TY - JOUR
T1 - Peripheral Monocytosis at Admission to Predict Cerebral Infarct and Poor Functional Outcomes in Subarachnoid Hemorrhage Patients
AU - Unda, Santiago R.
AU - Birnbaum, Jessie
AU - Labagnara, Kevin
AU - Wong, Megan
AU - Vaishnav, Dhrumil P.
AU - Altschul, David J.
N1 - Publisher Copyright:
© 2020
PY - 2020/6
Y1 - 2020/6
N2 - Objective: Increasing evidence points monocytes' role to be larger than thought in developing cerebral infarction (CI) after subarachnoid hemorrhage (SAH). However, there is no clinical evidence of the relationship between peripheral monocytes and CI and clinical outcomes. Therefore we determine whether an increase in monocytes in the acute phase is useful to predict CI and functional outcomes in SAH patients. Methods: We included 204 patients with an SAH diagnosis. We collected patient-related factors, comorbidities, Hunt-Hess grade, modified Fisher grade, treatment, delayed cerebral ischemia, CI, aneurysm characteristics, and peripheral monocytes from vein blood at admission. Poor outcomes were defined as modified Rankin Scale score ≥3. Results: Fifty (24.5%) patients had CI before discharge. In a multivariate model, increased monocytes at admission were significantly associated with CI after adjusting for IV-V Hunt-Hess grade and delayed cerebral ischemia (odds ratio: 3.193, 95% confidence interval: 1.069–9.532, P = 0.037). In receiver operating characteristic curve analysis, a monocyte count of 0.60 was identified as the best cutoff value to discriminate the development of CI (area under the curve = 0.622, P = 0.010; CI for monocytes <0.60 17.4% vs. CI for monocytes ≥0.60 29.1% P = 0.046). Admission monocytes ≥0.60 predicted poor functional outcomes at discharge (monocytes <0.60 52% vs. monocytes ≥0.60 64.7%) and at 12 months (monocytes <0.60 29.4% vs. monocytes ≥0.60 70.6%). Conclusions: Increased peripheral monocytes at admission is a risk factor for developing CI after SAH. Moreover, short- and long-term poor clinical outcomes were associated with higher monocyte count. Therefore monocytes could be a convenient biomarker for prognosis unfavorable outcomes and a possible target for new therapeutic strategies.
AB - Objective: Increasing evidence points monocytes' role to be larger than thought in developing cerebral infarction (CI) after subarachnoid hemorrhage (SAH). However, there is no clinical evidence of the relationship between peripheral monocytes and CI and clinical outcomes. Therefore we determine whether an increase in monocytes in the acute phase is useful to predict CI and functional outcomes in SAH patients. Methods: We included 204 patients with an SAH diagnosis. We collected patient-related factors, comorbidities, Hunt-Hess grade, modified Fisher grade, treatment, delayed cerebral ischemia, CI, aneurysm characteristics, and peripheral monocytes from vein blood at admission. Poor outcomes were defined as modified Rankin Scale score ≥3. Results: Fifty (24.5%) patients had CI before discharge. In a multivariate model, increased monocytes at admission were significantly associated with CI after adjusting for IV-V Hunt-Hess grade and delayed cerebral ischemia (odds ratio: 3.193, 95% confidence interval: 1.069–9.532, P = 0.037). In receiver operating characteristic curve analysis, a monocyte count of 0.60 was identified as the best cutoff value to discriminate the development of CI (area under the curve = 0.622, P = 0.010; CI for monocytes <0.60 17.4% vs. CI for monocytes ≥0.60 29.1% P = 0.046). Admission monocytes ≥0.60 predicted poor functional outcomes at discharge (monocytes <0.60 52% vs. monocytes ≥0.60 64.7%) and at 12 months (monocytes <0.60 29.4% vs. monocytes ≥0.60 70.6%). Conclusions: Increased peripheral monocytes at admission is a risk factor for developing CI after SAH. Moreover, short- and long-term poor clinical outcomes were associated with higher monocyte count. Therefore monocytes could be a convenient biomarker for prognosis unfavorable outcomes and a possible target for new therapeutic strategies.
KW - Clinical outcomes
KW - Monocytes
KW - Subarachnoid hemorrhage
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U2 - 10.1016/j.wneu.2020.02.170
DO - 10.1016/j.wneu.2020.02.170
M3 - Article
C2 - 32151773
AN - SCOPUS:85082549693
SN - 1878-8750
VL - 138
SP - e523-e529
JO - World Neurosurgery
JF - World Neurosurgery
ER -