Audience: cardiology clinicians and trainees. Evidence reviewed: September 2026.
Key message
In symptomatic obstructive hypertrophic cardiomyopathy (HCM), first confirm that dynamic left-ventricular outflow-tract (LVOT) obstruction explains the symptoms. Treatment then proceeds from physiology-aware medical therapy to specialist myosin-inhibitor or septal-reduction strategies, while sudden-death risk is assessed on a separate track.
1. Confirm the phenotype and mechanism
- Document maximal wall thickness, distribution of hypertrophy and LV systolic/diastolic function.
- Identify systolic anterior motion, mitral–septal contact and the mechanism/severity of mitral regurgitation.
- Measure resting and provoked LVOT gradients with correctly aligned CW Doppler. Exercise stress echocardiography is valuable when symptoms and resting/Valsalva gradients disagree.
- Use CMR for anatomy, apical disease, scar burden and alternative diagnoses.
- Exclude important mimics and contributors such as hypertension, valve disease, coronary disease, anaemia and arrhythmia.
2. Define what limits the patient
Record NYHA class, exertional chest pain, presyncope/syncope, palpitations and exercise capacity. Review volume status, blood pressure and drugs that reduce preload or afterload. New atrial fibrillation can sharply worsen filling and symptoms and requires prompt rhythm/rate and anticoagulation assessment.
3. Start physiology-directed treatment
A non-vasodilating beta-blocker is generally first-line for symptoms attributable to obstruction. Verapamil or diltiazem may be considered when beta-blockers are ineffective or not tolerated, but caution is required with hypotension, severe obstruction or advanced congestion. Disopyramide can reduce obstruction when added under expert supervision, with attention to anticholinergic effects and QT prolongation.
| Step | Decision | Safety focus |
|---|---|---|
| Initial drug | Non-vasodilating beta-blocker | Heart rate, blood pressure, conduction disease |
| Alternative | Verapamil or diltiazem in selected patients | Hypotension, pulmonary congestion, drug interactions |
| Add-on | Disopyramide in expert care | QT interval and anticholinergic burden |
| Advanced option | Cardiac myosin inhibitor where licensed and appropriate | Serial LVEF, interactions and mandated monitoring |
4. Escalate persistent severe symptoms
Patients with substantial symptoms despite maximally tolerated therapy should be referred to an experienced HCM centre. Options include a cardiac myosin inhibitor and septal reduction. Surgical myectomy is preferred when concomitant cardiac surgery or complex mitral/subvalvular anatomy requires correction. Alcohol septal ablation is an alternative for selected anatomy and risk profiles. Operator and centre experience materially affect outcomes.
5. Run parallel risk pathways
Sudden-cardiac-death risk assessment is not replaced by symptom control or gradient reduction. Evaluate previous cardiac arrest or sustained ventricular tachycardia, unexplained syncope, family history, maximal wall thickness, apical aneurysm, LV systolic dysfunction, non-sustained ventricular tachycardia and CMR scar within the applicable guideline framework. Also address genetics and family screening, atrial fibrillation, stroke prevention, pregnancy, exercise and endocarditis advice.
Selected references
- 2024 AHA/ACC multisociety HCM guideline.
- 2024 HCM guideline—PubMed record.
- 2023 ESC cardiomyopathy guideline.
Educational material only. Myosin-inhibitor and septal-reduction decisions require specialist HCM-centre assessment and current local prescribing guidance.
The Cardiac Compass 