Angiogenesis, the formation of new blood vessels from existing ones, plays an essential role in embryonic development. However, once the vascular network is fully developed, angiogenesis is only triggered locally and transiently under specific conditions, being mainly hypoxia. Notorious pathological conditions in which angiogenesis plays a role are cardiovascular diseases and cancer.

Neovascularization of atherosclerotic plaques contributes to the development of the plaques, increasing the risk of rupture. The clinical complications of atherosclerosis, e.g. myocardial infarction (MI) and stroke, are mainly caused by thrombus formation, which results from rupture of an atherosclerotic plaque and exposure of tissue factor to the blood. The formed blood clot can then either locally occlude the blood vessel or embolize and occlude a narrower vessel downstream. In both cases this manifests itself in the clinical symptoms of MI or stroke. It is thought that intraplaque microvessels contribute to the unstable plaque phenotype. Therefore, research into intraplaque angiogenesis and development of specific molecular imaging tracers could enable to distinguish unstable from stable plaques.

In MI however, angiogenesis plays a much more benign role, allowing neovascularization following myocardial ischemia. For this reason, therapeutic myocardial angiogenesis is being explored as a therapeutic option in ischemic heart disease.