Local Lesion-Related Factors and Restenosis After Coronary Angioplasty
Evidence From a Quantitative Angiographic Study in Patients With Unstable Angina Undergoing Double-Vessel Angioplasty
Background Restenosis rates are high when coronary angioplasty is performed in patients with unstable angina. The relative contributions of local and systemic factors to this excess risk of restenosis are unclear. To assess these, we compared changes in minimal lumen diameter and the incidence of restenosis, determined by quantitative coronary angiography, after coronary angioplasty at culprit and nonculprit lesions dilated in the course of a single procedure in patients with unstable angina.
Methods and Results We identified 67 consecutive patients with unstable angina in whom two lesions, in different vessels, were dilated during the same procedure. Lesions were designated as culprit or nonculprit on the basis of the location of ECG changes during chest pain combined with assessment of the angiographic characteristics of the lesions. With these criteria, 43 patients had identifiable culprit lesions. Stenosis severity before and immediately after angioplasty and at follow-up was assessed with quantitative angiography. Angiographic follow-up was performed in 91% (39 patients) of this subgroup. Culprit lesions were more severe (P<.02) than nonculprit lesions. The late loss at culprit lesions (0.87±0.75 mm) was significantly (P<.01) greater than the equivalent value for nonculprit lesions (0.33±0.69 mm). With a categorical definition (>50% stenosis at follow-up), restenosis occurred at 67% of culprit lesions and at 32% of nonculprit lesions (P<.01).
Conclusions The greater loss in minimal lumen diameter and the consequent higher rate of restenosis at culprit compared with nonculprit lesions suggest that local “lesion-related” factors are an important determinant of the high rate of restenosis when coronary angioplasty is performed in patients with unstable angina.
- Received June 20, 1994.
- Revision received August 30, 1994.
- Accepted September 23, 1994.
- Copyright © 1995 by American Heart Association