Lucas Chun Wah Fong1, Nicholas Ho Cheung Lee2, Andrew T Yan3, Ming-Yen Ng4. 1. Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China, fongcwlucas@outlook.com. 2. Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. 3. Department of Medicine, University of Toronto Division of Cardiology, St. Michael's Hospital, Toronto, Ontario, Canada. 4. Department of Diagnostic Radiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Abstract
INTRODUCTION: There have been inconsistent data on the direct comparison of prasugrel and ticagrelor. This meta-analysis was conducted to summarize the current available evidence. METHODS: We performed a meta-analysis (PROSPERO-registered CRD42020166810) of randomized trials up to February 2020 that compared prasugrel and ticagrelor in acute coronary syndrome with respect to the composite endpoint of myocardial infarction (MI), stroke, or cardiovascular death and secondary endpoints including MI, stroke, cardiovascular death, major bleeding (Bleeding Academic Research Consortium (BARC) type 2 or above), stent thrombosis, all-cause death, and other safety outcomes. RESULTS: Of the 11 eligible RCTs with 6,098 patients randomized to prasugrel (n = 3,050) or ticagrelor (n = 3,048), 180 and 207 had the composite endpoint events in the prasugrel arm and the ticagrelor arm, respectively, over a weighted mean follow-up period of 11 ± 2 months. Compared with prasugrel, the ticagrelor group had similar risk in the primary composite endpoint (risk ratio [RR] = 1.17; 95% CI = 0.96-1.42; p = 0.12, I2 = 0%). Compared to prasugrel, there was no significant difference associated with the ticagrelor groups with respect to stroke (RR = 1.05; 95% CI = 0.66-1.67; p = 0.84, I2 = 0%), cardiovascular death (RR = 1.01; 95% CI = 0.75-1.36; p = 0.95, I2 = 0%), BARC type 2 or above bleeding (RR = 1.16; 95% CI = 0.89-1.52; p = 0.26, I2 = 0%), stent thrombosis (RR = 1.58; 95% CI = 0.90-2.76; p = 0.11, I2 = 0%), and all-cause death (RR = 1.10; 95% CI = 0.86-1.43; p = 0.45, I2 = 0%) except MI (RR = 1.38; 95% CI = 1.05-1.81; p = 0.02, I2 = 0%) Conclusion: Compared with prasugrel, ticagrelor did not reduce the primary composite endpoint of MI, stroke, and cardiovascular death at a weighted mean follow-up of 11 months. There was no significant difference between the secondary outcomes except MI.
INTRODUCTION: There have been inconsistent data on the direct comparison of prasugrel and ticagrelor. This meta-analysis was conducted to summarize the current available evidence. METHODS: We performed a meta-analysis (PROSPERO-registered CRD42020166810) of randomized trials up to February 2020 that compared prasugrel and ticagrelor in acute coronary syndrome with respect to the composite endpoint of myocardial infarction (MI), stroke, or cardiovascular death and secondary endpoints including MI, stroke, cardiovascular death, major bleeding (Bleeding Academic Research Consortium (BARC) type 2 or above), stent thrombosis, all-cause death, and other safety outcomes. RESULTS: Of the 11 eligible RCTs with 6,098 patients randomized to prasugrel (n = 3,050) or ticagrelor (n = 3,048), 180 and 207 had the composite endpoint events in the prasugrel arm and the ticagrelor arm, respectively, over a weighted mean follow-up period of 11 ± 2 months. Compared with prasugrel, the ticagrelor group had similar risk in the primary composite endpoint (risk ratio [RR] = 1.17; 95% CI = 0.96-1.42; p = 0.12, I2 = 0%). Compared to prasugrel, there was no significant difference associated with the ticagrelor groups with respect to stroke (RR = 1.05; 95% CI = 0.66-1.67; p = 0.84, I2 = 0%), cardiovascular death (RR = 1.01; 95% CI = 0.75-1.36; p = 0.95, I2 = 0%), BARC type 2 or above bleeding (RR = 1.16; 95% CI = 0.89-1.52; p = 0.26, I2 = 0%), stent thrombosis (RR = 1.58; 95% CI = 0.90-2.76; p = 0.11, I2 = 0%), and all-cause death (RR = 1.10; 95% CI = 0.86-1.43; p = 0.45, I2 = 0%) except MI (RR = 1.38; 95% CI = 1.05-1.81; p = 0.02, I2 = 0%) Conclusion: Compared with prasugrel, ticagrelor did not reduce the primary composite endpoint of MI, stroke, and cardiovascular death at a weighted mean follow-up of 11 months. There was no significant difference between the secondary outcomes except MI.
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