Infarct expansion (IE) and ventricular remodelling (VR) are interdependent pathophysiologic processes in the heart following acute myocardial infarction (AMI), and may contribute to dilatation of the left ventricle, heart failure, left ventricular aneurysm and/or rupture, and poor prognosis. IE and VR are demonstrated by echocardiography, and are usually seen with large, transmural, anterior AMI, hypertension and persisting occlusion of the infarct-related coronary artery. All myocardial tissue components are involved in IE and VR, and local generation of growth factors, vasoactive mediators, oxygen-derived free radicals, and activation of the renin-aldosterone-angiotensin system may have pathophysiological significance. These mechanisms can provide the opportunity for therapy, and evidence suggests that treatment with angiotensin converting enzyme-inhibitors can attenuate IE and VR.