Prevention of Left Ventricular Remodeling After Myocardial Infarction.

摘要: Postinfarction left ventricular remodeling begins early after acute myocardial infarction and may continue for months to years afterward. Early re-establishment of flow in the occluded artery is associated with smaller cavity volumes reduced remodeling. Acute percutaneous coronary intervention (PCI) or thrombolytic therapy (for patients more than 1 hour away from a catheterization facility) as possible symptoms critical. Late reperfusion (PCI 12 hours infarction) prove useful, this will be determined by results ongoing clinical trials. Recurrent MI antiplatelet agents (aspirin most patients) 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Intravenous nitroglycerin limit (initial 24 hours) dilatation following infarction, but long-term use asymptomatic not efficacious. Betaadrenergic receptor antagonists angiotensin-converting enzyme (ACE) inhibitors have independent efficacy attenuating late phases The combined beta-blocker an ACE inhibitor has greater either agent alone, provided they are tolerated hemodynamically. Although angiotensin II similar fewer side effects, blockers should reserved intolerant In requiring diuretic therapy, spironolactone preferred because its salutary properties regarding extracellular matrix remodeling, specifically reducing fibrosis. Surgical revascularization without mitral valve repair useful selected severe ischemic regurgitation hibernating myocardium. New therapies directed at modulating process focus on manipulating components reduce deleterious impact process.