Author + information
- Robert W. Yeh, MD, MSc,
- Dean J. Kereiakes, MD and
- Laura Mauri, MD, MSc∗ ()
- ↵∗Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115
We thank Dr. Ganeshan and colleagues for their interest in our paper (1). In our subgroup analysis of the DAPT Study (Dual Antiplatelet Therapy Study) (1), continued thienopyridine therapy beyond 12 months after coronary stent placement provided consistent reductions in ischemic endpoints while increasing bleeding in patients presenting initially with or without myocardial infarction. Although not included in our original publication, we have performed the sensitivity analysis requested by Ganeshan and colleagues, grouping unstable angina patients with myocardial infarction patients (acute coronary syndrome [ACS] group). In this analysis, consistent reductions in ischemic endpoints were again observed with continued thienopyridine in both ACS and non-ACS patients (ACS group: stent thrombosis hazard ratio [HR]: 0.35; p < 0.001, myocardial infarction HR: 0.47; p < 0.001; non-ACS group: stent thrombosis HR: 0.25, p < 0.001, myocardial infarction HR: 0.61; p = 0.002; interaction p = NS for both comparisons). GUSTO (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) moderate or severe bleeding was increased with continued thienopyridine in both groups as well (ACS group HR: 2.01; p = 0.002; non-ACS group HR: 1.49; p = 0.024; interaction p = 0.31).
As Dr. Ganeshan and colleagues rightly point out, our study was a post-hoc subgroup analysis of a completed randomized clinical trial (2,3) and was not specifically powered to assess the interactions presented. Its conclusions should be interpreted with this in mind.
A large fraction of eligible patients were not randomized in the DAPT study, primarily due to patient and provider preference. Among myocardial infarction patients, those who were eligible, but not randomized, were similar in age, but were more often women (38.3% vs. 31.8%; p < 0.001), nonwhite (12.7% vs. 8.4%), and had higher rates of diabetes, prior stroke, congestive heart failure, and prior coronary revascularization (p < 0.001 for each), as compared with those randomized in the study. Similar results were observed among patients without myocardial infarction. These findings suggest that the randomized patients were somewhat lower risk for recurrent ischemic events than those who were enrolled. It is likely that had these eligible subjects also been randomized, a treatment effect of the same magnitude or larger would have been observed.
Please note: Dr. Yeh is a member of the advisory board for Abbott Vascular; and has received consulting fees from Gilead Sciences and Merck. Dr. Mauri has received institutional research grants from Abbott, Boston Scientific, Cordis, Medtronic, Eli Lilly/Daiichi-Sankyo, and Sanofi/Bristol-Myers Squibb; and has received personal fees from Medtronic, Recor, St. Jude Medical, and Biotronik. Dr. Kereiakes has reported that he has no relationships relevant to the contents of this paper to disclose. P.K. Shah, MD, FACC, served as Guest Editor for this paper.
- American College of Cardiology Foundation