摘要
Background/Aims: The aim of the study was to evaluate the differential roles of endothelial dysfunction and inflammation in intracranial atherosclerotic stroke (ICAS). Methods: We prospectively recruited 262 patients with acute cerebral infarcts caused by ICAS and 75 individuals with no history of stroke as controls. Markers of endothelial dysasymmetric dimethylarginine, ADMA) and inflammation (lipoprotein -associated phospholipase A2, Lp-PLA2) were measured. Acute ischemic lesions were measured in terms of their size, composition, and patterns. Subclinical microangiopathy (degree of leukoaraiosis) and macroangiopathy (presence/ number of asymptomatic stenoses) were graded in each patient. Results: Compared to normal controls, serum levels of ADMA (0.69 +/- 0.14 vs. 0.47 +/- 0.10, p < 0.001) and Lp-PLA2 (138.1 +/- 116.8 vs. 19.0 +/- 58.0, p < 0.001) were elevated in patients with ICAS. A high ADMA serum level was associated with greater prevalence of preclinical microangiopathy and macroangiopathy. Contrastingly, an elevated serum Lp-PLA2 level was associated with larger ischemic lesions, a greater number of lesions, and a larger cortical pattern. Conclusions: Endothelial dysfunction and inflammation have distinct effects in ICAS patents; endothelial dysfunction is associated with the underlying micro- and macro-atherosclerotic burden, whereas inflammation is associated with acute infarct volume and pattern.
- 出版日期2017