L-transposition of the great arteries presenting as severe preeclampsia.
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Biomedical subjects
D H Serfas
Publications and source records attributed to D H Serfas.
Nifedipine and conventional therapy for unstable angina pectoris: a randomized, double-blind comparison.
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 (13% for conventional vs 21% for nifedipine therapy), or (5) the percentage of patients who developed infarction (14% 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 less than .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 beta-blocker therapy and superiority of beta-blocker therapy in patients not previously receiving beta-blockers.
Angina Pectoris↗
Nifedipine therapy for patients with threatened and acute myocardial infarction: a randomized, double-blind, placebo-controlled comparison.
Preliminary clinical and laboratory observations suggest that nifedipine might prevent progression of threatened myocardial infarction by reversing coronary spasm or might limit necrosis during the course of acute myocardial infarction. We screened 3143 patients with ischemic pain of greater than 45 min duration and randomly assigned 105 eligible patients with threatened myocardial infarction and 66 with acute myocardial infarction to receive nifedipine (20 mg orally every 4 hr for 14 days) or placebo plus standard care. Treatment was started 4.6 +/- 0.1 hr after the onset of pain. Infarct size index was calculated by the MB-creatine kinase (CK) method and expressed as CK-geq/m2 +/- SE. The incidence of progression to infarction among patients with threatened myocardial infarction was not significantly altered by nifedipine (36 of 48 [75%] for placebo-treated and 43 of 57 [75%] for nifedipine-treated patients). Furthermore, infarct size index was similar among placebo- and nifedipine-treated patients (16.9 +/- 1.5 MB-CK-geq/m2, n = 65, and 17.0 +/- 1.5 MB-CK-geq/m2, n = 68, respectively) with threatened myocardial infarction who exhibited infarction and for those with acute myocardial infarction. Among the 171 eligible patients randomly assigned to drug or placebo, 6 month mortality did not differ significantly (8.5% for placebo vs 10.1% for nifedipine, NS), but mortality in the 2 weeks after randomization was significantly higher for nifedipine-treated patients (0% for placebo compared with 7.9% for nifedipine, p = .018).(ABSTRACT TRUNCATED AT 250 WORDS)
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