(Circulation. 2006;113:414-419.)
© 2006 American Heart Association, Inc.
Interventional Cardiology |
From the Department of Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul (M.-K.H., C.W.L., D.-W.P., K.-M.P., B.-K.L., Y.-H.K., J.-M.S., K.-H.H., D.-H.K., J.-K.S., J.-J.K., S.-W.P., S.-J.P.) and GangNeung (S.-S.C.), Korea, and Cardiovascular Research Foundation (G.S.M.), New York, NY.
Correspondence to Seung-Jung Park, MD, PhD, Departments of Medicine, University of Ulsan College of Medicine, Cardiac Center, Asan Medical Center, 388-1 Poongnap-dong, Songpa-gu, Seoul, 138-736, Korea. E-mail sjpark{at}amc.seoul.kr
Received May 19, 2005; revision received October 7, 2005; accepted November 4, 2005.
Background Late stent malapposition (LSM) after drug-eluting stent (DES) implantation has not been evaluated sufficiently in real-world practice.
Methods and Results We evaluated the incidence, mechanisms, predictors, and long-term prognosis of LSM after DES implantation in 557 patients (705 native lesions; sirolimus-eluting stent in 538 lesions and paclitaxel-eluting stent in 167 lesions) in whom intravascular ultrasound was performed at index and 6-month follow-up. LSM occurred in 82 patients with 85 lesions (12.1% overall, 95% CI 9.7% to 14.5%, 71 lesions (13.2%) in sirolimus-eluting stents and 14 lesions [8.4%] in paclitaxel-eluting stents, P=0.12]; the incidence was 25.0% (4/16) after directional coronary atherectomy before stenting, 27.5% (14/51) in chronic total occlusion lesions, and 31.8% (7/22) after primary stenting in acute myocardial infarction (P=0.13, P<0.001, and P=0.001, respectively, versus elective stenting with conventional balloon predilation, 9.7% [60/616]). There was an increase of external elastic membrane area (from 17.1±3.6 to 21.4±4.8 mm2, P<0.001) that was greater than the increase in plaque area (from 9.3±2.5 to 10.5±2.7 mm2, P<0.001). Independent predictors of LSM were total stent length, primary stenting in acute myocardial infarction, and chronic total occlusion lesions. Except for 1 death in the non-LSM group, there were no major adverse cardiac events in either LSM or non-LSM patients during a mean 10-month follow-up after detection of LSM.
Conclusions LSM occurs in 12% of cases after DES implantation. The predictors of LSM are total stent length, primary stenting in acute myocardial infarction, and chronic total occlusion lesions. LSM after DES implantation was not associated with any major adverse cardiac events during a subsequent 10-month (mean) follow-up.
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