Copenhaver Kaleigh, Silva Pinheiro do Nascimiento Juliana, Garg Rajeev K, Goldenberg Fernando, Shownkeen Harish, Potts Matthew, Jahromi Babak, Lindholm Paul F, Naidech Andrew M
Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL (K.C., J.S.P.N., A.M.N.).
Department of Neurological Sciences, Division of Neurocritical Care, Rush University Medical Center, Chicago, IL (R.K.G.).
Stroke. 2025 Jul 18. doi: 10.1161/STROKEAHA.125.051447.
Hematoma expansion (HE) is a preventable cause of disability and death in patients with acute intracerebral hemorrhage (ICH). Platelet activity is essential for coagulation, and antiplatelet medications (eg, aspirin, clopidogrel) increase HE risk. General markers of platelet activity are associated with later HE, but specific biomarkers of platelet activity could enhance our understanding. We hypothesized that hemostatic biomarkers of platelet activity would correlate with later HE.
We conducted a tri-center observational cohort study of spontaneous ICH patients with multiple imaging scans for HE calculation. The thromboelastography 6s Platelet Mapping assay assessed platelet activity with 3 biomarkers: (1) adenosine diphosphate receptor-induced platelet activation, (2) platelet-fibrin network clot strength measured by heparinized kaolin with heparinase, and (3) fibrinogen-only clot strength measured by activator F (ActF). Spearman rank measured the correlation between HE and platelet activity. A linear regression model predicted HE from ActF. We tested whether the relationship between ActF and HE interacted with pre-ICH antiplatelet medication.
Thirty-five patients were included. Eleven (35.48%) took pre-ICH antiplatelet medication. Heparinized kaolin with heparinase negatively correlated with HE (=-0.34, =0.02), indicating that stronger platelet-fibrin clots were associated with less subsequent HE. ActF's association with HE depended on pre-ICH antiplatelet medication use (interaction =0.005). More ActF (fibrinogen) was associated with less HE in patients who did not take pre-ICH antiplatelet medication.
Hemostatic biomarkers from the thromboelastography 6s Platelet Mapping assay predicted subsequent HE and may aid in determining neurosurgical need. Strengthening platelet-mediated coagulation may be a target for reducing HE and improving ICH outcomes.
血肿扩大(HE)是急性脑出血(ICH)患者致残和死亡的一个可预防原因。血小板活性对于凝血至关重要,而抗血小板药物(如阿司匹林、氯吡格雷)会增加HE风险。血小板活性的一般标志物与后期HE相关,但血小板活性的特定生物标志物可能会增进我们的理解。我们假设血小板活性的止血生物标志物将与后期HE相关。
我们对自发性ICH患者进行了一项三中心观察性队列研究,通过多次影像学扫描计算HE。血栓弹力图6s血小板功能分析用3种生物标志物评估血小板活性:(1)二磷酸腺苷受体诱导的血小板活化,(2)用肝素化高岭土和肝素酶测量的血小板 - 纤维蛋白网络凝块强度,以及(3)用激活剂F(ActF)测量的仅纤维蛋白原凝块强度。Spearman秩相关分析测量HE与血小板活性之间的相关性。线性回归模型根据ActF预测HE。我们测试了ActF与HE之间的关系是否与ICH前抗血小板药物相互作用。
纳入35例患者。11例(35.48%)在ICH前服用抗血小板药物。用肝素化高岭土和肝素酶测量的结果与HE呈负相关(r = -0.34,P = 0.02),表明更强的血小板 - 纤维蛋白凝块与随后较少的HE相关。ActF与HE的关联取决于ICH前抗血小板药物的使用情况(交互作用P = 0.005)。在未服用ICH前抗血小板药物的患者中,ActF(纤维蛋白原)越高与HE越少相关。
血栓弹力图6s血小板功能分析中的止血生物标志物可预测随后的HE,并可能有助于确定神经外科手术需求。增强血小板介导的凝血可能是减少HE和改善ICH预后的一个靶点。