Pathogenesis of restenosis.

Reopening of atherosclerotic vessels by a growing number and variety of intraluminal devices inflicts different degrees and types of trauma. The vascular wall responds acutely with sealing by activation of the clotting system, and in the long term with healing by migration, proliferation and synthetic activity of vascular wall cells. This is a physiologic response, and the astonishing capability of vascular tissue to restore a new channel in this way leads to permanent patency in over 70% of the interventions. In restenosis, the responses are similar in type, but different in degree: exuberant activation of the sealing mechanisms results in thrombosis and immediate occlusion, and excessive healing responses result in intimal hyperplasia and obstruction of the lumen within several months. The signals and factors involved in the initiation and, more importantly, in the termination of such responses are discussed. Although many of the factors capable of limiting an exaggerated and persistent cellular reaction are not yet known, adequate blood flow seems to play an important role in determining when the healing response should stop and the scar should stabilize.