ABSTRACT
The natural growth of collateral blood vessels in response to physiologically significant arterial luminal narrowing is a complex process, involving multiple cells and growth factors acting in an orchestrated and time-dependent manner.1-3 Local factors such ashypoxia, shear stress and inflammation stimulate angiogenesis, while systemic factors such as diabetes mellitus, aging and hypercholesterolemia have been clearly demonstrated to retard these reparative mechanisms.4-8 Although collateral bloodflow can reduce myocardial ischemia and infarct size, typically less than half of the normal maximal bloodflow is restored and thus, in a substantial number of patients, anginal symptoms persist. Despite great progress in the treatment of cardiovascular disease, there are increasing numbers of patients with advanced symptomatic coronary artery disease not amenable to conventional revascularization techniques. Current estimates suggest that 5-10% of patients referred to tertiary centers for coronary interventions are currently considered as ‘no-option’ patients and hence are potential candidates for therapeutic angiogenesis.
