a Department of Internal Medicine and Infectious Diseases , University Hospital of Patras , Rio , Patras , Greece.
b Department of Cardiology , University Hospital of Patras , Rio , Patras , Greece.
Platelets. 2018 Jan;29(1):76-78. doi: 10.1080/09537104.2017.1319919. Epub 2017 Jun 21.
High-on-treatment platelet reactivity (HPR) is associated with ischemic events in patients on antiplatelet therapy with a history of cardiovascular disease. On the other hand, recent data have associated sepsis with adverse cardiovascular events in patients admitted with bacteremia or respiratory infection. We aimed to assess P2Y-mediated platelet reactivity (PR) during sepsis and recovery in patients under clopidogrel. This was a prospective observational study. Incoming patients presenting with signs/symptoms of sepsis already on a maintenance dose of clopidogrel of 75 mg qd for cardiovascular events were included in this study. Patients were assessed for their PR on presentation and following septic syndrome, using the VerifyNow point-of-care P2Y assay. Patients were excluded in the presence of evidence of noncompliance to antiplatelet regimen or in need of discontinuation during this study. Twenty-two septic patients on clopidogrel were included in this study (Supplemental Figure S1). Clopidogrel was administered for previous stroke, coronary, and peripheral artery disease in 27.3, 40.9, and 31.8% of patients, respectively. The main site of infection was respiratory tract followed by urinary tract, while the same amounts of gram-negative and -positive pathogens were isolated. HPR was noted in 77% and 29% of patients during sepsis and recovery, respectively, presenting a significant decrease in P2Y reaction units values during follow-up [240.7 ± 58.3 versus 179.5 ± 58.4, 95% CI (-102.7, -39.76), p = 0.0002]. Five patients died of infection, while no adverse cardiovascular events were noted in our study. Our study shows that sepsis may favor HPR, which is reversed when recovery occurs. This finding may underlie the adverse cardiovascular events in patients admitted with sepsis, possibly requiring alteration of antiplatelet regimen during the inflammation period.
治疗中血小板高反应性（HPR）与心血管疾病病史患者的抗血小板治疗中发生缺血事件有关。另一方面，最近的数据表明，败血症与菌血症或呼吸道感染患者入院后的不良心血管事件有关。我们旨在评估败血症期间和恢复期间接受氯吡格雷治疗的患者的 P2Y 介导的血小板反应性（PR）。这是一项前瞻性观察研究。纳入了已经接受 75mg qd 氯吡格雷维持剂量治疗心血管疾病的患者，他们出现败血症的症状/体征。使用即时检验 P2Y 测定法在出现败血症和败血症综合征时评估患者的 PR。在存在抗血小板方案不依从或在研究期间需要停药的证据的情况下，患者被排除在外。这项研究共纳入了 22 名接受氯吡格雷治疗的败血症患者（补充图 S1）。氯吡格雷分别用于先前的中风、冠状动脉和外周动脉疾病患者的比例为 27.3%、40.9%和 31.8%。感染的主要部位是呼吸道，其次是泌尿道，而革兰氏阴性和阳性病原体的数量相同。败血症和恢复期间分别有 77%和 29%的患者出现 HPR，随访期间 P2Y 反应单位值显著下降[240.7 ± 58.3 与 179.5 ± 58.4，95%置信区间（-102.7，-39.76），p = 0.0002]。5 名患者因感染死亡，本研究未观察到不良心血管事件。我们的研究表明，败血症可能导致 HPR，而当恢复发生时 HPR 会逆转。这一发现可能是败血症患者入院后发生不良心血管事件的基础，可能需要在炎症期改变抗血小板方案。
