Nifedipine and conventional therapy for unstable angina pectoris: a randomized, double-blind comparison.

Abstract

To characterize the potential of nifedipine in the therapy of unstable angina pectoris we implemented a blinded, randomly assigned, titrated schedule of conventional therapy (propranolol, if not contraindicated, and isosorbide dinitrate) or nifedipine for 14 days in 126 patients hospitalized in a coronary care unit for ischemic chest pain of less than 45 min duration. There were no significant differences between conventionally and nifedipine-treated patients with regard to (1) the time to relief of pain as judged by life table analysis, (2) the decrease in anginal attacks per 24 hr from day 0 to day 2 ( -2.5 + 0.4 for conventional therapy vs; -2.8 + 0.3 for nifedipine), (3) the decrease in the number of nitroglycerin tablets consumed per 24 hr ( -2.0 ± 0.5 for conventional vs -2.1 ± 0.4 for nifedipine therapy), (4) the percentage of patients requiring morphine on day 1 (1 3% for conventional vs 21 % for nifedipine therapy), or (5) the percentage of patients who developed infarction (1 4% in both groups). Among the 27 patients who did not respond to initial conventional (n = 13) or nifedipine therapy (n = 14), five in each group became pain free when the opposite therapy (either nifedipine or conventional therapy) was added. In the subgroup of 67 patients who were receiving propranolol before randomization, addition of nifedipine was more effective in controlling pain than was an increase in conventional therapy (p = .026). In the subgroup of 59 patients not receiving prior propranolol, initiation of conventional therapy produced more rapid pain relief than initiation of nifedipine therapy alone (p < .001), which tended to increase heart rate. Thus, for the study population as a whole therapy with nifedipine alone was equivalent to conventional therapy for unstable angina, although this overall equivalence may result from a combination of superiority of nifedipine therapy in patients previously receiving ,/-blocker therapy and superiority of /3-blocker therapy in patients not previously receiving ,3-blockers. Circulation 69, No. 4, 728-739, 1984. UNSTABLE ANGINA, a syndrome intermediate in severity between stable angina pectoris and acute myocardial infarction, is well recognized. Heberden,' in his classic description of angina pectoris, noted that in some cases the pain occurred in patients at rest. Her-

Coronary vasomotor and clinical effects of nifedipine in effort, mixed and Prinzmetal angina

“…Several aspects, however, support the consistency of our findings: evaluation for each patient of the control level of attack frequency during the placebo period, which was compared with the attack frequency observed during nifedipine therapy: short duration of the trial which reduced the likelihood of coincidence with spontaneous remission [14]; and evidence that the clinical response in some cases was dose-related. This study confirms that: no pattern of the coronary atherosclerotic process is characteristic of the three forms of angina, and extent and severity of the disease do not predict the clinical response to calcium channel blockade [15,16]; patients with Prinzmetal angina exhibit a significantly more favorable response than those with classic exertional angina [17]; nifedipine fails to relieve exertional angina in a considerable number of cases [17,18] and is not better in treating mixed angina than in treating purely exertional angina [19]; therapy may be associated with increased angina frequency [10,17,18,20,21]; coronary segments of both normal and stenotic vessels show either increase, decrease, or no change in diameter in response to the calcium channel blocker [22][23][24]. Our main goal was to evaluate whether there is a relationship between the acute coronary vasomotor influences of nifedipine and the clinical response to treatment.…”

Meta-analyses of antihypertensive therapy: Are some of them misleading?

“…In one of the studies incorporated in the analysis, the authors included only short-term (2-week) rather then 6-month mortality [9,10]. Re-analysis, using 6-month data, led to disappearance of the statistical significance [8].…”

Nifedipine in acute myocardial infarction: an assessment of left ventricular function, infarct size, and infarct expansion. A double blind, randomised, placebo controlled trial.

“…'5 The initial preratment thallium scores in the nifedipine (7-8 (0.7) units) and placebo (7)(8)(9) (0-7) units) groups did not differ. The day 10 thallium score was lower in both groups and also did not differ significantly (nifedipine 5-3 (0-7), placebo 5-3 (0-7)).…”