Martin Orban1,2, Dietmar Trenk3, Tobias Geisler4, Johannes Rieber5, Martin Hadamitzky6, Lisa Gross1,2, Mathias Orban1,2, Danny Kupka1,2, Monika Baylacher1,2, Susan Müller1,2, Kurt Huber7, Lukasz Koltowski8, Zenon Huczek8, Jens Heyn9, Claudius Jacobshagen10, Dániel Aradi11, Steffen Massberg1,2, Dirk Sibbing1,2, Ralph Hein1,2. 1. Department of Cardiology, Ludwig-Maximilians University, Marchioninistraße 15, 81377 Munich, Germany. 2. DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Biedersteiner Straße 29, 80802 München, Germany. 3. Department of Cardiology and Angiology II, University Heart Centre Freiburg, Südring 15, 79189 Bad Krozingen, Germany. 4. Department of Cardiology and Cardiovascular Disease, University Hospital Tübingen, Otfried-Müller-Straße 10, 72076 Tübingen, Germany. 5. Department of Cardiology and Intensive Care Medicine, Heart Centre Bogenhausen, Englschalkinger Straße 77, 81925 München, Germany. 6. Department of Radiology, German Heart Center of Munich, Lazarettstraße 36, 80636 München, Germany. 7. 3 Department of Medicine, Cardiology and Intensive Care Medicine, Wilhelminen Hospital, and Sigmund Freud Private University, Medical School, Montleartstrasse 35-37, 1160 Vienna, Austria. 8. 1 Department of Cardiology, Medical University of Warsaw, Żwirki i Wigury 61, 02-091 Warszawa, Poland. 9. Department of Anesthesiology, Ludwig-Maximilians University, Marchioninistraße 15, 81377 Munich, Germany. 10. Department of Cardiology and Pneumology, Heart Centre/Georg-August-University Göttingen, 37073 Göttingen, Germany. 11. Department of Cardiology, Heart Centre Balatonfüred and Heart and Vascular Centre, Semmelweis University, Gyógy tér 2 8230 Balatonfüred, Budapest, Hungary.
Abstract
AIMS: Prior analyses disclosed variations in antiplatelet drug response and clinical outcomes between smokers and non-smokers, thus the safety and efficacy of any dual antiplatelet therapy (DAPT) de-escalation strategy may differ in relation to smoking status. Hence, we assessed the impact of smoking on clinical outcomes and adenosine diphosphate-induced platelet aggregation following guided de-escalation of DAPT in invasively managed acute coronary syndrome (ACS) patients. METHODS AND RESULTS: The multicentre TROPICAL-ACS trial randomized 2610 biomarker-positive ACS patients 1:1 to standard treatment with prasugrel for 12 months (control group) or aplatelet function testing guided de-escalation of DAPT. Current smokers (n = 1182) showed comparable event rates between study groups [6.6% vs. 6.6%; hazard ratio (HR) 1.0, 95% confidence interval (CI) 0.64-1.56, P > 0.99]. In non-smokers (n = 1428), a guided DAPT de-escalation was associated with a lower 1-year incidence of the primary endpoint [cardiovascular death, myocardial infarction, stroke, or bleeding ≥ Grade 2 according to Bleeding Academic Research Consortium (BARC) criteria] compared with control group patients (7.9% vs. 11.0%; HR 0.71, 95% CI 0.50-0.99, P = 0.048). This reduction was mainly driven by a lower rate of BARC ≥ Grade 2 bleedings (5.2% vs. 7.7%; HR 0.68, 95% CI 0.45-1.03, P = 0.066). There was no significant interaction of smoking status with treatment effects of guided DAPT de-escalation (Pint = 0.23). Adenosine diphosphate-induced platelet aggregation values were higher in current smokers [median 28 U, interquartile range (IQR: 20-40)] vs. non-smoker [median 24 U (16-25), P < 0.0001] in the control group and in current smokers [median 42 U, IQR (27-68)] vs. non-smoker [median 37 U, IQR (25-55), P < 0.001] in the monitoring group. CONCLUSION: Guided DAPT de-escalation appears to be equally safe and effective in smokers and non-smokers. Regardless of smoking status and especially for those patients deemed unsuitable for 1 year of potent platelet inhibition this DAPT strategy might be used as an alternative antiplatelet treatment regimen. Published on behalf of the European Society of Cardiology. All rights reserved.
RCT Entities:
AIMS: Prior analyses disclosed variations in antiplatelet drug response and clinical outcomes between smokers and non-smokers, thus the safety and efficacy of any dual antiplatelet therapy (DAPT) de-escalation strategy may differ in relation to smoking status. Hence, we assessed the impact of smoking on clinical outcomes and adenosine diphosphate-induced platelet aggregation following guided de-escalation of DAPT in invasively managed acute coronary syndrome (ACS) patients. METHODS AND RESULTS: The multicentre TROPICAL-ACS trial randomized 2610 biomarker-positive ACS patients 1:1 to standard treatment with prasugrel for 12 months (control group) or a platelet function testing guided de-escalation of DAPT. Current smokers (n = 1182) showed comparable event rates between study groups [6.6% vs. 6.6%; hazard ratio (HR) 1.0, 95% confidence interval (CI) 0.64-1.56, P > 0.99]. In non-smokers (n = 1428), a guided DAPT de-escalation was associated with a lower 1-year incidence of the primary endpoint [cardiovascular death, myocardial infarction, stroke, or bleeding ≥ Grade 2 according to Bleeding Academic Research Consortium (BARC) criteria] compared with control group patients (7.9% vs. 11.0%; HR 0.71, 95% CI 0.50-0.99, P = 0.048). This reduction was mainly driven by a lower rate of BARC ≥ Grade 2 bleedings (5.2% vs. 7.7%; HR 0.68, 95% CI 0.45-1.03, P = 0.066). There was no significant interaction of smoking status with treatment effects of guided DAPT de-escalation (Pint = 0.23). Adenosine diphosphate-induced platelet aggregation values were higher in current smokers [median 28 U, interquartile range (IQR: 20-40)] vs. non-smoker [median 24 U (16-25), P < 0.0001] in the control group and in current smokers [median 42 U, IQR (27-68)] vs. non-smoker [median 37 U, IQR (25-55), P < 0.001] in the monitoring group. CONCLUSION: Guided DAPT de-escalation appears to be equally safe and effective in smokers and non-smokers. Regardless of smoking status and especially for those patients deemed unsuitable for 1 year of potent platelet inhibition this DAPT strategy might be used as an alternative antiplatelet treatment regimen. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Rong Chang; Jinchun Wu; Xiaofei Zhang; Yi Ye; Wenqin Zhou; Yanmin Liu Journal: Evid Based Complement Alternat Med Date: 2021-10-31 Impact factor: 2.629