Cell and molecular events comprising collateral vessel development and remodeling (19.1)

Abstract

Although the relevance of coronary collaterals was debated for many years, more recent studies utilizing more acurate methods for measuring collateral flow have shown that collateral flow can minimize infarct size. The development of coronary collateral vessels by pressure gradients (fluid shear stress), involving the recruitment of multiple genes, including VEGF and FGF, is well documented. However, there is also more recent evidence that ischemia, independent of elevated shear stress can also stimulate collateral growth under certain conditions. Collateral growth is a form of arteriogenesis that involves: 1) endothelial deformation, 2) increases in NOS and NO, 3) VEGF activation of MCP‐1, 4) monocyte and T‐cell recruitment and migration and 5) remodeling of the vessel. The remodelinig process requires proliferation of endothelial cells and vascular smooth muscle, which results in an increase in vessel diamter. Important stimuli for collateral growth include brief, repeated, as well as gradual coronary artery occlusions.