Shaun G Goodman1, Philip E Aylward2, Michael Szarek3, Vakhtang Chumburidze4, Deepak L Bhatt5, Vera A Bittner6, Rafael Diaz7, Jay M Edelberg8, Corinne Hanotin9, Robert A Harrington10, J Wouter Jukema11, Sasko Kedev12, Alexia Letierce9, Angele Moryusef8, Robert Pordy13, Gabriel Arturo Ramos López14, Matthew T Roe15, Margus Viigimaa16, Harvey D White17, Andreas M Zeiher18, Ph Gabriel Steg19, Gregory G Schwartz20. 1. Canadian VIGOUR Centre, University of Alberta, Edmonton, Alberta, Canada and St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada. Electronic address: goodmans@smh.ca. 2. South Australian Health and Medical Research Institute, Flinders University and Medical Centre, Adelaide, South Australia, Australia. 3. State University of New York, Downstate School of Public Health, Brooklyn, New York. 4. Chapidze Emergency Cardiology Center, Tbilisi, Georgia. 5. Brigham and Women's Hospital Heart & Vascular Center and Harvard Medical School, Boston, Massachusetts. 6. Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama. 7. Estudios Cardiológicos Latinoamérica, Instituto Cardiovascular de Rosario, Rosario, Argentina. 8. Sanofi, Bridgewater, New Jersey. 9. Sanofi, Chilly-Mazarin, France. 10. Stanford Center for Clinical Research, Department of Medicine, Stanford University, Stanford, California. 11. Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands. 12. University Clinic of Cardiology, Skopje, Macedonia. 13. Regeneron Pharmaceuticals Inc., Tarrytown, New York. 14. Medical Office, Guadalajara, Jalisco, Mexico. 15. Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina; Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina. 16. SA Põhja-Eesti Regionaalhaigla, Tallinn, Estonia. 17. Green Lane Cardiovascular Services Auckland City Hospital, Auckland, New Zealand. 18. Department of Medicine III, Goethe University, Frankfurt am Main, Germany. 19. Assistance Publique-Hôpitaux de Paris, Hôpital Bichat, Paris, France; National Heart and Lung Institute, Imperial College, Royal Brompton Hospital, London, United Kingdom. 20. Division of Cardiology, University of Colorado School of Medicine, Aurora, Colorado.
Abstract
BACKGROUND:Patients with acute coronary syndrome (ACS) and history of coronary artery bypass grafting (CABG) are at high risk for recurrent cardiovascular events and death. OBJECTIVES: This study sought to determine the clinical benefit of adding alirocumab to statins in ACS patients with prior CABG in a pre-specified analysis of ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab). METHODS:Patients (n = 18,924) 1 to 12 months post-ACS with elevated atherogenic lipoprotein levels despite high-intensity statin therapy were randomized to alirocumab or placebo subcutaneously every 2 weeks. Median follow-up was 2.8 years. The primary composite endpoint of major adverse cardiovascular events (MACE) comprised coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, or unstable angina requiring hospitalization. All-cause death was a secondary endpoint. Patients were categorized by CABG status: no CABG (n = 16,896); index CABG after qualifying ACS, but before randomization (n = 1,025); or CABG before the qualifying ACS (n = 1,003). RESULTS: In each CABG category, hazard ratios (95% confidence intervals) for MACE (no CABG 0.86 [0.78 to 0.95], index CABG 0.85 [0.54 to 1.35], prior CABG 0.77 [0.61 to 0.98]) and death (0.88 [0.75 to 1.03], 0.85 [0.46 to 1.59], 0.67 [0.44 to 1.01], respectively) were consistent with the overall trial results (0.85 [0.78 to 0.93] and 0.85 [0.73 to 0.98], respectively). Absolute risk reductions (95% confidence intervals) differed across CABG categories for MACE (no CABG 1.3% [0.5% to 2.2%], index CABG 0.9% [-2.3% to 4.0%], prior CABG 6.4% [0.9% to 12.0%]) and for death (0.4% [-0.1% to 1.0%], 0.5% [-1.9% to 2.9%], and 3.6% [0.0% to 7.2%]). CONCLUSIONS: Among patients with recent ACS and elevated atherogenic lipoproteins despite intensive statin therapy, alirocumab was associated with large absolute reductions in MACE and death in those with CABG preceding the ACS event. (ODYSSEY OUTCOMES: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402).
RCT Entities:
BACKGROUND:Patients with acute coronary syndrome (ACS) and history of coronary artery bypass grafting (CABG) are at high risk for recurrent cardiovascular events and death. OBJECTIVES: This study sought to determine the clinical benefit of adding alirocumab to statins in ACS patients with prior CABG in a pre-specified analysis of ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab). METHODS:Patients (n = 18,924) 1 to 12 months post-ACS with elevated atherogenic lipoprotein levels despite high-intensity statin therapy were randomized to alirocumab or placebo subcutaneously every 2 weeks. Median follow-up was 2.8 years. The primary composite endpoint of major adverse cardiovascular events (MACE) comprised coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, or unstable angina requiring hospitalization. All-cause death was a secondary endpoint. Patients were categorized by CABG status: no CABG (n = 16,896); index CABG after qualifying ACS, but before randomization (n = 1,025); or CABG before the qualifying ACS (n = 1,003). RESULTS: In each CABG category, hazard ratios (95% confidence intervals) for MACE (no CABG 0.86 [0.78 to 0.95], index CABG 0.85 [0.54 to 1.35], prior CABG 0.77 [0.61 to 0.98]) and death (0.88 [0.75 to 1.03], 0.85 [0.46 to 1.59], 0.67 [0.44 to 1.01], respectively) were consistent with the overall trial results (0.85 [0.78 to 0.93] and 0.85 [0.73 to 0.98], respectively). Absolute risk reductions (95% confidence intervals) differed across CABG categories for MACE (no CABG 1.3% [0.5% to 2.2%], index CABG 0.9% [-2.3% to 4.0%], prior CABG 6.4% [0.9% to 12.0%]) and for death (0.4% [-0.1% to 1.0%], 0.5% [-1.9% to 2.9%], and 3.6% [0.0% to 7.2%]). CONCLUSIONS: Among patients with recent ACS and elevated atherogenic lipoproteins despite intensive statin therapy, alirocumab was associated with large absolute reductions in MACE and death in those with CABG preceding the ACS event. (ODYSSEY OUTCOMES: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402).
Authors: Wei Xie; Dan Li; Yaru Shi; Ning Yu; Yu Yan; Yingchao Zhang; Qiongli Yu; Yulin Li; Jie Du; Zhuofeng Lin; Fan Wu Journal: Front Cardiovasc Med Date: 2022-04-06
Authors: José Tuñón; Philippe Gabriel Steg; Deepak L Bhatt; Vera A Bittner; Rafael Díaz; Shaun G Goodman; J Wouter Jukema; Yong-Un Kim; Qian H Li; Christian Mueller; Alexander Parkhomenko; Robert Pordy; Piyamitr Sritara; Michael Szarek; Harvey D White; Andreas M Zeiher; Gregory G Schwartz Journal: Eur Heart J Date: 2020-11-07 Impact factor: 29.983