BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.