Pikija Slaven, Trkulja Vladimir, Mutzenbach Johannes Sebastian, McCoy Mark R, Ganger Patricia, Sellner Johann
Department of Neurology, Christian Doppler Medical Center, Paracelsus Medical University, Ignaz-Harrer-Str. 79, 5020, Salzburg, Austria.
Department for Pharmacology, School of Medicine, University of Zagreb, Zagreb, Croatia.
J Transl Med. 2016 Aug 30;14(1):250. doi: 10.1186/s12967-016-1006-6.
Understanding the underlying mechanism of thrombus formation and its components is critical for effective prevention and treatment of ischemic stroke. The generation of thrombotic clots requires conversion of soluble fibrinogen to an insoluble fibrin network. Quantitative features of intracranial clots causing acute ischemic stroke can be studied on non-contrast enhanced CT (NECT). Here, we evaluated on-admission fibrinogen and clot burden in relation to stroke severity, final infarct volume and in-hospital mortality.
We included 132 consecutive patients with ischemic stroke and presence of hyperdense artery sign admitted within 6 h from symptom onset. Radiological parameters including clot area (corresponding to clot burden) and final infarct volume were manually determined on NECT. National Institute of Health Stroke Scale (NIHSS) was used to quantify disease severity and short-term outcome.
Median patient age was 77, 58 % were women, and 63 % had an occlusion of the proximal middle cerebral artery segment. Thrombolysis was performed in 60 % and thrombectomy in 44 %. We identified several independent associations. Higher fibrinogen levels on admission were associated with smaller clot burden (p = 0.033) and lower NIHSS on admission (p = 0.022). Patients with lower fibrinogen had a higher clot burden (p = 0.028) and greater final infarct volume (p = 0.003). Higher fibrinogen was associated with a lower risk of in-hospital death or NIHSS score >15 if discharged alive (p = 0.028).
Our study suggests that intracranial clot burden in acute ischemic stroke is associated with fibrinogen consumption, and shows a complex relationship with disease severity, infarct size and in-hospital survival.
了解血栓形成的潜在机制及其组成部分对于有效预防和治疗缺血性中风至关重要。血栓性凝块的形成需要将可溶性纤维蛋白原转化为不溶性纤维蛋白网络。可在非增强CT（NECT）上研究导致急性缺血性中风的颅内凝块的定量特征。在此，我们评估了入院时纤维蛋白原和凝块负荷与中风严重程度、最终梗死体积和住院死亡率的关系。
我们纳入了132例症状发作后6小时内入院的缺血性中风且存在高密度动脉征的连续患者。在NECT上手动确定包括凝块面积（对应于凝块负荷）和最终梗死体积在内的放射学参数。使用美国国立卫生研究院卒中量表（NIHSS）来量化疾病严重程度和短期预后。
患者中位年龄为77岁，58%为女性，63%有大脑中动脉近端段闭塞。60%的患者进行了溶栓治疗，44%的患者进行了血栓切除术。我们发现了几个独立的关联。入院时较高的纤维蛋白原水平与较小的凝块负荷相关（p = 0.033）以及入院时较低的NIHSS评分相关（p = 0.022）。纤维蛋白原水平较低的患者凝块负荷较高（p = 0.028）且最终梗死体积较大（p = 0.003）。较高的纤维蛋白原与住院死亡风险较低或出院存活时NIHSS评分>15相关（p = 0.028）。
我们的研究表明，急性缺血性中风的颅内凝块负荷与纤维蛋白原消耗相关，并与疾病严重程度、梗死大小和住院生存率呈现复杂关系。
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