Matthew T Finn1, Björn Redfors2, Dimitri Karmpaliotis3, Ajay J Kirtane1, Philip Green4, Thomas McAndrew5, Mengdan Liu5, Michael B Cloney4, Bernhard Witzenbichler6, Giora Weisz7, Thomas D Stuckey8, Bruce R Brodie8, Michael J Rinaldi9, Franz-Josef Neumann10, D Christopher Metzger11, Timothy D Henry12, David A Cox13, Peter L Duffy14, Ernest L Mazzaferri15, Roxana Mehran16, Gregg W Stone1. 1. New York-Presbyterian Hospital/Columbia University Medical Center, New York, NY; Cardiovascular Research Foundation, New York, NY. 2. Cardiovascular Research Foundation, New York, NY; Department of Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden. 3. New York-Presbyterian Hospital/Columbia University Medical Center, New York, NY; Cardiovascular Research Foundation, New York, NY. Electronic address: dk2787@cumc.columbia.edu. 4. New York-Presbyterian Hospital/Columbia University Medical Center, New York, NY. 5. Cardiovascular Research Foundation, New York, NY. 6. Helios Amper-Klinikum, Dachau, Germany. 7. Montefiore Medical Center, Bronx, NY. 8. LeBauer-Brodie Center for Cardiovascular Research and Education/Cone Health, Greensboro, NC. 9. Sanger Heart and Vascular Institute/Atrium Health, Charlotte, NC. 10. Heart Center Bad Krozingen, Bad Krozingen, Germany. 11. Ballad Health CVA Heart Institute, Kingsport, TN. 12. Minneapolis Heart Institute Foundation at Abbott Northwestern Hospital, MN; Cedars-Sinai Heart Institute, Los Angeles, CA. 13. CVA Brookwood Baptist Hospital, Birmingham, AL. 14. Reid Heart Center, FirstHealth of the Carolinas, Pinehurst, NC. 15. The Ohio State University Wexner Medical Center, Columbus, OH. 16. Cardiovascular Research Foundation, New York, NY; Icahn School of Medicine at Mount Sinai, New York, NY.
Abstract
BACKGROUND: Chronic total occlusion (CTO) percutaneous coronary intervention (PCI) typically requires a greater number of stents and longer stent length than non-CTO PCI, placing these patients at greater risk for adverse ischemic events. We sought to determine whether the association between high platelet reactivity (HPR) and the risk of ischemic events is stronger after CTO than non-CTO PCI. METHODS: Patients undergoing successful PCI in the multicenter ADAPT-DES study were stratified according to whether they underwent PCI of a CTO. HPR was defined as VerifyNow platelet reaction units >208. The study primary endpoint was the 2-year risk target vessel failure ([TVF] defined as cardiac death, myocardial infarction, or target lesion revascularization). RESULTS: CTO PCI was performed in 400 of 8448 patients. HPR was present in 34.5% of CTO PCI patients and 43.1% of non-CTO PCI patients (P = .0007). Patients undergoing CTO PCI with versus without HPR had significantly higher 2-year rates of TVF (15.0% versus 8.3%, P = .04) without significant differences in bleeding. HPR was an independent predictor of 2-year TVF (adjusted HR 1.16, 95% CI 1.02-1.34, P = .03) whereas CTO PCI was not (adjusted HR 0.89, 95% CI 0.65-1.22, P = .48). There was a significant interaction between CTO versus non-CTO PCI and PRU as a continuous variable for 2-year TVF (Pinteraction = 0.02). CONCLUSIONS: In ADAPT-DES, HPR was associated with an increased 2-year risk of TVF after PCI, an association that was at least as strong after CTO PCI compared with non-CTO PCI.
BACKGROUND:Chronic total occlusion (CTO) percutaneous coronary intervention (PCI) typically requires a greater number of stents and longer stent length than non-CTO PCI, placing these patients at greater risk for adverse ischemic events. We sought to determine whether the association between high platelet reactivity (HPR) and the risk of ischemic events is stronger after CTO than non-CTO PCI. METHODS:Patients undergoing successful PCI in the multicenter ADAPT-DES study were stratified according to whether they underwent PCI of a CTO. HPR was defined as VerifyNow platelet reaction units >208. The study primary endpoint was the 2-year risk target vessel failure ([TVF] defined as cardiac death, myocardial infarction, or target lesion revascularization). RESULTS: CTO PCI was performed in 400 of 8448 patients. HPR was present in 34.5% of CTO PCI patients and 43.1% of non-CTO PCI patients (P = .0007). Patients undergoing CTO PCI with versus without HPR had significantly higher 2-year rates of TVF (15.0% versus 8.3%, P = .04) without significant differences in bleeding. HPR was an independent predictor of 2-year TVF (adjusted HR 1.16, 95% CI 1.02-1.34, P = .03) whereas CTO PCI was not (adjusted HR 0.89, 95% CI 0.65-1.22, P = .48). There was a significant interaction between CTO versus non-CTO PCI and PRU as a continuous variable for 2-year TVF (Pinteraction = 0.02). CONCLUSIONS: In ADAPT-DES, HPR was associated with an increased 2-year risk of TVF after PCI, an association that was at least as strong after CTO PCI compared with non-CTO PCI.