Thrombosis In Myocardial Infarction Study Group-Brigham and Women's Hospital, Boston, Massachusetts; Instituto do Coracao (InCor), Hospital das Clinicas da Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Instituto do Coracao (InCor), Hospital das Clinicas da Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
J Am Coll Cardiol. 2020 Jan 28;75(3):289-300. doi: 10.1016/j.jacc.2019.11.035.
Mechanistic studies have shown that morphine blunts the antiplatelet effects of oral adenosine diphosphate receptor blockers. However, the clinical relevance of this interaction is controversial.
This study sought to explore the association between morphine and ischemic events in 5,438 patients treated with concomitant clopidogrel presenting with non-ST-segment elevation acute coronary syndromes (NSTEACS) in the EARLY ACS (Early Glycoprotein IIb/IIIa Inhibition in Patients With Non-ST-Segment Elevation Acute Coronary Syndrome) trial. Patients not treated with clopidogrel (n = 3,462) were used as negative controls.
Endpoints were the composite of death, myocardial infarction (MI), recurrent ischemia, or thrombotic bailout at 96 h (4-way endpoint) and the composite of death or MI at 30 days.
In patients treated with clopidogrel, morphine use was associated with higher rates of the 4-way endpoint at 96 h (adjusted odds ratio [OR]: 1.40; 95% confidence interval [CI]: 1.04 to 1.87; p = 0.026). There was a trend for higher rates of death or MI at 30 days (adjusted OR: 1.29; 95% CI: 0.98 to 1.70; p = 0.072), driven by events in the first 48 h (adjusted hazard ratio: 1.54; 95% CI: 1.07 to 2.23; p = 0.021). In patients not treated with clopidogrel, morphine was not associated with either the 4-way endpoint at 96 h (adjusted OR: 1.05; 95% CI: 0.74 to 1.49; p = 0.79; p = 0.36 ) or death or MI at 30 days (adjusted OR: 1.07; 95% CI: 0.77 to 1.48; p = 0.70; p = 0.46).
When used concomitantly with clopidogrel pre-treatment, morphine was associated with higher rates of ischemic events in patients with NSTEACS. (EARLY ACS: Early Glycoprotein IIb/IIIa Inhibition in Patients With Non-ST-Segment Elevation Acute Coronary Syndrome; NCT00089895).
机制研究表明,吗啡会削弱口服二磷酸腺苷受体阻滞剂的抗血小板作用。然而,这种相互作用的临床相关性仍存在争议。
本研究旨在探讨吗啡与 5438 例同时接受氯吡格雷治疗的非 ST 段抬高急性冠状动脉综合征(NSTEACS)患者缺血事件之间的关系,这些患者来自 EARLY ACS(非 ST 段抬高急性冠状动脉综合征患者早期糖蛋白 IIb/IIIa 抑制)试验。未接受氯吡格雷治疗的患者(n=3462)作为阴性对照。
终点是 96 小时时的死亡、心肌梗死(MI)、复发性缺血或血栓形成补救的复合终点(四向终点)和 30 天时的死亡或 MI 复合终点。
在接受氯吡格雷治疗的患者中,吗啡的使用与 96 小时时四向终点的发生率较高相关(校正优势比[OR]:1.40;95%置信区间[CI]:1.04 至 1.87;p=0.026)。30 天时死亡或 MI 的发生率也有升高趋势(校正 OR:1.29;95%CI:0.98 至 1.70;p=0.072),这主要归因于前 48 小时的事件(校正风险比:1.54;95%CI:1.07 至 2.23;p=0.021)。在未接受氯吡格雷治疗的患者中,吗啡与 96 小时时四向终点(校正 OR:1.05;95%CI:0.74 至 1.49;p=0.79;p=0.36)或 30 天时死亡或 MI(校正 OR:1.07;95%CI:0.77 至 1.48;p=0.70;p=0.46)均无相关性。
在与氯吡格雷预治疗同时使用时,吗啡与 NSTEACS 患者的缺血事件发生率增加相关。(EARLY ACS:非 ST 段抬高急性冠状动脉综合征患者早期糖蛋白 IIb/IIIa 抑制;NCT00089895)。