Pathogenesis of restenosis. A correlation of clinical observations with cellular responses

Angioplasty enlarges the lumen of atherosclerotic arteries, but also causes trauma and a response to injury in the form of fibrocellular intimal hyperplasia. Migration and growth of smooth muscle cells is a healing and repair process, filling the tissue gaps and molding a new lumen according to the local hemodynamic conditions. In addition to these reactive fibrocellular parts, tissue removed from restenosis sites also contains large amounts of old plaque components, as well as fresh thrombotic material, indicating that loose parts of the old vessel wall can contribute substantially to the restenosis by displacement as well as by their thrombogenicity. Excessive catheter trauma favors this reocclusion process by creating large dissections; however, insufficient dilatation does not leave enough space for the necessary fibrocellular healing. Current instrumentation cannot yet control the extent of the trauma well enough, and many proposed follow-up medical treatments aimed at preventing a variety of suspected restenosis mechanisms have not substantially improved the restenosis rate. So far, the most successful treatment of restenosis has been repeat angioplasty, often repeated several times, with excellent final results.