Evolution of infarct size during the early use of nifedipine in patients with acute myocardial infarction: the Norwegian Nifedipine Multicenter Trial.

In a multicenter double-blind study, 227 patients with suspected acute myocardial infarction (AMI) were randomized within 12 hr from onset of symptoms to treatment with nifedipine (112 patients) or placebo (115 patients). AMI was confirmed in 74 patients on nifedipine and in 83 on placebo. Patients with AMI received nifedipine 5.5 +/- 2.9 hr (mean +/- SD) after onset of symptoms. Infarct size was assessed by the release of creatine kinase isoenzyme MB (CK-MB). Infarct size index (CK-MB geq/m2) was 25 +/- 16 (n = 71) in the nifedipine group and 23 +/- 13 (n = 77) in the placebo group (NS). After the first 10 mg of nifedipine systolic blood pressure fell from 147 +/- 30 to 135 +/- 28 mm Hg (p less than .01) and heart rate rose from 75 +/- 18 to 79 +/- 19 beats/min (p less than .01). No change was observed after the first placebo dose. The treatment was continued for 6 weeks. Over this period there were 10 deaths in each group. Early treatment with nifedipine in patients with AMI does not seem to reduce infarct size as determined by enzyme level.

The antithrombotic effect of heparin in deep venous thrombosis: relation to four heparin assays.

In a prospective study, 280 patients with phlebographically proven deep venous thrombosis received intravenous heparin infusion; 224 of the patients were subjected to control phlebography after 5-8 days of treatment. Females above 70 years showed least phlebographic improvement despite similar heparin dosage and heparin activity. Heparin activity in daily drawn blood samples was determined by four different assays. Chromogenic substrate (CS) assay (Coatest heparin), activated partial thromboplastin time (Cephotest), and thrombin time with recalcified plasma (CaTT) showed weak but significant correlations with thrombus resolution judged by phlebography (p = 0.004, 0.003 and 0.018, respectively). A linear prediction equation showed that the phlebographic result was about equally influenced by the mean dose and by the result of any of the three heparin assays. Thrombin time with citrated plasma showed no correlation. CS assay and CaTT showed significantly lower mean heparin activity in patients with (n = 13) than without clinically diagnosed pulmonary embolism (p = 0.012 and 0.001, respectively).