Mechanism of angioplasty and its relation to restenosis

Balloon angioplasty enlarges atherosclerotic narrowings in the vast majority of patients in whom it is attempted at an acceptably low complication rate. Experimental and human pathologic studies have confirmed that angioplasty enlarges the lumen by stretching the vessel wall. Often this stretching process causes plaque fracture due to inelastic components of the atheroma. Denudation of the endothelium is also a consistent observation. While enlarging the lumen, this vascular trauma promotes marked platelet adhesion and aggregation that is dependent on the degree of vascular damage. Most platelets accumulate early within the first few hours. Subsequently, thrombus formation and smooth muscle cell proliferation can occur with the formation of a new fibrocellular occlusive process. Experimentally, antiplatelet therapy can significantly reduce platelet deposition and can reduce the incidence of restenosis. Although restenosis is a multifactoral process, prevention seems possible when platelet accumulation, thrombus formation and smooth muscle cell proliferation can be inhibited through drug or mechanical means.