Ramos-Lopes Joana, Varela Ricardo, Pascoal Rui, Rodrigues Fernando, Coelho José, Almendra Luciano, Duque Cristina, Rodrigues Bruno, Machado Cristina, Nunes Carla, Carmo-Macário Maria, Santo Gustavo, Silva Fernando, Sargento-Freitas João
Departments of Neurology.
Clinical Pathology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal.
Neurologist. 2021 Mar 4;26(2):32-35. doi: 10.1097/NRL.0000000000000329.
Lipoprotein-associated phospholipase A2 (Lp-PLA2), which is involved in the inflammatory atherosclerotic process, has emerged as an independent risk factor for atheromatous vascular events. Its impact on coronary disease has already been demonstrated, however, its influence in cerebrovascular etiology is still unknown. We aimed to observe and describe the potential association between Lp-PLA2 levels and the etiologic subtype of ischemic stroke.
Unicentric, observational, and prospective cohort study of consecutive patients with acute ischemic stroke, admitted in a comprehensive stroke center. Patients with incomplete investigation or coexisting causes were excluded. Lp-PLA2 was dosed in peripheral blood between day 3 and 14 postevent with "Lp-PLA2-SNIBE" kit. Statistical significance was set for P<0.05.
A total of 96 patients were enrolled, with mean age of 75.31±11.88 years, 41 males (42.7%); 12.5% with lacunar stroke, 16.7% atherothrombotic, 46.9% cardioembolic, and 24% embolic stroke of undetermined source (ESUS). The level of Lp-PLA2 was different between etiologies (F=2.982, P=0.035), being lower in ESUS (143.3±42.8 ng/mL). There were no significant associations with previous vascular risk factors, history of ischemic stroke and modified-Rankin scale (mRS) score 3 months postevent. In ESUS patients, Lp-PLA2 was not associated with cervical ultrasound findings or frequent supraventricular extrasystoles.
Lp-PLA2 levels are different between etiologic subtypes of ischemic stroke, being lower in ESUS patients. The results of this study reinforce the existence of distinct pathophysiological mechanisms in patients with ESUS. Multicenter clinical trials with larger sample sizes are needed to clarify the role Lp-PLA2 on the etiology of stroke.
脂蛋白相关磷脂酶A2（Lp-PLA2）参与炎症性动脉粥样硬化过程，已成为动脉粥样硬化性血管事件的独立危险因素。其对冠心病的影响已经得到证实，然而，其在脑血管病因学中的影响仍不清楚。我们旨在观察并描述Lp-PLA2水平与缺血性卒中病因亚型之间的潜在关联。
在一家综合卒中中心对连续的急性缺血性卒中患者进行单中心、观察性和前瞻性队列研究。排除检查不完整或存在并存病因的患者。在事件发生后第3天至第14天之间，使用“Lp-PLA2-SNIBE”试剂盒检测外周血中的Lp-PLA2。设定P<0.05为具有统计学意义。
共纳入96例患者，平均年龄75.31±11.88岁，男性41例（42.7%）；腔隙性卒中患者占12.5%，动脉粥样硬化血栓形成患者占16.7%，心源性栓塞患者占46.9%，不明来源栓塞性卒中（ESUS）患者占24%。不同病因之间Lp-PLA2水平存在差异（F=2.982，P=0.035），ESUS患者的Lp-PLA2水平较低（143.3±42.8 ng/mL）。与既往血管危险因素、缺血性卒中病史及事件发生后3个月的改良Rankin量表（mRS）评分均无显著关联。在ESUS患者中，Lp-PLA2与颈部超声检查结果或频发室上性早搏无关。
缺血性卒中不同病因亚型之间Lp-PLA2水平存在差异，ESUS患者的Lp-PLA2水平较低。本研究结果进一步证实了ESUS患者存在不同的病理生理机制。需要开展更大样本量的多中心临床试验来阐明Lp-PLA2在卒中病因学中的作用。
