Left ventricular function after coronary artery reperfusion

Abstract

Left ventricular dysfunction and dilation after reperfusion relate to the amount of infarcted and dysfunctional myocardium and will continue to be important determinants of morbidity and mortality. There is marked heterogeneity in the anatomic and pathophysiologic presentation of patients with acute myocardial infarction prior to thrombolyste, and many of these individual settings resemble those in animal species with various degrees of collateral formation. Three major determinants of infarct size are responsible for this heterogeneity and include the risk area, the duration of the coronary occlusion, and the level of the residual coronary blood flow via collaterals or a partially patent artery. All 3 of these determinants will influence the initial and late results of reperfusion therapy on infarct size and ventricular function. However, in addition to late or unsuccessful thrombolysis, there are other important factors determining outcome: inadequate reflow, residual coronary stenosis, and coronary reocclusion, factors that can be associated with late progressive left ventricular dilation and dysfunction. The risk factors for left ventricular dysfunction and dilation after reperfusion can now be identified, and such patients should undergo coronary angiography prior to hospital discharge and, if appropriate, revascularization of the infarct-related artery (and perhaps other vessels). In other patients, if serial studies reveal progressive left ventricular failure and dilation late after reperfusion, despite therapy with an angiotensin-converting enzyme (ACE) inhibitor, and if repeat coronary angiography identifies significant coronary stenoses and areas of hibernating or stunned myocardium, revascularization may limit progression of dilation and improve left ventricular function. Thus, many events occur during the evolution of myocardial infarction and after thrombolysis for which treatment is possible, and there is good reason to expect that left ventricular function can be improved well beyond the modest increase now observed with thrombolytic therapy. This, in turn, could have a further significant impact on morbidity and mortality after reperfusion.