Acute myocardial infarction can produce alterations in the topography of the left ventricle both in the infarcted and remote areas. These changes as a whole, have been termed ventricular remodelling. Attention has been focused on myocyte alterations due to the remodelling process, but the myocardial wall also contains fibroblasts, which produce collagen and elastin fibers, and endothelial and smooth muscle cells which are the main constituents of the vascular wall. In left ventricular hypertrophy, a form of myocardial remodelling, structural changes of myocytes, cardiac interstitium as well as the coronary microcirculation have been found (vascular remodelling). In vivo, the function of coronary microcirculation can be evaluated by measuring myocardial blood flow and coronary reserve. In fact the study of coronary reserve in patients with left ventricular hypertrophy disclosed microcirculatory dysfunction which probably represents the functional counterpart of the structural changes already described. Positron emission tomography (PET) can noninvasively quantitate myocardial blood flow and coronary reserve in humans. Recently studies with PET disclosed microcirculatory alterations also in patients with coronary artery disease (CAD) in the absence of gross myocardial hypertrophy. In particular, after myocardial infarction, coronary vasodilator capacity has been shown to be impaired not only in the infarcted areas but also in the remote ones subtended by angiographically normal vessels. A blunted coronary reserve has been identified with PET also in remote regions from ischemia in patients with stable angina and single vessel CAD.