Clinical benefit of angiotensin converting enzyme inhibition after acute myocardial infarction: myocardial reperfusion revisited. 1996

J Renkin
Division of Intensive Care, University of Louvain Medical School, St Luc University Hospital, Brussels, Belgium.

BACKGROUND Beneficial effect has been reported from angiotensin converting enzyme (ACE) inhibition after acute myocardial infarction (AMI) in several experimental and large clinical studies showing improvements in haemodynamics, left ventricular remodelling and mortality. However, this benefit has not been prospectively evaluated after AMI effectively reperfused using current coronary recanalization techniques. OBJECTIVE The clinical relevance of reperfusion therapies including thrombolysis or percutaneous transluminal coronary angioplasty relates to their ability to limit infarct size and left ventricular dysfunction and reduce infarct-related morbidity and mortality. The clinical issue is to determine whether ACE inhibitors should be routinely proposed as an adjunct therapy in patients with a patent infarct-related vessel after AMI. Three placebo-controlled randomized trials addressed this issue in evaluating the left ventricular remodelling process (i.e. left ventricular volumes and ejection fraction changes) during a 3 to 4-month follow-up period. The Captopril and Thrombolysis Study and the Captopril plus Tissue plasminogen activator after Myocardial Infarction trials failed to show any significant preventive effect of early captopril therapy on remodelling in patients admitted for anterior AMI and treated with conventional use of streptokinase and alteplase, respectively. In the Salvage from Perindopril in Reperfused Infarction Trial, no beneficial effect on global left ventricular remodelling was observed from perindopril therapy in a population with effective myocardial reperfusion confirmed at angiography and moderately depressed left ventricular function. However, in this study ACE inhibition seemed to favourably alter remodeling in a subgroup of AMI patients with anterior location and large infarct size despite successful reperfusion. CONCLUSIONS Recommendation for ACE inhibition as a routine adjunct therapy to reperfusion techniques is not supported by current data on short-term left ventricular function changes.

UI MeSH Term Description Entries
D009203 Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION). Cardiovascular Stroke,Heart Attack,Myocardial Infarct,Cardiovascular Strokes,Heart Attacks,Infarct, Myocardial,Infarction, Myocardial,Infarctions, Myocardial,Infarcts, Myocardial,Myocardial Infarctions,Myocardial Infarcts,Stroke, Cardiovascular,Strokes, Cardiovascular
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000806 Angiotensin-Converting Enzyme Inhibitors A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. ACE Inhibitor,ACE Inhibitors,Angiotensin Converting Enzyme Inhibitor,Angiotensin I-Converting Enzyme Inhibitor,Angiotensin-Converting Enzyme Inhibitor,Kininase II Inhibitor,Kininase II Inhibitors,Angiotensin I-Converting Enzyme Inhibitors,Angiotensin-Converting Enzyme Antagonists,Antagonists, Angiotensin-Converting Enzyme,Antagonists, Kininase II,Inhibitors, ACE,Inhibitors, Angiotensin-Converting Enzyme,Inhibitors, Kininase II,Kininase II Antagonists,Angiotensin Converting Enzyme Antagonists,Angiotensin Converting Enzyme Inhibitors,Angiotensin I Converting Enzyme Inhibitor,Angiotensin I Converting Enzyme Inhibitors,Antagonists, Angiotensin Converting Enzyme,Enzyme Antagonists, Angiotensin-Converting,Enzyme Inhibitor, Angiotensin-Converting,Enzyme Inhibitors, Angiotensin-Converting,II Inhibitor, Kininase,Inhibitor, ACE,Inhibitor, Angiotensin-Converting Enzyme,Inhibitor, Kininase II,Inhibitors, Angiotensin Converting Enzyme
D015425 Myocardial Reperfusion Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY. Coronary Reperfusion,Reperfusion, Myocardial,Coronary Reperfusions,Myocardial Reperfusions,Reperfusion, Coronary,Reperfusions, Coronary,Reperfusions, Myocardial
D016277 Ventricular Function, Left The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance. Left Ventricular Function,Function, Left Ventricular,Functions, Left Ventricular,Left Ventricular Functions,Ventricular Functions, Left

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