The effect of 20 mg dose of intravenous verapamil was studied over a range of heart rates in 12 patients with hypertrophic cardiomyopathy. Six patients had an appreciable left ventricular outflow tract gradient and six did not. The drug reduced myocardial oxygen consumption in proportion to a reduction in the development of left ventricular pressure. The negative inotropic effect of verapamil was counteracted by the drug's non-specific vasodilator activity, so that cardiac index was unaltered at any heart rate and as a result myocardial efficiency was unaffected by the drug. Verapamil did not consistently alter myocardial metabolism. Some patients showed improvement in anaerobic myocardial metabolism after verapamil but an equal number showed impairment of lactate metabolism. It was not possible to predict from clinical features, echocardiographic findings, or haemodynamic variables measured before administration of verapamil which patients would demonstrate haemodynamic or metabolic improvement after the drug. In this short term study no mechanism was demonstrated by which patients with hypertrophic cardiomyopathy might obtain a consistent improvement from treatment with verapamil.
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