A matricellular
protein galectin-3 is involved in tissue injury and
inflammation, but the role of
galectin-3 remains unclear in
aneurysmal subarachnoid hemorrhage (SAH). The purpose of this study was to assess whether acute-stage
galectin-3 levels were associated with the subsequent development of neurovascular events and outcome after SAH. This study included 83 consecutive patients diagnosed with aneurysmal SAH of resuscitated World Federation of Neurological Surgeons (WFNS) grades 1-3. Plasma
galectin-3 levels were once measured on days 1-3 (the day after clipping or coiling). Fifteen patients had poor outcomes, which were associated with increasing age, female, pre-onset morbidity, worse WFNS grade, modified Fisher computed tomography scale, acute
hydrocephalus, and higher
galectin-3 levels compared with good outcomes. Multivariate analyses revealed that plasma
galectin-3 was an independent determinant for poor outcome (odds ratio, 3.08; 95% confidence interval, 1.58-6.00; p = 0.001). Among post-SAH neurovascular events occurring on day 4 and thereafter, delayed
cerebral ischemia and
infarction, but not angiographic vasospasm and shunt-dependent
hydrocephalus, showed significantly higher plasma
galectin-3 levels on days 1-3. The receiver operating characteristic curve indicated that plasma
galectin-3 with a cutoff value of 3.30 or 3.48 ng/ml predicted delayed
cerebral infarction development or poor outcome (specificity, 62.5%, 70.6%; sensitivity, 90.9%, 73.3%, respectively). The findings suggest that plasma
galectin-3 levels on days 1-3 would be a useful
biomarker for predicting subsequent development of delayed
cerebral infarction and eventual poor outcome and provide a new candidate, which may mediate between post-SAH early
brain injury or
inflammation and delayed
cerebral infarction without vasospasm.