After acute myocardial infarction, left ventricular filling pressure is elevated because of systolic and/or diastolic dysfunction. The severity of the left ventricular dysfunction is influenced not only by infarct size and location but also by biochemical, neurohormonal, and peripheral vascular responses to infarction. Short-term vasodilator therapy improves left ventricular dysfunction and may influence favorably long-term prognosis in the presence of severe systolic dysfunction but not with predominant diastolic dysfunction. The chronic systolic dysfunction which may follow acute myocardial infarction also is influenced favorably by chronic vasodilator therapy.