Mechanism of relief of pacing induced angina with oral verapamil: reduced oxygen demand.

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Abstract
To evaluate the influence of oral verapamil (80 and 120 mg) on angina threshold, coronary blood flow, myocardial oxygen consumption and left ventricular function, we subjected 13 patients with effort angina and fixed obstructive coronary artery disease to atrial pacing at progressively higher heart rates. After 120 mg of verapamil, the time to onset of angina and the heart rate at the onset of ST-segment depression increased by 18% (p less than 0.005) and 10% (p less than 0.001), respectively, without any change in the angina threshold (rate-pressure product at the onset of angina). The rate-pressure product, coronary blood flow and myocardial oxygen consumption were lower at rest and at pre-angina heart rates but not when the angina threshold was reached. Thus, the beneficial effect of verapamil was primarily due to decreased myocardial oxygen demand rather than to increased coronary blood flow. The decreased demand resulted from a lower arterial pressure at each pacing rate. In these patients without heart failure, left ventricular pump function did not deteriorate. This beneficial response was less with 80 mg of oral verapamil. These findings suggest that oral verapamil has a potential role in the management of patients with effort angina due to fixed obstructive coronary artery disease.