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

Cardiovascular Disease syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Cardiovascular Disease in American Board of Internal Medicine Certification (ABIM Board Certification), not a summary of it.

1. 1

   Ischemic Heart Disease & Acute Coronary Syndromes

   4 topics

   • Stable Ischemic Heart Disease
     • Chronic stable angina assessment and risk stratification
     • Pretest probability and noninvasive testing selection
     • Optimal medical therapy and indications for revascularization
   • Acute Coronary Syndromes
     • STEMI recognition and reperfusion strategy
     • NSTEMI/unstable angina risk scores (TIMI, GRACE)
     • Antiplatelet and anticoagulation regimens
   • Secondary Prevention
     • Statin and lipid-lowering targets
     • Cardiac rehabilitation and lifestyle modification
   • Mechanical and ischemic complications of MI
2. 2

   Heart Failure & Cardiomyopathies

   4 topics

   • HFrEF: guideline-directed medical therapy
     • ARNI, beta-blockers, MRA, SGLT2 inhibitors
     • Device therapy (ICD, CRT) indications
   • HFpEF diagnosis and management
   • Acute decompensated heart failure and cardiogenic shock
   • Cardiomyopathies
     • Dilated, hypertrophic, restrictive phenotypes
     • Infiltrative disease (amyloid, sarcoid, hemochromatosis)
3. 3

   Arrhythmias & Conduction Disorders

   5 topics

   • Atrial fibrillation and flutter
     • Rate vs rhythm control
     • CHA2DS2-VASc and anticoagulation decisions
   • Supraventricular tachycardias
   • Ventricular arrhythmias and sudden cardiac death prevention
   • Bradyarrhythmias and pacing indications
   • Long QT and inherited channelopathies
4. 4

   Valvular & Structural Heart Disease

   4 topics

   • Aortic stenosis and regurgitation
     • Severity grading by echocardiography
     • Timing of valve replacement (SAVR vs TAVR)
   • Mitral valve disease
   • Infective endocarditis diagnosis and management
   • Prosthetic valve evaluation and anticoagulation
5. 5

   Vascular Disease & Hypertension

   5 topics

   • Hypertension diagnosis, staging, and pharmacotherapy
   • Secondary hypertension workup
   • Aortic aneurysm and dissection
   • Peripheral arterial disease
   • Pericardial disease and tamponade

Cardiovascular Disease flashcards for American Board of Internal Medicine Certification (ABIM Board Certification)

23 of 61 cards from the Cardiovascular Disease deck — real questions with worked answers.

1. In stable ischemic heart disease, which two classes of medications are proven to reduce mortality/cardiovascular events (not just symptoms)?

   Aspirin (antiplatelet) and high-intensity statins reduce events. Beta-blockers, nitrates, ranolazine, and calcium channel blockers are primarily antianginal/symptomatic. ACE inhibitors/ARBs reduce events in those with LV dysfunction, diabetes, HTN, or CKD.

2. When is revascularization (vs optimal medical therapy alone) indicated to improve survival in stable ischemic heart disease?

   Survival benefit is established for: left main disease (>=50% stenosis), multivessel disease with reduced LVEF, and proximal LAD disease. Per ISCHEMIA trial, in stable patients with moderate-severe ischemia but preserved EF and no left main disease, routine revascularization does not reduce death/MI over OMT.

3. What ECG and biomarker findings distinguish unstable angina from NSTEMI?

   Both have ischemic symptoms without ST elevation (may show ST depression or T-wave inversion). Unstable angina has NEGATIVE troponin; NSTEMI has ELEVATED (positive) troponin indicating myocardial necrosis.

4. What is the immediate management priority for a STEMI, and what are the target reperfusion times?

   Emergent reperfusion. Primary PCI is preferred with goal door-to-balloon <=90 min (or <=120 min if transfer needed). If PCI unavailable within 120 min, give fibrinolytics within 30 min of arrival (door-to-needle), then transfer for PCI.

5. In acute coronary syndrome, when should supplemental oxygen be administered?

   Only when oxygen saturation is <90% (or <94% by some guidelines) or the patient has respiratory distress. Routine oxygen in normoxemic patients provides no benefit and may be harmful.

6. What is the standard dual antiplatelet therapy (DAPT) duration after drug-eluting stent placement for ACS?

   Aspirin indefinitely plus a P2Y12 inhibitor (ticagrelor or prasugrel preferred over clopidogrel) for at least 12 months. Duration may be shortened for high bleeding risk or extended for high ischemic risk.

7. Why is prasugrel contraindicated in patients with prior stroke or TIA?

   Prasugrel increases the risk of intracranial and major bleeding; in patients with prior stroke/TIA it causes net harm. It is also generally avoided in patients >=75 years or <60 kg.

8. List the five core components of secondary prevention after myocardial infarction.

   1) High-intensity statin (LDL goal <70, often <55 mg/dL); 2) Antiplatelet therapy (aspirin +/- P2Y12); 3) Beta-blocker; 4) ACE inhibitor/ARB (especially if EF reduced, HTN, DM, CKD); 5) Lifestyle: smoking cessation, cardiac rehab, diet, exercise, BP/glucose control.

9. Which non-statin lipid-lowering agents are added for secondary prevention when LDL remains above goal on maximal statin therapy?

   Ezetimibe first (oral), then a PCSK9 inhibitor (evolocumab/alirocumab) for very high-risk patients. Bempedoic acid and inclisiran are additional options.

10. A patient develops a new harsh holosystolic murmur and acute pulmonary edema 3-5 days after an MI. What two mechanical complications must be distinguished, and how?

    Ventricular septal rupture vs acute mitral regurgitation (papillary muscle rupture). Distinguish by echocardiography; a right heart catheter shows an oxygen 'step-up' in the RV with VSR but a prominent v-wave (PCWP) with acute MR. Both require emergent surgery.

11. What is the typical timing and presentation of free wall rupture after acute MI?

    Occurs days 1-7 (peak 3-5 days), more common in first transmural MI, elderly, women, and late reperfusion. Presents as sudden hemodynamic collapse, pulseless electrical activity, and cardiac tamponade. Usually fatal; requires emergent pericardiocentesis and surgery.

12. Which artery occlusion classically causes right ventricular infarction, and how does management differ?

    Proximal right coronary artery (RCA). RV infarction causes hypotension with clear lungs and elevated JVP; it is preload-dependent. Treat with IV fluids; AVOID nitrates and diuretics, which reduce preload and worsen hypotension.

13. What ECG lead set should be obtained when inferior STEMI is present, and what does it detect?

    Right-sided leads (especially V4R) to detect RV infarction, and posterior leads (V7-V9) to detect posterior MI. ST elevation in V4R indicates RV involvement.

14. List the four pillars (drug classes) of guideline-directed medical therapy for HFrEF.

    1) ARNI (sacubitril/valsartan) or ACEi/ARB; 2) Beta-blocker (carvedilol, metoprolol succinate, or bisoprolol); 3) Mineralocorticoid receptor antagonist (spironolactone/eplerenone); 4) SGLT2 inhibitor (dapagliflozin/empagliflozin).

15. What washout period is required when switching from an ACE inhibitor to an ARNI (sacubitril/valsartan), and why?

    A 36-hour washout from the ACE inhibitor is required to avoid overlapping neprilysin and ACE inhibition, which markedly increases angioedema risk.

16. In HFrEF, when is an implantable cardioverter-defibrillator (ICD) indicated for primary prevention?

    LVEF <=35% despite >=3 months of optimal GDMT, NYHA class II-III (or class I if EF <=30% ischemic), with reasonable expectation of survival >1 year. For nonischemic cardiomyopathy, wait 3 months on GDMT; for post-MI, wait at least 40 days.

17. What are the indications for cardiac resynchronization therapy (CRT) in HFrEF?

    LVEF <=35%, sinus rhythm, LBBB with QRS >=150 ms, and NYHA class II-IV symptoms on GDMT. Greatest benefit with LBBB and QRS >=150 ms; benefit is less for non-LBBB or QRS 120-149 ms.

18. Which additional HFrEF therapies are indicated specifically in self-identified Black patients and in those with persistent symptoms?

    Hydralazine plus isosorbide dinitrate added to GDMT improves outcomes in Black patients with NYHA III-IV. Ivabradine is added for sinus rhythm with heart rate >=70 despite maximal beta-blocker.

19. What diagnostic score/criteria support a diagnosis of HFpEF in a patient with dyspnea and preserved EF?

    HFpEF requires EF >=50%, evidence of elevated filling pressures, and structural/functional abnormalities. The H2FPEF and HFA-PEFF scores incorporate obesity, atrial fibrillation, age, pulmonary hypertension, elevated filling pressures, and echo findings (e.g., E/e', LA enlargement, elevated NT-proBNP).

20. Which drug class has the strongest evidence for reducing heart failure hospitalizations in HFpEF?

    SGLT2 inhibitors (empagliflozin, dapagliflozin) reduce HF hospitalizations across the full EF spectrum, including HFpEF. Management also targets comorbidities: BP control, diuretics for congestion, AF management, and weight loss.

21. 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.

22. 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).

23. 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.

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