Limitation of infarct size by decrease of afterload with prazosin.
To investigate the possibility of limiting infarct size by decreasing afterload 32 normotensive patients with uncomplicated acute myocardial infarction (AMI) were put on prazosin and compared with 32 control patients. Blood pressure fell significantly lower in the prazosin group without increase of heart rate. The mean daily and peak levels of serum aspartate transaminase and lactic dehydrogenase and the calculated from the 12 lead ECG mean daily sum of ST segment elevation, number of leads with ST greater than or equal to 0.1 mV, mean ST elevation, number of new Q waves greater than or equal to 0.03 s and the loss of height of R waves were significantly less in the prazosin group. ST segment re-elevation occurring on 2nd-3rd day in the control group was absent or minimal in the prazosin group. The enzyme levels and the change of the ECG variables correlated fairly well with the change of blood pressure. These findings indicate that, at least in the selectively good risk cases of our material, reduction of afterload without increase of heart rate induced by prazosin may favorably influence the balance of myocardial oxygen supply and demand early in AMI and prevent death of jeopardized ischaemic tissue, thus limiting the final extent of the infarct.
D000328:Adult; D000368:Aged; D001219:Aspartate Aminotransferases / Q000097:blood; D004562:Electrocardiography; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy*; D011224:Prazosin / Q000627:therapeutic use*; D011799:Quinazolines / Q000627:therapeutic use*
D011799:Quinazolines; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D011224:Prazosin