RESTENOSIS is both bane and embarrassment to cardiologists. Despite the effectiveness of percutaneous transluminal coronary angioplasty (PTCA) as a means of treating coronary artery disease, its long-term benefits remain tempered by restenosis, which develops in 30% to 50% of patients within 6 months after the procedure is done.
During the nearly 2 decades that PTCA has been performed, cardiologists have attempted to decrease this disconcerting number, proposing various theories and devising trials to test them. Studies recently reported at the American College of Cardiology meeting in Orlando, Fla, make evident the need to revise traditionally held views on the pathophysiology of restenosis. Obviously, a better understanding of how and why restenosis occurs is key to finding rational ways of preventing or treating it.
The prevailing view is that the angioplasty procedure damages the coronary wall, leading to platelet activation, which causes vascular smooth muscle cells to proliferate and