Abstract TP120: Elevated Lipoprotein-Associated Phospholipase A2 is Differentially Associated With Symptomatic Intracranial Atherosclerosis

Abstract

Background and Objective: Intracranial atherosclerotic disease (ICAD) is a common etiology of stroke in China. Lipoprotein-associated phospholipaseA2 (Lp-PLA2), an inflammatory enzyme expressed in atherosclerotic plaques, has been linked to an increased risk of ischemic stroke. Relatively few studies have explored the relationship between Lp-PLA2 and various ischemic stroke subtypes. We aimed to determine the association between the serum Lp-PLA2 mass and the main types of symptomatic large vessel atherosclerosis. Methods: In this cross-sectional study, we reviewed data on 126 eligible acute ischemic stroke patients consecutively admitted to a single medical center in China from March 2014 to February 2016. Clinical symptoms, signs and traditional risk factors of cerebrovascular diseases were recorded. The level of serum lipids, homocysteine and glucose etc. were collected. Serum Lp-PLA2 and high-sensitivity C-reactive protein (hs-CRP) were measured. According to the results of CT angiography, patients were divided into four different groups: 1) no artery stenosis (N), 2) both intracranial and extracranial artery stenosis (B), 3) intracranial artery stenosis (I), 4) extracranial artery stenosis (E). The association of serum Lp-PLA2 and other inflammatory markers to ICAD were analyzed with Pearson correlation test. Results: Lp-PLA2 expression in the ICAD group was higher than other three groups (I vs. N vs. B vs. E: 112.22±66.79 ug/l vs. 81.70±38.50 ug/l vs.89.25±52.15 ug/l vs. 106.11± 57.76 ug/l, p=0.025). When Lp-PLA2 was above the median level, the presence of ICAD was higher than other three groups (Q3: 16[50.0%] vs. 1[3.1%] vs. 9[28.1%] vs. 6[18.8%], P=0.002; Q4: 15[48.4%] vs. 5[16.1%] vs. 8[25.8%] vs. 3[9.7%], P=0.014). In ICAD group, Lp-PLA2 mass was positively correlated with hs-CRP (r=0.899, P <0.001), and inversely correlated with total cholesterol (r=-0.307, P =0.028) and apoliprotein B (r=-0.320, P =0.022). Conclusions: Lp-PLA2 is differentially associated with ICAD compared to extracranial artery stenosis or no stenosis, which suggests that inflammation may play a greater role in the pathophysiology of ICAD versus these other symptomatic stroke categories.