A 35-year-old man presents with exertional syncope and a family history of sudden cardiac death. Echocardiogram shows asymmetric septal hypertrophy with an interventricular septum of 22 mm, systolic anterior motion (SAM) of the mitral valve, and LVOT gradient of 65 mmHg at rest. The PRIMARY mechanism of syncope in this condition is:

• A Diastolic dysfunction causing pulmonary oedema
• B Mitral regurgitation causing left atrial hypertension
• C LV outflow tract obstruction causing reduced cardiac output during exertion ✓
• D Coronary artery spasm causing ischaemia

Explanation

Hypertrophic obstructive cardiomyopathy (HOCM) causes exertional syncope through dynamic LVOT obstruction, which worsens during exercise due to increased contractility, reduced preload (catecholamine-mediated vasodilation), and sympathetic activation — causing SAM of the mitral valve to contact the septum and further narrowing the LVOT. Reduced cardiac output during peak demand leads to syncope or near-syncope. This same mechanism explains why Valsalva manoeuvre worsens the murmur. Diastolic dysfunction contributes to symptoms but not the primary mechanism of syncope. Ventricular arrhythmias (VT/VF) are an additional mechanism for sudden death and syncope.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.