Inflammatory markers in progressing lacunar stroke
Background: The mechanisms underlying neurologic deterioration in patients with lacunar infarction have not been established. While accumulating evidence suggest a role for inflammatory-mediated damage after brain ischemia, whether inflammation also intervenes in lacunar stroke progression remains unsettled. Objective: We sought to investigate the role of inflammatory markers in the progression of lacunar infarctions Methods: We studied within the first 24 hours after the onset of symptoms 113 consecutive patients (mean age 69.7±9.3, 57% males) with lacunar stroke defined by clinical and CT/MRI criteria (lacunar syndrome + lesion of < 15mm in appropriate location). Neurological deterioration was defined as a fall of 1 or more points in Canadian Stroke Scale (CSS) between inclusion and 48 hours. Interleukine 6 (IL-6), tumor necrosis factor-α (TNF-α) and ICAM-1 were determined by ELISA in blood samples obtained on admission. Results: At follow up, 27 patients (23.9%) progressed on the CSS. Among risk factors and clinical characteristics, only a history of hypertension, and a lack of prior treatment with aspirin, were significantly more frequent in patients with neurologic deterioration (p<0.05). Serum TNF-α (17.3±5.02 vs 8.7±4.7 pg/mL), IL-6 (29.2±7.2 vs 13.7±7.5 pg/mL) and ICAM-1 (270.6±65.0 vs 160.6±29.8 pg/mL) were significantly higher in patients who progressed (p<0.001). Logistic regression analyses adjusted for history of hypertension and prior aspirin intake showed that TNF−α [OR=1.36, 95% CI (1.20–1.53)], IL-6 [OR=1.25, 95% CI (1.14–1.36)] and ICAM-1 [by 10 pg/mL, OR=2.85, 95% CI (2.79–2.91)] were related to lacunar stroke progression. Conclusions: Our results suggest that inflammation contributes to the progression of lacunar infarctions. Further studies will establish the mechanisms underlying this provocative finding that opens a new therapeutic avenue in lacunar stroke.