Pravastatin in acute ischaemic syndromes: results of a randomised placebo-controlled trial.

Therapy with individual 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) has been shown conclusively to diminish coronary event rates and mortality in both primary and secondary prevention. To date, scant attention has been paid to whether initiation of such regimens in the hospital phase of acute coronary syndromes might confer cardioprotective benefits. The purpose of this study was to determine the safety and tolerability of early initiation of statin therapy in patients with acute coronary syndromes. In this randomised, double-blind, three-month, pilot study, 100 patients with acute myocardial infarction or unstable angina and low-density lipoprotein cholesterol > 3.5 mmol/l were randomly assigned to pravastatin 40 mg daily or placebo initiated within 48 hours of hospital admission. Pravastatin proved safe and well tolerated in these patients, who were well matched at baseline. No statistically significant differences in death, MI and drug-related adverse events were observed in the pravastatin group compared with control subjects. This pilot study shows that therapy with pravastatin early after an acute coronary event is safe and well tolerated. Larger, long-term studies are needed to confirm these findings.

Atrial natriuretic peptide after myocardial infarction.

Plasma concentrations of atrial natriuretic peptide (ANP) after acute myocardial infarction were measured at fixed times during 48 hours in 38 patients admitted to the hospital within 4.4 hours after the onset of symptoms. Three hours after admission, the mean concentration of ANP was significantly lower than that at the time of admission. Thereafter it rose steadily until 15 hours after admission. ANP concentrations measured in each patient at the time of admission and the individual mean ANP concentrations during the first 48 hours after admission correlated weakly but significantly with the size of the infarct and the left ventricular function. Neither the site of the infarct, the occurrence of reperfusion, nor the number of coronary vessels affected influenced the ANP concentration. In 24 patients in whom cardiac catheterization was performed, no relationship between ANP concentrations and left ventricular pressures was observed. Determination of ANP concentrations seems to be of little value in assessing cardiac function after acute myocardial infarction.

Reciprocal changes in atrial natriuretic peptide levels and plasma renin activity during treatment of pulmonary embolism.

We followed atrial natriuretic peptide (ANP) levels in 12 patients during anticoagulant treatment of pulmonary embolism. In each patient with this disorder ANP decreased during treatment. Concomitantly, plasma renin activity (PRA) markedly rose. The decrease in ANP was significantly related to the rise in PRA. No consistent changes in ANP or in PRA were observed in five patients with peripheral venous thrombosis receiving the same anticoagulant treatment. Plasma aldosterone levels did not change in either group.