Guido Parodi1, Benedetta Bellandi2, Ioanna Xanthopoulou2, Piera Capranzano2, Davide Capodanno2, Renato Valenti2, Katerina Stavrou2, Angela Migliorini2, David Antoniucci2, Corrado Tamburino2, Dimitrios Alexopoulos2. 1. From the Department of Heart and Vessels, Careggi University Hospital, Florence, Italy (G.P., B.B., R.V., A.M., D. Antoniucci); Post-graduate School in Cardiology, University of Florence, Italy (G.P.); Department of Cardiology, Patras University Hospital, Patras, Greece (I.X., K.S., D. Alexopoulos); and Cardiology Department, Ferrarotto Hospital, University of Catania, Catania, Italy (P.C., D.C., C.T.). parodiguido@gmail.com. 2. From the Department of Heart and Vessels, Careggi University Hospital, Florence, Italy (G.P., B.B., R.V., A.M., D. Antoniucci); Post-graduate School in Cardiology, University of Florence, Italy (G.P.); Department of Cardiology, Patras University Hospital, Patras, Greece (I.X., K.S., D. Alexopoulos); and Cardiology Department, Ferrarotto Hospital, University of Catania, Catania, Italy (P.C., D.C., C.T.).
Abstract
BACKGROUND: Morphine is recommended in patients with ST-segment-elevation myocardial infarction, including those undergoing primary percutaneous coronary intervention. Suboptimal antiplatelet effect during and after primary percutaneous coronary intervention is associated with increased thrombotic complications. It was hypothesized a potential drug-drug interaction between morphine and antiplatelet agents. We sought to assess platelet inhibition after a loading dose of the currently recommended antiplatelet agents in ST-segment-elevation myocardial infarction patients according to morphine use. METHODS AND RESULTS: Three hundred patients undergoing primary percutaneous coronary intervention receiving either prasugrel (n = 95) or ticagrelor (n = 205) loading dose had platelet reactivity assessed by VerifyNow 1, 2, and 4 hours after loading dose. Patients treated with morphine (n = 95; 32%) had a higher incidence of vomit (15% versus 2%; P = 0.001). P2Y12 reactivity units 2 hours after the loading dose was 187 (153-221) and 133 (102-165) in patient with and without morphine (P < 0.001); the difference persisted after excluding patients with vomit (P < 0.0001). High residual platelet reactivity (P2Y12 reactivity units ≥ 208) at 2 hours was found in 53% and 29% patients with and without morphine (P < 0.001) and without difference between prasugrel and ticagrelor patients. The independent predictors of high residual platelet reactivity at 2 hours were morphine use (odds ratio, 2.91 [1.71-4.97]; P < 0.0001) and age (odds ratio, 1.03 [1.01-1.05]; P = 0.010). Morphine remained associated with high residual platelet reactivity after propensity score adjustment (c-statistic, 0.68; 95% confidence interval, 0.66-0.70; P = 0.879 for Hosmer-Lemeshow test). CONCLUSIONS: In patients with ST-segment-elevation myocardial infarction, morphine use is associated with a delayed onset of action of the oral antiplatelet agents. This association persisted after adjusting for the propensity to receive morphine and after excluding patients with vomit.
BACKGROUND:Morphine is recommended in patients with ST-segment-elevation myocardial infarction, including those undergoing primary percutaneous coronary intervention. Suboptimal antiplatelet effect during and after primary percutaneous coronary intervention is associated with increased thrombotic complications. It was hypothesized a potential drug-drug interaction between morphine and antiplatelet agents. We sought to assess platelet inhibition after a loading dose of the currently recommended antiplatelet agents in ST-segment-elevation myocardial infarctionpatients according to morphine use. METHODS AND RESULTS: Three hundred patients undergoing primary percutaneous coronary intervention receiving either prasugrel (n = 95) or ticagrelor (n = 205) loading dose had platelet reactivity assessed by VerifyNow 1, 2, and 4 hours after loading dose. Patients treated with morphine (n = 95; 32%) had a higher incidence of vomit (15% versus 2%; P = 0.001). P2Y12 reactivity units 2 hours after the loading dose was 187 (153-221) and 133 (102-165) in patient with and without morphine (P < 0.001); the difference persisted after excluding patients with vomit (P < 0.0001). High residual platelet reactivity (P2Y12 reactivity units ≥ 208) at 2 hours was found in 53% and 29% patients with and without morphine (P < 0.001) and without difference between prasugrel and ticagrelorpatients. The independent predictors of high residual platelet reactivity at 2 hours were morphine use (odds ratio, 2.91 [1.71-4.97]; P < 0.0001) and age (odds ratio, 1.03 [1.01-1.05]; P = 0.010). Morphine remained associated with high residual platelet reactivity after propensity score adjustment (c-statistic, 0.68; 95% confidence interval, 0.66-0.70; P = 0.879 for Hosmer-Lemeshow test). CONCLUSIONS: In patients with ST-segment-elevation myocardial infarction, morphine use is associated with a delayed onset of action of the oral antiplatelet agents. This association persisted after adjusting for the propensity to receive morphine and after excluding patients with vomit.
Authors: Christopher R Kelly; Ajay J Kirtane; Jennifer Stant; Gregg W Stone; Robert M Minutello; S Chiu Wong; Honeyleen Manuzon; Roxanne Gerow-Smith; Nancy Kelley; LeRoy E Rabbani Journal: Crit Pathw Cardiol Date: 2017-03
Authors: Anne Henrieke Tavenier; Renicus Suffridus Hermanides; Jan Paul Ottervanger; Peter Gerrit Johannes Ter Horst; Elvin Kedhi; Adriaan W J van 't Hof Journal: Drug Saf Date: 2018-12 Impact factor: 5.606