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The ABIM Cardiovascular Disease Certification Exam is unusual among internal medicine subspecialty boards in one specific way: roughly ten hours of multiple-choice testing plus a dedicated ECG and imaging component that tests something different from ordinary clinical recall — the ability to look at a rhythm strip, an echo clip description, or a coronary angiogram and go straight to the right interpretation, fast. This ABIM Cardiovascular Disease Practice Test gives you 770 original questions built around that full scope: coronary disease, heart failure, arrhythmias, valvular disease, and dedicated ECG/echocardiography/angiography interpretation, each with a full explanation of the clinical reasoning behind the answer.
What Is the ABIM Cardiovascular Disease Certification Exam?
| Detail | Current Information |
|---|---|
| Format | Full day of multiple-choice testing plus a separate ECG/imaging component |
| Multiple-choice sessions | Four 2-hour sessions, ~10 hours total |
| ECG/imaging component | Up to 75 questions, ~10 unscored |
| ECG/imaging weighting | ~48% ECGs, 37% echocardiograms, 15% coronary angiograms |
| Scoring | Pass/fail on the exam as a whole — no separate passing score required for the ECG/imaging component alone |
| Unanswered questions | Scored as incorrect — always answer every question |
| 2026 exam dates | October 13–14, 2026 |
| 2026 regular registration | December 1, 2025 – June 15, 2026 |
| 2026 late registration | June 16–28, 2026, with an additional non-refundable fee |
One detail worth internalizing early: your pass/fail decision is based on the exam as a whole, not a separate cutoff for the ECG/imaging section. Content-area feedback is provided for your own diagnostic purposes, but it’s not directly comparable to your overall score — so don’t assume a weak content-area breakdown on your score report means you failed that section specifically.
What’s Covered on the Exam
Core clinical domains include coronary artery disease and acute coronary syndromes, chronic coronary syndromes, heart failure and cardiomyopathies, arrhythmias and conduction disorders, valvular heart disease, hypertension and risk reduction, pulmonary hypertension and right-heart disease, pericardial disorders, adult congenital heart disease, aortic disease, preventive cardiology, peripheral arterial disease, and cardiovascular pharmacology.
The dedicated ECG/imaging blueprint deserves separate attention because it’s tested differently:
- ECGs (~48% of this component): rhythm and conduction patterns, ischemic changes, ST/T/U-wave abnormalities, pacemaker function, hypertrophy and axis findings
- Echocardiograms (~37%): chamber size and systolic function, valvular lesions via Doppler and structural findings, cardiomyopathy patterns
- Coronary angiograms (~15%): coronary anatomy, lesion characteristics, angiographic abnormalities
ABIM reviews and updates this blueprint annually, so treat it as a current framework rather than an unchanging list — always confirm you’re studying the version in effect for your exam year.
Eligibility Requirements
To sit for the ABIM Cardiovascular Disease Certification Exam, physicians must:
- Hold prior ABIM certification in internal medicine
- Complete accredited cardiovascular disease fellowship training — currently 36 months total, including 24 months of clinical training, with specified procedural experience in ECG, echocardiography, right- and left-heart catheterization, and diagnostic coronary angiography
- Complete training through a program accredited by ACGME, the Royal College of Physicians and Surgeons of Canada, or the Collège des médecins du Québec
- Demonstrate clinical competence, procedural skills, and appropriate professional/ethical conduct
- Hold a valid, unrestricted, unchallenged medical license
Confirm your specific status through your ABIM Physician Portal, since eligibility policies can be updated.
How to Register
- Confirm eligibility and fellowship completion requirements are met.
- Register through the ABIM Physician Portal during the applicable window — for 2026, regular registration runs December 1, 2025 through June 15, 2026.
- Late registration (June 16–28, 2026) is available with an additional non-refundable fee.
- Schedule your appointment through Pearson VUE — appointments fill first-come, first-served.
- Review current ABIM testing-center and identification requirements before your appointment.
How to Study for This Exam
- Treat the ECG/imaging component as its own discipline, not an extension of the multiple-choice section — describe what you actually see (rhythm, rate, intervals, axis, morphology for ECGs; chamber size, function, valve anatomy, Doppler findings for echo; coronary anatomy and lesion characteristics for angiography) before jumping to a diagnosis. This disciplined, step-by-step process is what holds up on unfamiliar cases.
- Weight your image practice roughly to the blueprint — ECGs get the most emphasis (~48%), followed by echocardiography (~37%) and angiography (~15%), so don’t let angiography crowd out ECG practice time just because it feels more procedurally interesting.
- Practice distinguishing closely related diagnoses deliberately — true-severe vs. pseudo-severe AS, Wellens vs. non-specific T-wave inversion, primary vs. secondary MR — these paired distinctions are exactly where board-level difficulty concentrates.
- Answer every practice question, including guesses — since unanswered questions score as incorrect on the real exam, build the habit of committing to a best answer under practice conditions too.
- Review missed questions for the reasoning gap, not just the correct letter — a wrong ECG read is often a process failure (skipped a step) rather than a knowledge failure, and that’s worth diagnosing specifically.
- Use timed blocks as your date approaches, especially for image-based questions, since interpretation speed genuinely matters across a 10-hour testing day.
Exam Day Tips
- Read the entire clinical stem before committing to an answer — identify exactly what’s being asked (diagnosis? next step? mechanism?) before evaluating options.
- For image-based questions, examine the entire image systematically before fixating on one finding.
- Answer every question — unanswered items are scored as incorrect, so a reasoned guess always beats a blank.
- Don’t over-defend an unlikely distractor; move on and return to uncertain questions if time allows.
- Review current ABIM identification, scheduling, and testing-center policies before your appointment, since procedures can be updated.
Common Mistakes to Avoid
- Memorizing answer patterns instead of the clinical reasoning behind them
- Treating ECG interpretation as memorization rather than a repeatable systematic process
- Neglecting echocardiographic and angiographic interpretation in favor of purely clinical questions
- Assuming one isolated finding always establishes the diagnosis
- Failing to distinguish closely related cardiovascular syndromes
- Practicing only untimed questions and never building genuine pacing under pressure
- Leaving image interpretation practice until the final days
- Relying on outdated exam-format information instead of the current ABIM blueprint
Is the ABIM Cardiovascular Disease Exam Difficult?
It’s demanding because it spans an unusually broad cardiovascular knowledge base and requires a distinct interpretive skill set for the ECG/imaging component that ordinary clinical vignettes don’t test. Difficulty tends to concentrate less around recognizing a condition in isolation and more around distinguishing closely related diagnoses, interpreting images efficiently under time pressure, and applying findings to a specific clinical presentation rather than a textbook description. A structured practice routine that treats image interpretation as its own skill — not an afterthought to clinical study — tends to close this gap faster than volume alone.
Sample Questions and Answers
Question 1. A 68-year-old man with hypertension, type 2 diabetes, and chronic kidney disease presents with 90 minutes of substernal chest pressure radiating to the left arm. ECG shows 2-mm ST-segment elevations in leads II, III, and aVF with reciprocal ST depression in leads I and aVL. Blood pressure is 86/58 mm Hg, heart rate 54/min, and lungs are clear. He has elevated jugular venous pressure and clear lung fields. Which of the following is the most appropriate immediate management?
A. Intravenous nitroglycerin
B. Emergent coronary angiography with primary PCI
C. Intravenous furosemide
D. Intravenous metoprolol
Correct Answer: B. Emergent coronary angiography with primary PCI
Answer Explanation: Option B is correct because this patient has an inferior STEMI complicated by hypotension and clinical findings suggesting right ventricular involvement. Acute coronary occlusion requires urgent reperfusion, and primary PCI is the preferred reperfusion strategy when it can be performed promptly. The elevated JVP, clear lungs, hypotension, and inferior infarction strongly suggest right ventricular infarction, commonly involving the proximal right coronary artery. Nitroglycerin can worsen hypotension by reducing preload and should be avoided in suspected right ventricular infarction with low blood pressure. Furosemide would further reduce preload without treating the coronary occlusion. Intravenous metoprolol is inappropriate during acute hemodynamic instability and bradycardia.
Why the other options are incorrect:
Option A is inappropriate because venodilation may markedly reduce preload and worsen right ventricular output and hypotension.
Option C is incorrect because there is no evidence of pulmonary congestion, and diuresis could worsen preload dependence.
Option D is contraindicated because the patient is hypotensive and bradycardic during an acute infarction.
Study Guide:
Inferior STEMI with hypotension, elevated JVP, and clear lungs should raise immediate concern for right ventricular infarction.
Avoid preload-reducing medications such as nitrates in unstable right ventricular infarction.
Urgent reperfusion is the definitive treatment for an acute coronary occlusion.
Always interpret the ECG together with the hemodynamic examination.
Question 2. A 72-year-old woman with heart failure with reduced ejection fraction has an LVEF of 30% despite treatment with sacubitril/valsartan, carvedilol, spironolactone, and dapagliflozin. She is euvolemic and has no recent hospitalizations. ECG shows sinus rhythm with a left bundle branch block and QRS duration of 168 ms. Which intervention is most appropriate to reduce mortality and heart-failure-related events?
A. Cardiac resynchronization therapy
B. Digoxin
C. Verapamil
D. Routine dual antiplatelet therapy
Correct Answer: A. Cardiac resynchronization therapy
Answer Explanation: Option A is correct because this patient has symptomatic HFrEF with persistently reduced LVEF despite guideline-directed medical therapy, sinus rhythm, and a markedly prolonged QRS with LBBB morphology. Cardiac resynchronization therapy can improve ventricular synchrony, reduce heart-failure hospitalizations, and improve survival in appropriately selected patients. A QRS duration of at least 150 ms with LBBB morphology is particularly associated with benefit. The other choices do not address the underlying electrical dyssynchrony. Digoxin may reduce hospitalizations in selected patients but does not provide the same mortality benefit. Verapamil can worsen systolic function. Dual antiplatelet therapy has no role in routine chronic HFrEF without another indication.
Why the other options are incorrect:
Option B may have a role for selected symptomatic patients but does not correct electrical dyssynchrony or provide the indicated device-based benefit.
Option C can depress myocardial contractility and is generally unsuitable in significant systolic heart failure.
Option D is unnecessary without an acute coronary syndrome, PCI, or another established indication.
Study Guide:
Remember the importance of QRS duration and morphology when evaluating advanced HFrEF.
LBBB with a markedly prolonged QRS identifies patients who may benefit substantially from CRT.
CRT is considered after appropriate guideline-directed medical therapy and clinical assessment.
Device selection also depends on expected survival, functional status, rhythm, and ventricular function.
Question 3. A 64-year-old woman presents with sudden palpitations and lightheadedness. ECG demonstrates a regular wide-complex tachycardia at 190/min. Blood pressure is 78/46 mm Hg, and she is diaphoretic and confused. There is no immediately available history of structural heart disease. What is the most appropriate next step?
A. Intravenous adenosine
B. Intravenous amiodarone over 30 minutes
C. Immediate synchronized cardioversion
D. Carotid sinus massage
Correct Answer: C. Immediate synchronized cardioversion
Answer Explanation: Option C is correct because the patient has an unstable tachyarrhythmia manifested by hypotension, altered mental status, and diaphoresis. Immediate synchronized cardioversion is indicated for an unstable tachycardia with a pulse. A regular wide-complex tachycardia should generally be presumed to be ventricular tachycardia until proven otherwise, particularly in adults. Pharmacologic treatment is too slow and potentially hazardous in a hemodynamically unstable patient. Although adenosine can occasionally help diagnose or terminate certain regular supraventricular tachycardias with aberrancy, it should not delay electrical therapy in an unstable patient. Vagal maneuvers are also inappropriate when there is significant hemodynamic compromise.
Why the other options are incorrect:
Option A may be considered diagnostically in selected stable regular monomorphic wide-complex tachycardias but should not delay cardioversion in an unstable patient.
Option B is too slow for a patient with shock and altered mental status.
Option D is inappropriate because the patient is unstable and the rhythm may be ventricular tachycardia.
Study Guide:
The first question in tachycardia is whether the patient is hemodynamically stable.
Hypotension, altered mental status, ischemic symptoms, or shock indicate instability.
Unstable tachycardia with a pulse requires synchronized cardioversion.
Regular wide-complex tachycardia should be treated as ventricular tachycardia unless a supraventricular origin is clearly established.
Question 4. A 76-year-old man with hypertension and hyperlipidemia develops exertional dyspnea and intermittent exertional chest discomfort. Examination reveals a harsh crescendo-decrescendo systolic murmur at the right upper sternal border radiating to the carotids. Echocardiography shows an aortic valve area of 0.7 cm², mean gradient of 48 mm Hg, and LVEF of 58%. Which of the following is the most appropriate management?
A. Annual echocardiography without intervention
B. Surgical or transcatheter aortic valve replacement
C. Long-term nitrate therapy as definitive treatment
D. Balloon valvotomy as definitive therapy
Correct Answer: B. Surgical or transcatheter aortic valve replacement
Answer Explanation: Option B is correct because this patient has symptomatic severe aortic stenosis. An aortic valve area below 1.0 cm² together with a high transvalvular gradient establishes severe obstruction in the appropriate clinical context. Once severe aortic stenosis becomes symptomatic, valve replacement is indicated because medical therapy does not correct the fixed mechanical obstruction and symptomatic severe disease carries substantial risk of adverse outcomes. The choice between surgical and transcatheter replacement depends on age, anatomy, surgical risk, life expectancy, comorbidities, and patient preferences. Surveillance alone is inappropriate in symptomatic severe disease. Balloon valvotomy has a limited contemporary role, particularly as a bridge in selected patients rather than definitive treatment for degenerative adult aortic stenosis.
Why the other options are incorrect:
Option A is inadequate because the patient already has symptoms attributable to severe obstruction.
Option C does not correct the fixed valvular obstruction and should not be considered definitive therapy.
Option D generally provides temporary benefit and is not the standard definitive treatment for degenerative severe aortic stenosis.
Study Guide:
Severe aortic stenosis is defined using valve area, gradients, velocity, flow, and clinical context.
Symptoms such as exertional dyspnea, angina, or syncope are major management triggers.
Valve replacement is the definitive treatment for symptomatic severe AS.
The procedure should be individualized according to anatomy, operative risk, age, expected longevity, and preferences.
Question 5. A 59-year-old man with hypertension presents with episodic palpitations. His ECG during symptoms shows atrial fibrillation with a ventricular rate of 150/min. He has no chest pain, pulmonary edema, hypotension, or ischemic ECG changes. His CHA₂DS₂-VASc score is 2. Which of the following is the most appropriate long-term strategy?
A. Aspirin alone
B. No antithrombotic therapy because the AF is intermittent
C. Oral anticoagulation for stroke prevention
D. Long-term clopidogrel monotherapy
Correct Answer: C. Oral anticoagulation for stroke prevention
Answer Explanation: Option C is correct because stroke risk in atrial fibrillation is determined by established thromboembolic risk factors rather than whether AF is paroxysmal or persistent. This patient has sufficient risk to warrant oral anticoagulation, assuming there is no contraindication. Direct oral anticoagulants are generally preferred over warfarin for most patients with nonvalvular AF, although specific clinical circumstances may favor warfarin. Aspirin and clopidogrel are substantially less effective for prevention of AF-related embolic stroke and are not substitutes for anticoagulation when anticoagulation is indicated. Rate or rhythm control addresses symptoms and ventricular response but does not eliminate the need for stroke prevention when thromboembolic risk remains elevated.
Why the other options are incorrect:
Option A provides inadequate stroke prevention for a patient with an indication for oral anticoagulation.
Option B is incorrect because paroxysmal AF carries thromboembolic risk comparable to other AF patterns when risk factors are present.
Option D is not an adequate substitute for anticoagulation in AF-related stroke prevention.
Study Guide:
Do not use AF pattern alone to determine anticoagulation decisions.
Assess thromboembolic risk systematically and reassess it over time as clinical factors change.
Direct oral anticoagulants are commonly preferred in eligible patients with nonvalvular AF.
Anticoagulation and rate/rhythm control answer different clinical questions.
Question 6. A 67-year-old man presents with fever, malaise, and a new systolic murmur. He has a history of a prosthetic aortic valve. Blood cultures grow Staphylococcus aureus. Transesophageal echocardiography demonstrates a mobile vegetation with a small periannular abscess. Despite appropriate intravenous antibiotics, he develops new second-degree AV block. Which complication most directly explains the conduction abnormality?
A. Aortic root abscess extending into the conduction system
B. Acute pulmonary embolism
C. Left atrial enlargement
D. Functional mitral regurgitation
Correct Answer: A. Aortic root abscess extending into the conduction system
Answer Explanation: Option A is correct because new conduction abnormalities in a patient with infective endocarditis, particularly prosthetic-valve endocarditis involving the aortic valve, strongly suggest extension of infection into the periannular region. The atrioventricular conduction system lies close to the aortic annulus and membranous septum, making new AV block a warning sign for an aortic root or periannular abscess. Transesophageal echocardiography is particularly valuable for detecting prosthetic-valve complications. This is a high-risk complication that generally requires urgent multidisciplinary evaluation and often surgical intervention in addition to antimicrobial therapy. The other choices do not anatomically explain new AV conduction disease in this setting.
Why the other options are incorrect:
Option B can produce acute hemodynamic compromise but does not explain new AV block with a periannular abscess.
Option C may predispose to atrial arrhythmias but does not cause this conduction abnormality.
Option D can result from valve dysfunction but does not account for new AV block.
Study Guide:
New AV block during aortic-valve endocarditis is a major warning sign for periannular extension.
Prosthetic-valve endocarditis has a higher risk of abscess and invasive complications.
TEE is especially important when prosthetic material or complications are suspected.
Conduction abnormalities should prompt urgent evaluation for aortic root involvement.
Question 7. A 45-year-old woman with no previous cardiac history presents with exertional dyspnea and near-syncope. ECG shows sinus rhythm with voltage criteria for LV hypertrophy and deep T-wave inversions in the lateral leads. Echocardiography demonstrates asymmetric septal hypertrophy measuring 20 mm, systolic anterior motion of the mitral valve, and a resting LV outflow tract gradient of 70 mm Hg. Which medication is most appropriate for initial symptom control?
A. Nifedipine
B. Carvedilol
C. Digoxin
D. Isosorbide dinitrate
Correct Answer: B. Carvedilol
Answer Explanation: Option B is correct because the patient has obstructive hypertrophic cardiomyopathy with significant LV outflow tract obstruction. A nonvasodilating beta blocker is generally used initially to reduce heart rate, prolong diastolic filling, and decrease the dynamic obstruction associated with hypercontractility. Carvedilol may be used cautiously, although agent selection should account for its vasodilating properties; conventional nonvasodilating beta blockers such as metoprolol are often preferred. Vasodilators and medications that substantially reduce preload can worsen obstruction by decreasing LV cavity size. Digoxin may increase contractility and can aggravate dynamic obstruction. Persistent severe symptoms despite medical therapy may prompt consideration of advanced therapies at experienced HCM centers.
Why the other options are incorrect:
Option A can reduce afterload and worsen dynamic LV outflow obstruction in susceptible patients.
Option C increases contractility and may exacerbate the obstruction.
Option D decreases preload and can worsen the degree of dynamic obstruction.
Study Guide:
Obstructive HCM is highly sensitive to changes in preload and contractility.
Beta blockade can reduce symptoms by slowing heart rate and improving filling.
Avoid unnecessary preload reduction and positive inotropy in significant LVOT obstruction.
Persistent severe symptoms require assessment for specialized HCM therapies.
ABIM Cardiovascular Disease ECG/Imaging component
Question 8 — ECG. A 68-year-old man presents with sudden substernal chest pressure. The ECG shows ST-segment elevation in leads II, III, and aVF, with ST-segment depression in leads I and aVL. There is also ST-segment elevation in V4R. Which ECG diagnosis best explains the findings?
A. Acute inferior myocardial infarction with right ventricular involvement
B. Acute anterior myocardial infarction
C. Acute lateral myocardial infarction
D. Acute pericarditis
E. Posterior myocardial infarction alone
F. Acute pulmonary embolism
Best Answer: A
Answer Explanation:
The combination of ST elevation in II, III, and aVF with reciprocal depression in I and aVL identifies an acute inferior myocardial infarction. ST elevation in V4R indicates right ventricular involvement, most commonly from proximal right coronary artery occlusion. In an appropriate clinical setting, this ECG pattern should prompt urgent reperfusion management while avoiding therapies that markedly reduce preload if the patient is hypotensive. The right-sided lead is particularly useful because standard 12-lead ECG findings may not fully reveal RV involvement. The greater ST elevation in lead III than II also favors an RCA culprit in an inferior infarction.
Why the other options are incorrect:
B. Anterior infarction produces ST elevation primarily in V1–V4.
C. Lateral infarction produces changes in I, aVL, V5, and V6.
D. Pericarditis generally causes diffuse ST elevation with PR-segment changes rather than localized inferior elevation with reciprocal changes.
E. Posterior infarction produces ST depression in V1–V3 with posterior confirmation.
F. Pulmonary embolism does not produce this classic territorial ST-elevation pattern.
Study Guide:
Inferior STEMI is recognized by ST elevation in II, III, and aVF.
V4R elevation indicates right ventricular involvement.
Compare lead III with II and look for reciprocal changes when identifying the culprit territory.
Question 9 — ECG. A 74-year-old woman presents with palpitations and presyncope. The ECG demonstrates a regular tachycardia at approximately 150 beats/min. The QRS complexes are narrow. Between QRS complexes, sawtooth atrial activity is most clearly visible in the inferior leads. Which rhythm should be selected?
A. Atrial fibrillation
B. Typical atrial flutter with 2:1 AV conduction
C. AV nodal reentrant tachycardia
D. Sinus tachycardia
E. Multifocal atrial tachycardia
F. Ventricular tachycardia
Best Answer: B
Answer Explanation:
A regular narrow-complex tachycardia around 150 beats/min with characteristic sawtooth flutter waves in the inferior leads is typical atrial flutter with 2:1 AV conduction. The atrial rate is usually approximately 300 beats/min, with every second atrial impulse conducted to the ventricles. The regularity can make the rhythm resemble sinus tachycardia or AVNRT, particularly when flutter waves are hidden within the QRS or T waves. Careful inspection of the inferior leads and V1 may reveal the continuous atrial activity. Recognizing flutter is important because anticoagulation considerations follow the same general thromboembolic-risk framework used for atrial fibrillation.
Why the other options are incorrect:
A. AF produces an irregularly irregular ventricular response.
C. AVNRT is usually a regular narrow tachycardia without continuous sawtooth atrial activity.
D. Sinus tachycardia has discrete P waves preceding each QRS.
E. MAT has an irregular rhythm and at least three distinct P-wave morphologies.
F. VT is generally wide-complex.
Study Guide:
Typical flutter has an atrial rate near 300/min.
2:1 conduction commonly produces a ventricular rate near 150/min.
Inferior-lead flutter waves are a major diagnostic clue.
Question 10 — Echocardiogram. A patient with suspected constrictive pericarditis undergoes Doppler echocardiography. Mitral inflow demonstrates marked respiratory variation, with decreased early diastolic mitral inflow during inspiration. Tissue Doppler shows preserved or increased medial mitral annular e′ velocity. Which diagnosis is most likely?
A. Constrictive pericarditis
B. Restrictive cardiomyopathy
C. Severe isolated mitral stenosis
D. Dilated cardiomyopathy
E. Acute myocardial infarction
F. Hypertrophic obstructive cardiomyopathy
Best Answer: A
Answer Explanation:
Constrictive pericarditis produces abnormal ventricular interdependence because the rigid pericardium limits total cardiac volume. During inspiration, increased right-sided filling shifts the septum toward the LV and reduces LV filling, producing respiratory variation in mitral inflow. A preserved or increased medial mitral annular e′ velocity, sometimes called annulus reversus or paradoxus in appropriate contexts, can help distinguish constriction from myocardial restrictive disease. In restrictive cardiomyopathy, myocardial relaxation is impaired and tissue Doppler e′ is typically reduced. The diagnosis should be integrated with hepatic vein Doppler, septal motion, and clinical findings.
Why the other options are incorrect:
B. Restrictive cardiomyopathy generally causes reduced annular e′ rather than preserved medial relaxation.
C. Mitral stenosis produces fixed obstruction to transmitral flow.
D. Dilated cardiomyopathy produces chamber dilation and systolic dysfunction.
E. MI can impair relaxation but does not produce this characteristic ventricular interdependence.
F. HOCM produces dynamic LVOT obstruction rather than constrictive filling physiology.
Study Guide:
Constrictive pericarditis causes exaggerated ventricular interdependence.
Respiratory variation in mitral inflow is an important clue.
Preserved medial e′ helps distinguish constriction from myocardial restriction.
Question 11 — Coronary Angiogram. Coronary angiography demonstrates diffuse, transient narrowing of multiple epicardial coronary segments during an episode of chest pain. The narrowing resolves completely after intracoronary nitroglycerin. Which diagnosis is most likely?
A. Fixed multivessel atherosclerotic disease
B. Coronary vasospasm
C. Spontaneous coronary artery dissection
D. Coronary embolism
E. Left-main plaque rupture
F. Coronary artery fistula
Best Answer: B
Answer Explanation:
Diffuse or focal reversible narrowing of epicardial coronary arteries that resolves after intracoronary nitroglycerin is characteristic of coronary vasospasm. Vasospastic angina can cause transient myocardial ischemia and ST-segment elevation during episodes despite the absence of fixed obstructive disease. Calcium-channel blockers are the main preventive therapy, with nitrates used when needed. The dramatic angiographic response to nitroglycerin helps distinguish vasospasm from fixed atherosclerotic stenosis, SCAD, or thrombotic occlusion. Smoking is a major modifiable risk factor and should be specifically addressed.
Why the other options are incorrect:
A. Fixed atherosclerotic lesions do not disappear after nitroglycerin.
C. SCAD does not typically resolve immediately with vasodilation.
D. Embolic occlusion produces an abrupt filling defect or occlusion.
E. Plaque rupture does not produce completely reversible diffuse narrowing with nitroglycerin.
F. A fistula is an abnormal vascular connection rather than transient stenosis.
Study Guide:
Reversible epicardial narrowing strongly suggests coronary spasm.
Nitroglycerin can demonstrate reversibility during angiography.
Calcium-channel blockers are first-line preventive therapy.
Question 12 — ECG. A 66-year-old man presents with acute chest pain. The ECG shows ST-segment elevation in leads I and aVL with reciprocal ST-segment depression in leads III and aVF. Which myocardial territory is most likely involved?
A. Inferior wall
B. High lateral wall
C. Right ventricle
D. Posterior wall
E. Septal wall
F. Right atrium
Best Answer: B
Answer Explanation:
ST-segment elevation in leads I and aVL localizes acute ischemic injury to the high lateral myocardial territory. Reciprocal ST depression in the inferior leads strengthens the interpretation that these changes represent an acute coronary syndrome rather than nonspecific repolarization. The circumflex or a diagonal branch of the LAD can supply this territory depending on coronary anatomy. Lead aVL is particularly useful because it can reveal subtle high-lateral infarction that may be overlooked if attention is focused only on the standard precordial leads. Clinical symptoms, serial ECGs, and troponin measurements should be integrated with the ECG interpretation.
Why the other options are incorrect:
A. Inferior infarction primarily produces ST elevation in II, III, and aVF.
C. RV infarction is suggested by right-sided leads such as V4R.
D. Posterior infarction produces reciprocal anterior ST depression with tall R waves.
E. Septal injury generally involves V1–V2.
F. Right atrial disease does not produce this territorial ST-elevation pattern.
Study Guide:
Leads I and aVL represent the high lateral territory.
Reciprocal inferior ST depression supports acute ischemia.
Always examine aVL when localizing subtle lateral infarction.


