF 30-60% or LVESD >=40 mm.

What are the modified Duke criteria for diagnosing infective endocarditis?

Major: typical organism in 2 separate blood cultures (or persistent bacteremia) and endocardial involvement (vegetation/abscess/new regurgitation on echo). Minor: predisposing condition, fever >=38C, vascular phenomena, immunologic phenomena, suggestive microbiology. Definite IE = 2 major, or 1 major + 3 minor, or 5 minor.

What are the major indications for surgery in infective endocarditis?

Heart failure from valve dysfunction; uncontrolled/persistent infection or perivalvular abscess; difficult organisms (fungal, multidrug-resistant); recurrent emboli or large mobile vegetation (>10 mm) despite appropriate antibiotics; and prosthetic valve endocarditis with complications.

Which cardiac conditions warrant antibiotic prophylaxis before high-risk dental procedures?

Prosthetic heart valves (including TAVR) or prosthetic material for repair; prior infective endocarditis; unrepaired cyanotic congenital heart disease (or repaired with residual defects); and cardiac transplant recipients with valvulopathy. Standard regimen is amoxicillin 2 g PO 30-60 min before the procedure.

What is the recommended anticoagulation and target INR for mechanical prosthetic heart valves?

Lifelong warfarin (DOACs are contraindicated). Mechanical aortic valve: INR 2.5 (range 2.0-3.0). Mechanical mitral valve or any valve with added risk factors: INR 3.0 (range 2.5-3.5). Low-dose aspirin is added. Bioprosthetic valves typically need only short-term anticoagulation or antiplatelet therapy.

How is hypertension staged per the 2017 ACC/AHA guideline?

Normal <120/<80; Elevated 120-129/<80; Stage 1 HTN 130-139 or 80-89; Stage 2 HTN >=140 or >=90. Diagnosis requires proper out-of-office or repeated measurements. Hypertensive crisis is >=180/>=120.

What are the recommended first-line antihypertensive drug classes, and which is preferred in Black patients without HF/CKD?

First-line: thiazide diuretics, ACE inhibitors, ARBs, and dihydropyridine calcium channel blockers. In Black patients without heart failure or CKD, a thiazide diuretic or calcium channel blocker is preferred for initial monotherapy over ACEi/ARB.

What clinical clues should prompt a workup for secondary hypertension?

Resistant HTN (uncontrolled on 3 drugs including a diuretic), onset <30 or sudden onset, severe/malignant HTN, abrupt loss of control, hypokalemia, abdominal bruit, or target-organ damage out of proportion. Common causes: primary aldosteronism, renovascular disease, OSA, pheochromocytoma, renal parenchymal disease.

What is the screening test for primary aldosteronism, the most common secondary cause of hypertension?

Plasma aldosterone-to-renin ratio (ARR); an elevated aldosterone with suppressed renin is suggestive. Confirm with salt loading/saline suppression testing, then adrenal CT and adrenal vein sampling to localize before considering adrenalectomy.

Compare the presentation and immediate management of Stanford type A vs type B aortic dissection.

Type A involves the ascending aorta - surgical emergency (risk of tamponade, AR, coronary/cerebral malperfusion). Type B is distal to the left subclavian - managed medically with rapid IV beta-blockade (e.g., esmolol/labetalol) to lower heart rate and BP, surgery/endovascular for complications (malperfusion, rupture).

What are the size thresholds for elective repair of an abdominal aortic aneurysm (AAA)?

Repair when AAA diameter >=5.5 cm in men (>=5.0 cm in women), rapid growth (>0.5 cm in 6 months or >1 cm/year), or symptomatic/tender aneurysm. One-time ultrasound screening is recommended for men aged 65-75 who have ever smoked.

What is the ankle-brachial index (ABI), and how do values classify peripheral arterial disease?

ABI = highest ankle systolic pressure / highest brachial systolic pressure. Normal 1.0-1.4; borderline 0.91-0.99; PAD <=0.90; severe ischemia <0.40. ABI >1.40 suggests noncompressible, calcified vessels (common in diabetes/CKD).

What is the medical management of symptomatic peripheral arterial disease (claudication)?

Risk factor modification (smoking cessation is essential), high-intensity statin, antiplatelet therapy (aspirin or clopidogrel), control of HTN/diabetes, supervised exercise therapy, and cilostazol for claudication symptoms. Low-dose rivaroxaban plus aspirin reduces limb/cardiovascular events. Revascularization for lifestyle-limiting or critical limb ischemia.

What are the classic ECG and physical exam findings of acute pericarditis?

Diffuse concave-upward ST elevation with PR-segment depression (and PR elevation in aVR); a pericardial friction rub; pleuritic chest pain that improves leaning forward. Treatment is NSAIDs plus colchicine (colchicine reduces recurrence).

What is Beck's triad and the hemodynamic hallmark of cardiac tamponade?

Beck's triad: hypotension, muffled heart sounds, and elevated JVP (distended neck veins). The hallmark is pulsus paradoxus (>10 mmHg drop in systolic BP on inspiration) with echo showing diastolic RV/RA collapse. Treatment is urgent pericardiocentesis.