BACKGROUND AND PURPOSE: Subarachnoid hemorrhage (SAH) frequently results in myocardial necrosis with release of cardiac enzymes. Historically, this necrosis has been attributed to coronary artery disease, coronary vasospasm, or oxygen supply-demand mismatch. Experimental evidence, however, indicates that excessive release of norepinephrine from the myocardial sympathetic nerves is the most likely cause. We hypothesized that myocardial necrosis after SAH is a neurally mediated process that is dependent on the severity of neurological injury. METHODS: Consecutive patients admitted with SAH were enrolled prospectively. Predictor variables reflecting demographic (age, sex, body surface area), hemodynamic (heart rate, systolic blood pressure), treatment (phenylephrine dose), and neurological (Hunt-Hess score) factors were recorded. Serial cardiac troponin I measurements and echocardiography were performed on days 1, 3, and 6 after enrollment. Troponin level was treated as a dichotomous outcome variable. We performed univariate and multivariate analyses on the relationships between the predictor variables and troponin level. RESULTS: The study included 223 patients with an average age of 54 years. Twenty percent of the subjects had troponin I levels >1.0 microg/L (range, 0.3 to 50 microg/L). By multivariate logistic regression, a Hunt-Hess score >2, female sex, larger body surface area and left ventricular mass, lower systolic blood pressure, and higher heart rate and phenylephrine dose were independent predictors of troponin elevation. CONCLUSIONS: The degree of neurological injury as measured by the Hunt-Hess grade is a strong, independent predictor of myocardial necrosis after SAH. This finding supports the hypothesis that cardiac injury after SAH is a neurally mediated process.
BACKGROUND AND PURPOSE:Subarachnoid hemorrhage (SAH) frequently results in myocardial necrosis with release of cardiac enzymes. Historically, this necrosis has been attributed to coronary artery disease, coronary vasospasm, or oxygen supply-demand mismatch. Experimental evidence, however, indicates that excessive release of norepinephrine from the myocardial sympathetic nerves is the most likely cause. We hypothesized that myocardial necrosis after SAH is a neurally mediated process that is dependent on the severity of neurological injury. METHODS: Consecutive patients admitted with SAH were enrolled prospectively. Predictor variables reflecting demographic (age, sex, body surface area), hemodynamic (heart rate, systolic blood pressure), treatment (phenylephrine dose), and neurological (Hunt-Hess score) factors were recorded. Serial cardiac troponin I measurements and echocardiography were performed on days 1, 3, and 6 after enrollment. Troponin level was treated as a dichotomous outcome variable. We performed univariate and multivariate analyses on the relationships between the predictor variables and troponin level. RESULTS: The study included 223 patients with an average age of 54 years. Twenty percent of the subjects had troponin I levels >1.0 microg/L (range, 0.3 to 50 microg/L). By multivariate logistic regression, a Hunt-Hess score >2, female sex, larger body surface area and left ventricular mass, lower systolic blood pressure, and higher heart rate and phenylephrine dose were independent predictors of troponin elevation. CONCLUSIONS: The degree of neurological injury as measured by the Hunt-Hess grade is a strong, independent predictor of myocardial necrosis after SAH. This finding supports the hypothesis that cardiac injury after SAH is a neurally mediated process.
Authors: Avinash Kothavale; Nader M Banki; Alexander Kopelnik; Sirisha Yarlagadda; Michael T Lawton; Nerissa Ko; Wade S Smith; Barbara Drew; Elyse Foster; Jonathan G Zaroff Journal: Neurocrit Care Date: 2006 Impact factor: 3.210
Authors: Michael Moussouttas; Edwin W Lai; John Khoury; Thanh T Huynh; Keith Dombrowski; Karel Pacak Journal: Neurocrit Care Date: 2012-06 Impact factor: 3.210