Author + information
- Received July 12, 2017
- Revision received August 29, 2017
- Accepted September 6, 2017
- Published online October 23, 2017.
- Robert W. Yeh, MD, MSca,b,∗ (, )
- Dean J. Kereiakes, MDc,
- P. Gabriel Steg, MDd,e,f,
- Donald E. Cutlip, MDa,b,
- Kevin J. Croce, MD, PhDg,
- Joseph M. Massaro, PhDb,h,
- Laura Mauri, MD, MScb,g,
- on behalf of the DAPT Study Investigators
- aRichard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Beth Israel Deaconess Medical Center, Boston, Massachusetts
- bBaim Institute for Clinical Research, Boston, Massachusetts
- cChrist Hospital Heart and Vascular Center and the Lindner Center for Research and Education, Cincinnati, Ohio
- dUniversité Paris-Diderot, INSERM U-1148, Paris, France
- eHôpital Bichat, Département Hospitalo-Universitaire FIRE, Assistance Publique–Hôpitaux de Paris, Paris, France
- fNHLI, Imperial College, Royal Brompton Hospital, London, United Kingdom
- gBrigham and Women’s Hospital, Boston, Massachusetts
- hBoston University School of Public Health, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. Robert W. Yeh, Richard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Beth Israel Deaconess Medical Center, 375 Longwood Avenue, 4th Floor, Boston, Massachusetts 02215.
Background Subjects undergoing coronary stenting with complex lesion anatomy may experience different risks and benefits with prolonged dual antiplatelet therapy.
Objectives The authors assessed the effect of 30 months versus 12 months of dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) based on the presence or absence of anatomically-complex target lesions.
Methods In the DAPT Study, combined myocardial infarction (MI) or stent thrombosis and moderate/severe bleeding were assessed in enrolled (n = 25,416) and randomized (n = 11,554) subjects. Complex lesions had any of the following characteristics: unprotected left main, >2 lesions/vessel, length ≥30 mm, bifurcation with side branch ≥2.5 mm, vein bypass graft, or thrombus-containing lesion. Events were evaluated according to increasing number of complexity characteristics and compared according to DAPT score.
Results Enrolled subjects with more complex target lesions had higher rates of MI or stent thrombosis in the first 12 months after PCI (3.9% vs. 2.4%; p < 0.001). Among those who were event-free at 12 months, rates of MI or stent thrombosis between 12 and 30 months were similar between those with versus without complex anatomy (3.5% vs. 2.9%; p = 0.07). Reduction of MI or stent thrombosis with continued thienopyridine beyond 12 months versus placebo was similar for subjects with (2.5% vs. 4.5%; hazard ratio: 0.55; 95% confidence interval: 0.38 to 0.79; p = 0.001) and without (2.0% vs. 3.8%; hazard ratio: 0.52; 95% confidence interval: 0.39 to 0.69; p < 0.001) anatomic complexity (pinteraction = 0.81), as was increase in moderate/severe bleeding (pinteraction = 0.44). Among subjects with anatomic complexity, those with DAPT scores ≥2 randomized to continued thienopyridine had greater reductions in MI or stent thrombosis (3.0% vs. 6.1%; p < 0.001) compared with subjects with scores <2 (1.7% vs. 2.3%; p = 0.42; p value comparing risk differences = 0.03).
Conclusions Complex target-lesion anatomy is associated with increased ischemic events, particularly within the first year after PCI. Among those without events in the first 12 months, the benefits of extending DAPT were similar in subjects with and without complex lesions. A high DAPT score identified those experiencing the most benefit from extended treatment among patients with and without complex anatomy. (The Dual Antiplatelet Therapy Study [DAPT Study]; NCT00977938)
- complex lesions
- dual antiplatelet therapy
- dual antiplatelet therapy score
- percutaneous coronary intervention
This study was sponsored by the Baim Institute for Clinical Research; and was funded by Abbott, Boston Scientific Corporation, Cordis Corporation, Medtronic, Inc., Bristol-Myers Squibb Company/Sanofi Pharmaceuticals Partnership, Eli Lilly and Company, Daiichi Sankyo Company Limited, and the U.S. Department of Health and Human Services (1RO1FD003870-01). Dr. Yeh has received research funding from Boston Scientific and Abiomed; and has served as a consultant for Abbott Vascular and Boston Scientific. Dr. Kereiakes has served as a consultant for and received research funding from Boston Scientific Corporation and Abbott Vascular. Dr. Steg has received research grants from Merck, Sanofi, and Servier; has received consulting fees from Amarin, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi-Sankyo, Janssen, Lilly, Merck, Novartis, Pfizer, Regeneron, Sanofi, and Servier; and has received speaking fees from Amgen, AstraZeneca, Bayer, Bristol-Myers Squibb, Merck, Pfizer, Regeneron, and Sanofi. Dr. Cutlip has received contracted research support from Medtronic, Celonova, and Boston Scientific. Dr. Mauri has received grant funding from Amgen, Abbott, Boston Scientific, Boehringer Ingelheim, Biotronik, Corvia, and Recor; has received honoraria from Daiichi-Sankyo and Sanofi; and has served as a consultant for Amgen, Boehringer Ingelheim, Corvia, and Recor. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received July 12, 2017.
- Revision received August 29, 2017.
- Accepted September 6, 2017.
- 2017 American College of Cardiology Foundation