ABSTRACT
The two major clinical targets for therapeutic angiogenesis in humans at present are cardiac and peripheral skeletal muscle. Chronic myocardial ischemia is almost universally caused by atherosclerotic coronary artery disease (CAD) and may manifest as ‘‘angina pectoris’’, an exertional chest discomfort that is relieved by rest. In more severe cases myocardial ischemia may manifest as angina with minimal exertion or even at rest, life-threatening ischemic dysrhythmia, and/or reversible ischemic myocardial dysfunction. Finally, small-vessel disease or microvascular dysfunction may also cause chronic myocardial ischemia. Importantly, while increases in myocardial perfusion would be expected to attenuate the adverse impact of an acute myocardial infarction, the biological time-scale for angiogenesis probably exceeds the time required to salvage myocardium, but BFGF could be considered as an agent that can block apoptosis and thereby have a beneficial effect on the long-term outcome of this disease.
