Acute myocardial infarction (AMI) is characterized by regional myocardial damage which may lead to systolic and diastolic dysfunction with a subsequent risk of left ventricular (LV) remodeling, local and systemic neurohormonal activation, vascular dysfunction and development of heart failure. The pathophysiology and prognosis of LV systolic dysfunction after AMI has been the focus of research for several decades. Insights from these studies have led to several therapeutic interventions that improve outcome. In addition to depressed systolic function, clinical or radiographic evidence of heart failure is a consistent and powerful predictor of outcome in patients following AMI. Pulmonary congestion after AMI reflects raised LV filling pressures but is frequently seen after what appears to be only minor myocardial damage. The pathophysiological mechanism for this is incompletely understood but may involve impaired active relaxation of the myocardium and increased LV chamber stiffness, hence, abnormalities in diastolic function. Abnormal LV diastolic function especially when chamber stiffness is increased is characterized by a disproportionate increase in filling pressure during exercise and an inadequate increase of cardiac output. During ventricular diastole the left atrium acts as a conduit between the left ventricle and the pulmonary veins. Thus in case of increased filling pressures left atrial pressure is elevated exposing the pulmonary vascular bed to increased pressures. In accordance pulmonary artery pressure is frequently increased after AMI, even when systolic function is preserved.