Abstract

In this issue of Neurocritical Care , the University of California San Francisco group makes another important contribution to our understanding of neurocardiology (see pp. 199 – 205 for the article by Kothavale et al.). Cardiac dysfunction after subarachnoid hemorrhage (SAH), neurogenic stunned myocardium (NSM) (1) , may have a major impact on critical care. These data provide a model for further study, answer some important questions, and raise interesting new pathways for further research. A large number of patients with SAH were prospectively followed with standardized data collection. Although treatment decisions are hard to derive from nonrandomized data, observational studies generally do not suffer from selection bias because few patients (or their families) decline to participate. The authors point out that regional wall motion abnormalities (RWMAs), a form of NSM, were common. They reiterate the association between higher Hunt & Hess grade and mild elevations in cardiac troponin I (cTi) (2) . The additional prognostic significance of neurostimulant use and tachycardia lend further support to the hypothesis that a sympathetic surge leads to NSM. Cocaine has a central mechanism of action on the heart (3) , and the adverse effects of a combination of cocaine and SAH are probably synergistic. These data further support the idea that cTi — fast, cheap, and prognostic (4) — should be measured in all patients with SAH. Phenylephrine use was associated with a dose-dependent increase in RWMA. These data cannot tell us if it is cause or effect, but this is an important distinction. If NSM leads Editorial Neurocritical Care Copyright © 2006 Humana Press Inc. All rights of any nature whatsoever are reserved. ISSN 1541-6933/06/4:197–198 ISSN 1556-0961 (Online) DOI: 10.1385/Neurocrit. Care 2006;04:197–198

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