Ventricular remodeling following myocardial infarction: a description of the pathologic process, current investigation, and suggested therapy.
The pathophysiologic process of ventricular remodeling after AMI involves an alteration in myocardial cell contraction. The stretching and redistribution of myocardial cells in the ischemic area promote dyssynergic contraction and an overall reduction in ventricular function. Expansion of the infarcted area and volume-overload hypertrophy of the uninfarcted area remodel the shape of the ventricle. Ventricular enlargement and dilation are associated with early mortality and morbidity. This has prompted further study to identify measures that can attenuate the process. Limited investigation on human subjects suggests that ACE inhibition reduces ventricular wall stress and preserves ventricular shape and function. A multicenter trial, SAVE, is under way to study the effects of long-term captopril therapy for patients suffering from AMI. This study and future investigations will focus on inhibition of ventricular remodeling following AMI in the hope of reducing symptomatic CHF and mortality.
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D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D006331:Heart Diseases / Q000517:prevention & control; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D009203:Myocardial Infarction / Q000451:nursing / Q000473:pathology* / Q000503:physiopathology*; D016276:Ventricular Function
D000806:Angiotensin-Converting Enzyme Inhibitors