Published online before print January 22, 2004, doi: 10.1161/01.STR.0000114874.96688.54
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(Stroke. 2004;35:548.)
© 2004 American Heart Association, Inc.
Original Contributions |
Predictors of Neurocardiogenic Injury After Subarachnoid Hemorrhage
From the Division of Cardiology (P.T., A.K., N.B., E.F., W.P., J.Z.), Division of Neuroradiology (K.O., N.K.), Department of Neurology (D.G.), Department of Neurological Surgery (M.T.L.), and Division of Physiological Nursing (B.D.), UCSF Medical Center, San Francisco, Calif.
Reprint requests to Jonathan Zaroff, MD, 505 Parnassus Ave, Moffitt Suite 1177, San Francisco, CA 94117–0124. E-mail Zaroff{at}medicine.ucsf.edu
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 µg/L (range, 0.3 to 50 µg/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.
Key Words: heart failure, congestive • subarachnoid hemorrhage • troponin
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