Noninvasive evaluation of the effect of timolol on left ventricular performance after myocardial infarction and the consequence for prognosis.

Left ventricular performance was evaluated noninvasively in 111 patients participating at one study center in the Norwegian Multicenter Study on Timolol After Myocardial Infarction. Systolic time intervals were measured in 55 patients treated with timolol and in 56 patients receiving placebo. Measurements were made before randomization, and after 1, 3 and 12 months of treatment. During the treatment period, the pre-ejection period/left ventricular ejection time ratio was significantly lower in the timolol-treated group, indicating better left ventricular function than in the placebo-treated patients. In the 27 patients who died during the follow-up period of 50 to 72 months, there was a significant increase in the pre-ejection period/left ventricular ejection time ratio from baseline to the last performed recording, indicating a deterioration in left ventricular performance in these patients. No such change occurred in the group that survived the entire follow-up period. Deterioration of left ventricular function is related to a high long-term mortality rate after myocardial infarction, and left ventricular function is better preserved in patients treated with timolol than in patients receiving placebo.

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.

Systolic time intervals in acute myocardial infarction.

Systolic time intervals (STI) have been measured in 50 individuals without heart disease. Electromechanical systole (QS2), left ventricular ejection time (LVET) and preejection period (PEP), but not PEP/LVET, were correlated to heart rate (HR). Regression equations were made and used when correcting STI for HR in two groups of patients: a) 51 patients with acute myocardial infarction (AMI) b) 22 patients with chest pains, but no AMI. STI was measured on the first 4 days, on the 7th day, on the day of discharge and at a control about 60 days later. In the AMI group there was a reduction in left ventricular performance from the 1st to the 4th day, and the difference in shortening of LVET was significant (p less than 0.001), while PEP and PEP/LVET increased from the 1st to the 3rd day (p less than 0.001). Between the AMI and the control groups there were significant differences (p less than 0.001) in LVET and PEP/LVET on the 3rd, 4th and 7th day, and in PEP on the 3rd and 4th day. STI was not found to separate clinical groups with heart failure of different severity. The survivors had a lower (p less than 0.05) PEP/LVET on the 1st day than those who died. The various localization of the infarction made no difference in STI. LVET was found to be strongly correlated (p less than 0.001) to the hydroxybutyric dehydrogenase values.