Aims: Endothelial dysfunction and inflammation play a major role in the progression of atherosclerosis. This study aimed 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 dysfunction (asymmetric 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 tandem 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. Although there was a significant correlation between ADMA and Lp-PLA2 levels in patients with ICAS (r2 = 0.235, P <0.001), some patients showed high Lp-PLA2 but low ADMA levels, while others showed high ADMA but low Lp-PLA2 levels. A high ADMA serum level was associated with a 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.
Conclusion: 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.