Confusable diagnoses · PANCE / PANRE

Aortic Stenosis vs Hypertrophic Cardiomyopathy

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

Aortic Stenosis and Hypertrophic Cardiomyopathy are easy to mix up on the boards. Here's a side-by-side comparison — presentation, workup, imaging, and first-line treatment — drawn from our full outlines.

Aortic Stenosis vs Hypertrophic Cardiomyopathy at a glance

  • Aortic Stenosis: Obstruction to LV outflow; classic SAD triad (Syncope, Angina, Dyspnea) signals need for AVR.
  • Hypertrophic Cardiomyopathy: Genetic LVH (often asymmetric septal) with dynamic LVOT obstruction — leading cause of SCD in young athletes.

Try two board-style questions on Aortic Stenosis vs Hypertrophic Cardiomyopathy

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Question 1CardiovascularEasy
A 72-year-old woman with severe aortic stenosis develops new symptoms. Which symptom triad in severe aortic stenosis (AS) is a Class I indication for aortic valve replacement?
  • AOrthopnea, hepatomegaly, and ascites
  • BFatigue, palpitations, and peripheral edema
  • CPalpitations, night sweats, and weight loss
  • DAngina, syncope, and dyspnea
Reveal answer & full explanation
Correct answer: D — Angina, syncope, and dyspnea
  • AOrthopnea, hepatomegaly, and ascites
  • BFatigue, palpitations, and peripheral edema
  • CPalpitations, night sweats, and weight loss
  • DAngina, syncope, and dyspnea✓

Why Angina, syncope, and dyspnea is correct

  • The classic aortic stenosis (AS) symptomatic triad is angina, syncope (often exertional), and dyspnea/heart failure
  • Onset of any symptom in severe AS markedly worsens prognosis: median survival is 5 years with angina, 3 years with syncope, and 2 years with dyspnea without intervention
  • Onset of any of these symptoms is a Class I indication for valve replacement

Why the others are wrong

  • A) Orthopnea, hepatomegaly, and ascites — these are signs of right heart failure (HF) and are unrelated to the classic AS symptomatic triad
  • B) Fatigue, palpitations, and peripheral edema — this nonspecific cluster suggests atrial fibrillation or right-sided volume overload; none of the three is part of the triad whose onset defines symptomatic severe AS and triggers a Class I indication
  • C) Palpitations, night sweats, and weight loss — constitutional symptoms of this kind point toward infective endocarditis or malignancy rather than the outflow obstruction symptoms that mandate valve replacement
Question 2CardiovascularMedium
A 21-year-old man with hypertrophic cardiomyopathy is being risk-stratified for sudden cardiac death. Which feature most strongly supports the placement of an implantable cardioverter-defibrillator for primary prevention?
  • AResting left ventricular outflow tract (LVOT) gradient of 25 mmHg
  • BMaximal left ventricular (LV) wall thickness of 14 mm
  • CSymmetric septal hypertrophy
  • DFamily history of sudden cardiac death in a first-degree relative
Reveal answer & full explanation
Correct answer: D — Family history of sudden cardiac death in a first-degree relative
  • AResting left ventricular outflow tract (LVOT) gradient of 25 mmHg
  • BMaximal left ventricular (LV) wall thickness of 14 mm
  • CSymmetric septal hypertrophy
  • DFamily history of sudden cardiac death in a first-degree relative✓

Why family history of sudden cardiac death in a first-degree relative is correct

  • Under the 2024 AHA/ACC hypertrophic cardiomyopathy (HCM) guideline, a primary-prevention implantable cardioverter-defibrillator (ICD) is reasonable when there is ≥1 major sudden cardiac death (SCD) risk factor: HCM-related sudden death in a first-degree or close relative ≤50 years old, unexplained syncope suspected to be arrhythmic, massive left ventricular (LV) hypertrophy (≥30 mm), LV apical aneurysm, or LV ejection fraction <50%.
  • In adults, nonsustained ventricular tachycardia on monitoring and extensive late gadolinium enhancement on cardiac magnetic resonance (CMR) are weaker modifiers used only when the ICD decision is otherwise uncertain; abnormal blood pressure response to exercise is no longer part of risk stratification.

Why the others are wrong

  • Resting left ventricular outflow tract (LVOT) gradient of 25 mmHg — A low resting LVOT gradient of 25 mmHg does not by itself justify an ICD.
  • Maximal left ventricular (LV) wall thickness of 14 mm — Mild hypertrophy of 14 mm does not by itself justify an ICD; the threshold for massive hypertrophy is ≥30 mm.
  • Symmetric septal hypertrophy — Symmetric vs asymmetric hypertrophy is a morphologic description, not a risk marker for SCD.
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Side-by-side comparison

FeatureAortic StenosisHypertrophic Cardiomyopathy
At a glanceObstruction to LV outflow; classic SAD triad (Syncope, Angina, Dyspnea) signals need for AVR.Genetic LVH (often asymmetric septal) with dynamic LVOT obstruction — leading cause of SCD in young athletes.
Classic presentationCrescendo-decrescendo systolic ejection murmur at RUSB radiating to carotids, pulsus parvus et tardus, late-peaking murmur in severe disease.; Classic SAD triad (onset of any symptom marks severe AS and dramatically worsens prognosis):; • Syncope — exertional; from inability to augment CO across fixed obstruction; • Angina — from…Often asymptomatic; HCM detected on screening or after sudden death of a family member; Exertional dyspnea, fatigue (most common symptom); Anginal chest pain; Palpitations, presyncope, syncope (especially exertional — ominous); Sudden cardiac death may be the first manifestation; Brisk, bisferiens carotid pulse (spike-and-dome);…
Workup / key labsStandard CV labs: lipid panel, A1c, BMP, BNP; Pre-operative workup if AVR plannedAdult: maximum LV wall thickness ≥15 mm unexplained by loading conditions, or ≥13 mm with affected family member or positive genetic testing. Obstructive HCM = peak LVOT gradient ≥30 mmHg at rest or with provocation (Valsalva, standing, exercise); ≥50 mmHg is hemodynamically significant and is the threshold for septal reduction therapy…
ImagingECG: LVH with strain (left precordial T-wave inversions), left atrial enlargement, occasionally LBBB or AV block from septal calcification; CXR: cardiomegaly late; aortic root calcification visible on lateral; Transthoracic echocardiogram (KEY DIAGNOSTIC TEST):; • Mild: AVA >1.5 cm², mean gradient <20 mmHg, peak velocity <3 m/s; •…Transthoracic echo — diagnostic; document septal thickness, LVOT gradient at rest and with provocation (Valsalva, exercise), SAM, MR; Cardiac MRI with late gadolinium enhancement — extent of fibrosis and SCD risk stratification, mass quantification, apical HCM identification; ECG — LVH with strain, deep narrow Q waves (septal…
First-line treatmentAsymptomatic AS — no proven benefit from medical therapy to slow progression; Treat concomitant HTN per standard guideline-directed therapy (ACEi/ARB acceptable), starting at a low dose and titrating slowly with close BP monitoring (Class 1); avoid abrupt preload reduction such as nitrates in severe AS; Lipid-lowering therapy does NOT…Avoid dehydration, excess alcohol, and sudden standing; mild-to-moderate exercise is encouraged, and vigorous or competitive sports are decided by shared decision-making with an HCM expert rather than blanket disqualification (2024 AHA/ACC); Symptomatic obstructive HCM: non-vasodilating beta-blocker (metoprolol, atenolol, propranolol)…

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Full outlines

Aortic Stenosis Hypertrophic Cardiomyopathy (HCM) All 514 diagnoses

Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.