Author + information
- Received March 18, 1986
- Revision received September 10, 1986
- Accepted October 1, 1986
- Published online April 1, 1987.
- ↵‡Address for reprints: Robert M. Califf, MD, P.O. Box 31123, Duke University Medical Center, Durham, North Carolina, 27710.
Although initial success rates for coronary angioplasty have improved, the rate of restenosis within 6 months of the procedure has persisted at 30 to 40%. The relation of restenosis to initial success, recurrence of symptoms and risk factors suggests that high grade or total lesions, long lesions, lesions in the proximal left anterior descending artery or in saphenous grafts, and the absence of intimai dissection after angioplasty are associated with an increased risk of restenosis. Unstable angina, male sex and diabetes are clinical factors associated with a greater risk of restenosis. Pathologic specimens suggest that plaque splitting and disruption are found acutely after angioplasty, but that restenosis occurs as an ex- cessive reparative, proliferative response of smooth muscle cells leading to recurrent luminal narrowing.
A prospective analysis of therapeutic interventions to prevent restenosis, such as administrating antiplatelet and lipid-lowering agents, intensive diabetic therapy and administration of calcium antagonists, is proposed. Problems with timing of studies, design and sample size are considered. Current recommendations for antirestenosis therapy include antiplatelet therapy before and after angioplasty, administration of heparin in some patients and intensive risk factor intervention for the 6 months after the procedure.
- Received March 18, 1986.
- Revision received September 10, 1986.
- Accepted October 1, 1986.
- American College of Cardiology Foundation