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Restenosis after Arterial Injury Caused by Coronary Stenting in Patients with Diabetes Mellitus

Joseph P. Carrozza, MD; Richard E. Kuntz, MD; Robert F. Fishman, MD; and Donald S. Baim, MD
[+] Article and Author Information

From Beth Israel Hospital, Boston, Massachusetts. Requests for Reprints: Joseph P. Carrozza, Jr., MD, Cardiovascular Division, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215. Acknowledgment: The authors thank Ms. Cynthia Senerchia for assistance with data collection and analysis. Grant Support: In part by physician investigator award 13-603-901 from the Massachusetts Affiliate of the American Heart Association (Dr. Carrozza).


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1993;118(5):344-349. doi:10.7326/0003-4819-118-5-199303010-00004
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Objective: To determine whether diabetic patients, when compared with nondiabetic patients, have a higher incidence of restenosis after coronary stenting, and, if so, whether restenosis is attributable to lesion or procedural differences or to a greater biologic tendency for late loss of minimum diameter in diabetic patients.

Design: Case series.

Setting: Tertiary care referral center.

Patients: Two hundred twenty consecutive patients with coronary artery disease who were referred for placement of a Palmaz-Schatz stent in either a native coronary artery or a saphenous vein graft.

Results: Based on a traditional dichotomous definition of restenosis (≥ 50% stenosis at follow-up), lesions in diabetic patients had a significantly greater restenosis rate (55%) than lesions in nondiabetic patients (20%; P = 0.001). Vessel size, lesion length, pre-procedure lesion severity, procedural outcome, and acute gain (the difference between minimum lumen diameter before and after the procedure) were similar in the diabetic and nondiabetic groups. However, at follow-up, stents in diabetic patients had a smaller lumen diameter (1.66 ± 1.18 mm) compared with those in nondiabetic patients (2.24 ± 0.93 mm; P = 0.004), as well as a greater percent stenosis (49% compared with 32%; P = 0.002). Thus, the increased restenosis rate in stents in diabetic patients (55% compared with 20%; P = 0.001) is secondary to increased late loss of minimum lumen diameter (1.66 ± 1.28 mm compared with 1.23 ± 0.97 mm; P = 0.04).

Conclusions: After arterial injury produced by stent placement, diabetic patients have a significantly greater incidence of restenosis because of greater late loss at the treatment site. Because elastic recoil or vasospasm contributes little to stent restenosis, the increased late loss of minimum lumen diameter in diabetic patients suggests that they have a greater predisposition to intimal hyperplasia.

Figures

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Figure 1.
Restenosis in diabetic and nondiabetic patients according to the terms of the geometric model.

The model is described in the Methods section. The top of the bar shows the mean reference artery diameter, and the black area represents the minimum lumen diameter before treatment (pre-procedure). The incremental gain in lumen diameter before and immediately after stenting represents the acute gain. Late loss, calculated as the difference in minimum lumen diameter immediately after placement and at follow-up (hatched area), was significantly greater in diabetic patients.

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Figure 2.
Loss index in diabetic and nondiabetic patients.

The loss index is calculated as late loss divided by acute gain.

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Figure 3.
Cumulative distribution of percent stenosis in stents at follow-up for diabetic and nondiabetic patients.

Angiographic restenosis (50% diameter stenosis) was significantly greater in diabetic patients.

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