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Efficacy of calcium channel blocker therapy for angina pectoris resulting from small-vessel coronary artery disease and abnormal vasodilator reserve.

Abnormal vasodilator reserve of the coronary microcirculation is a frequent mechanism of angina pectoris in patients with angiographically normal coronary arteries. To assess the effect of calcium channel blocking agents on symptoms and exercise capacity, 26 patients shown to have angina pectoris because of abnormally small coronary arteries and limited vasodilator reserve underwent randomized, double-blind, placebo-controlled outpatient study, with 1 month for each period. An unblinded lead-in phase determined the best dose of verapamil (17 patients) or nifedipine (9 patients). Exercise testing using bicycle ergometry was performed at the end of each period. Four patients interrupted the placebo period and 1 patient interrupted both placebo and drug period because of frequent and severe chest pain. While receiving calcium channel blocker drugs, patients who completed both phases of the study recorded fewer episodes of angina (21 +/- 21 vs 35 +/- 27, p less than 0.001) and consumed fewer nitroglycerin tablets (23 +/- 27 vs 41 +/- 50, p less than 0.001) than during the placebo period. Exercise duration was slightly but significantly prolonged (278 +/- 129 vs 231 +/- 136 seconds, p less than 0.025) during drug treatment compared with placebo, and significantly fewer patients terminated exercise with chest pain while receiving drug treatment. Subjectively, 22 of 26 patients felt better on the calcium channel blocker than on placebo. Thus, calcium channel blocker therapy appears to be beneficial in controlling angina and improving exercise tolerance in patients with angina pectoris resulting from abnormally small coronary arteries and limited vasodilator reserve.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Influence of rifampicin on antihypertensive effects of dihydropiridine calcium-channel blockers in four elderly patients].

Rifamicin, an antituberculosis agent, is one of the most potent inducers of hepatic drug-oxidation enzymes. Rifampicin can reduce the efficacy of several therapeutically important drugs (including verapamil and diltiazem) by accelerating systemic elimination or by increasing hepatic first-pass metabolism. Because dihydropyridine calcium-channel blockers are mainly metabolized by the liver, rifampicin may also increase the extraction of these drugs and thereby reduce their antihypertensive effects. Here we report four possible cases of interaction between rifampicin and dihydropiridine calcium-channel blockers. Rifampicin was given to treat tuberculosis in four elderly hypertensive patients whose blood pressure was well-controlled by one or more dihydropiridine calcium-channel blockers (nisoldipine, nifedipine, or barnidipine and manidipine), shortly after the start of antituberculosis therapy, their blood pressures rose. Either much greater doses of dihydropyridines or additional antihypertensive agents had to be given to keep blood pressure under control. After withdrawal of rifampicin, blood pressure fell in all patients and the doses of the antihypertensive agents had to be reduced. These findings indicate that rifampicin may lessen the antihypertensive effects of dihydropiridine calcium-channel blockers.

Aged↗

[Calcium channel blockers in the treatment of ischemic heart disease].

After a brief review of the pathophysiological properties of calcium channel blockers on the ischaemic heart muscle the author deals with the therapeutic effect of blockers on coronary spasms and at the same time on vasodilatation of arteries in the systemic circulation. Their effect is manifested also by the favourable action on the arteriosclerotic process proper, the clinically significant retardation of atherogenesis, stabilization of atherosclerotic plaques. The author pays special attention to the new calcium channel blocker-amlodipine which as to its pharmacokinetic properties is superior to all hitherto used types of blockers.

Calcium Channel Blockers↗