Aortic Stenosis vs Hypertrophic Cardiomyopathy
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.
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Side-by-side comparison
| Feature | Aortic Stenosis | Hypertrophic Cardiomyopathy |
|---|---|---|
| At a glance | Obstruction 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 presentation | Crescendo-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 labs | Standard CV labs: lipid panel, A1c, BMP, BNP; Pre-operative workup if AVR planned | Adult: maximum LV wall thickness ≥15 mm unexplained by loading conditions, or ≥13 mm with affected family member or positive genetic testing. LVOT gradient ≥30 mmHg at rest or ≥50 mmHg with provocation defines obstructive HCM.; Basic labs; consider genetic testing in proband and cascade screen of first-degree relatives; BNP/NT-proBNP… |
| Imaging | ECG: 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 treatment | Asymptomatic AS — no proven benefit from medical therapy to slow progression; Treat concomitant HTN cautiously (avoid afterload reduction that worsens output across fixed obstruction); preferred agents: ACEi/ARB at low dose, titrated carefully; Lipid-lowering therapy does NOT slow progression of calcific AS (multiple negative trials);… | Avoid dehydration, alcohol, sudden standing, and intense competitive athletics (per 2020 ACC/AHA — shared decision-making for participation); Symptomatic obstructive HCM: non-vasodilating beta-blocker (metoprolol, atenolol, propranolol) titrated to symptoms and HR; Non-dihydropyridine CCB (verapamil, diltiazem) if beta-blocker not… |
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