Abstract

Twenty-seven hospitalized patients with typical variant angina were studied to evaluate the efficacy of nifedipine, diltiazem and verapamil in blocking ergonovine-induced episodes of variant angina and to determine if the results of incremental ergonovine testing during treatment correlated with the clinical response. The ergonovine test result was positive (that is, with S-T elevation) in all 27 patients during a control period without medication. During a subsequent treatment period with nifedipine (20 mg every 6 hours), the test result converted to negative at the maximal ergonovine dose of 0.4 mg in 11 patients, remained positive but at two or more ergonovine dose levels higher than those during the control test in 11, and was unimproved in 5 other patients. Identical results occurred when ergonovine tests were repeated during treatment with diltiazem, 120 mg every 8 hours. During treatment with verapamil, 160 mg every 8 hours, the test result was negative in 8 patients, positive at two or more ergonovine dose levels higher than those during the control test in 10 patients and positive at a dose similar to that of the control test in the remaining 9. Variant anginal attacks occurred during none of the 30 drug treatment periods associated with a negative ergonovine test, during only 1 of the 24 treatment periods associated with a positive test at high ergonovine dose levels (0.2 to 0.4 mg), and during 12 of the 27 treatment periods with a positive test at 0.1 mg or less of ergonovine ( p <0.001). During the 7 month (range 1 to 15) follow-up period, 14 of 15 patients treated with a drug that had converted the ergonovine test response to negative remained angina-free, compared with only 4 of 12 treated with a drug associated with a persistently positive test ( p <0.01). Thus, nifedipine, diltiazem and verapamil can partially or totally block ergonovine-induced angina and S-T elevation in most patients with variant angina. The results of ergonovine testing during treatment with these drugs correlate with the clinical response to therapy.

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