Abstract

Introduction: Up to 50% of subarachnoid hemorrhage (SAH) patients develop cardiac injury. The relationship between early systemic inflammation and cardiac injury after SAH is unknown. Here we examined changes in blood leukocyte counts and their relationship to cardiac dysfunction. Methods: We reviewed the medical records of 288 SAH patients admitted to our Comprehensive Stroke Center. Patients were dichotomized based on elevated (≥0.04ng/mL) or normal (<0.04ng/mL) troponin I (TnI). Demographics and labs from admission were then compared among the two groups by Chi-Square or Mann-Whitney test. Ejection fraction (EF) was stratified into low (<50%), normal (50-70%), or high (>70%) from echocardiogram data. We performed univariate and multivariate logistic regression to establish the relationship between blood leukocyte counts and cardiac injury. Results: Of 288 SAH patients, 241 had TnI levels performed at the time of admission and 119 (49.4%) of these had elevated TnI on admission. Patients with elevated TnI were significantly older, had higher grade SAH, abnormal EF, and were more likely to have hypertension and dyslipidemia. 10 (4.1%) had low EF while 58 (24.1%) had high EF on admission echocardiogram. In univariate analysis, total leukocyte count (p<0.0001), absolute neutrophil count (p=0.037), absolute monocyte count (p=0.014), and neutrophil-lymphocyte ratio (p=0.010) were associated with elevated TnI. Multivariate analysis adjusting for covariates showed that only total leukocyte count remained a significant predictor of elevated TnI (OR = 1.104, 95% CI= 1.020 - 1.195; p=0.014). Receiver operating characteristic (ROC) analysis demonstrated that adjusted total leukocyte count distinguishes between SAH patients with normal and elevated TnI (area under the curve = 0.787, p=0.001), with the optimal cutoff being 0.521 (sensitivity of 67.0% and specificity of 80.6%). Conclusions: Blood total leukocyte count is an independent predictor of cardiac injury in SAH patients. This highlights the role of inflammation in mediating cardiac dysfunction after brain hemorrhage, and raises questions regarding the potential of anti-inflammatory therapy for cardioprotection in SAH.

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