Early ACE-inhibition in myocardial infarction. Possible role of bradykinin.
Restoration of coronary blood flow in the ischemic myocardium is absolutely needed to prevent irreversible cellular damage but on the other hand may have potentially hazardous consequences. Since thrombolysis during myocardial infarction is designed to salvage a maximal number of myocardial cells threatened by ischemia, a concommitant intervention which reduces cellular damage due to reperfusion will improve the net result of such procedure. The adjunctive use of ACE-inhibitors with thrombolytic therapy early during acute myocardial infarction offers theoretic advantages. This article summarizes the results indicating that ACE-inhibitors do play an important role in cardioprotection in the acute phase of myocardial ischemia followed by reperfusion. Probably, their effect on bradykinin breakdown is at least partly responsible for this effect.
van Gilst
W H
WH
Department of Clinical Pharmacology, University of Groningen, The Netherlands.
de Graeff
P A
PA
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001920:Bradykinin / Q000502:physiology*; D003326:Coronary Circulation / Q000187:drug effects; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy*; D011453:Prostaglandins / Q000378:metabolism
D000806:Angiotensin-Converting Enzyme Inhibitors; D011453:Prostaglandins; D001920:Bradykinin