Pathophysiology of collateral development.

The formation of collateral arteries in patients suffering from occlusive atherosclerotic vascular diseases has been frequently reported. The growth of these collateral arteries has been termed 'arteriogenesis'. Clinical observations and investigations using various animal models support the hypothesis that the mechanism of arteriogenesis is based on the remodelling of pre-existing collateral anastomoses. This process seems to be mainly triggered by fluid shear stress which is induced by the altered blood flow conditions after an arterial occlusion. Early arteriogenesis involves the activation of collateral endothelial cells, the attraction of leukocytes to the collateral vascular wall and subsequently their invasion into the perivascular space of the collateral vessel. In a second phase, proliferation of vascular cells is initiated by growth factors mainly released from accumulated leukocytes. Furthermore, tissue degradation and changes in the extracellular matrix are observed. Unravelling the mechanisms of arteriogenesis is crucial to the development of successful therapeutic approaches for the treatment of patients with ischemic vascular diseases.