Modification of left ventricular response to pacing tachycardia by nifedipine in patients with coronary artery disease

The calcium blocking agent nifedipine was shown to protect the isolated left ventricle against the development of altered diastolic compliance during severe global ischemia. To assess the influence of nifedipine during myocardial ischemia in human subjects, we studied the effect of nifedipine (20 mg sublingually) on the hemodynamic response to pacing tachycardia (heart rate 66 ± 4 to 143 ± 4 beats per minute) in 17 patients with multivessel coronary artery disease. Typical anginal pain occurred in all patients during pacing tachycardia before nifedipine, but in only 3 of 17 patients during pacing after nifedipine. In 11 patients a significant (≥ 5 mm Hg) increase in postpacing left ventricular end-diastolic pressure (LVEDP, 15 ± 2 mm Hg to 28 ± 2 mm Hg, p < 0.01) developed, and was associated with an upward shift of the left ventricular diastolic pressure-volume curve. In these patients, pretreatment with nifedipine did not alter resting LVEDP or aortic pressure, but did attenuate or abolish the increase in LVEDP and the shift in left ventricular diastolic pressure-volume curves after pacing tachycardia to the same rate and for the same duration. The antianginal effect of nifedipine was not associated with a reduction in contractility, because there was no change in LV + dp/dt after nifedipine. However, the increase in left ventricular systolic pressure achieved in response to pacing tachycardia was less after nifedipine. We conclude that nifedipine favorably modifies the symptomatic and hemodynamic response to pacing tachycardia in patients with coronary artery disease. The mechanism is uncertain and could involve a direct myocardial effect, peripheral vasodilation, coronary vasodilation or a combination of these effects.