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Hypertrophic cardiomyopathy is a disease caused by a number of mutations in the genes encoding cardiac sarcomeric proteins[1]. Twenty-five percent of patients with hypertrophic cardiomiopathy have evidence of obstruction of the left ventricular outflow tract[2]. Diastolic dysfunction and myocardial ischaemia are pathophysiological features of the disease responsible for reduced exercise capacity and functional limi-tation[3,4]. The physiological significance of left ventricu-lar outflow tract obstruction is still not fully confirmed. Increased left ventricular filling pressure, documented in patients with hypertrophic obstructive cardiomyopathy during exercise[5], suggests that left ventricular outflow tract obstruction contributes to exercise limitation. Patients with hypertrophic obstructive cardio-myopathy frequently complain of exertional dyspnoea, angina, and syncope. The therapeutic options for theEuropean Heart Journal (2000) 21, 770–777 doi:10.1053/euhj.1999.1905, available online a