[Remodeling of the left ventricle after myocardial infarction].
Cardiac remodeling following myocardial infarction denotes changes of left ventricular shape, chamber size and wall thickness. It involves both the infarcted and the noninfarcted segments. This process begins at the time of acute myocardial infarction, progresses by stages, and can lead to congestive heart failure. The major determinants of lest ventricular remodeling are infarct size and transmural, adequacy of the healing process, mechanical deformation forces, and progressive ventricular dilation. Infarct expansion is a relatively frequent, early occurring alteration of the ventricular shape. It denotes thinning and lengthening of the infarct segment. The progressive ventricular remodeling can be halted by reactive hypertrophy of the viable myocytes, on condition that it is appropriate. The left ventricular increase results from myocytes hypertrophy, partly their hyperplasia, and increase of fibrosis. Major ways of action in order to limit the cardiac remodeling after myocardial infarction are: reperfusion of the infarct-related vessel by thrombolysis, nitrate therapy, and angiotensin-converting enzyme inhibitors administration. Maximum benefit is when therapy is begun very early.
Droździak
E
E
Kliniki Choroby Wieńcowej Instytutu Kardiologii CMUJ w Krakowie.
Piwowarska
W
W
D000222:Adaptation, Physiological; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology*; D009203:Myocardial Infarction / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology
D000806:Angiotensin-Converting Enzyme Inhibitors
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