Platelet-vessel wall interactions in the development of restenosis after coronary angioplasty

Acute occlusion and restenosis of the dilated coronary segment remain serious unsolved complications that can occur after coronary angioplasty. Acute occlusion is seen in approximately 3-5% of patients and restenosis in 13-47% of patients undergoing this procedure. While the causes of these complications are incompletely understood, platelets and their interactions with the vessel wall appear to be important. The mechanism of stenosis dilatation involves a splitting or tearing of the atherosclerotic plaque as well as desquamation of the endothelial layer of the vessel wall. Therefore, superficial as well as deep arterial injury occurs as a result of angioplasty. Acute occlusion and restenosis appear to be the biological response to this injury. Following even subtle injury to the endothelial layer, platelets adhere to the vessel wall and become activated, releasing substances such as platelet derived growth factor which stimulates intimal hyperplasia and re-growth of the atherosclerotic plaque. Deeper injury results in increased platelet deposition and mural thrombus formation. Rheologic factors including oscillatory shear forces and high local shear rates resulting from residual stenosis and intimal dissection further promote platelet activation and thrombus formation. Both the rheologic factors and the thrombogenic properties of the vessel wall and circulating blood promote restenosis and acute occlusion. Studies using animal models have demonstrated that platelet inhibitor drugs used in addition to heparin can reduce the amount of platelet deposition at the time of angioplasty, and may have a favorable effect on the occurrence of acute occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)