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This Article Figures Only Full Text Full Text (PDF) CME: Take the course for this article: Volume 66, Number 9, May 9, 2006 All Versions of this Article: 01.wnl.0000206077.13705.6dv1 66/9/1325    most recent Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Related articles in Neurology Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ay, H. Articles by Sorensen, A. G. Search for Related Content PubMed PubMed Citation Articles by Ay, H. Articles by Sorensen, A. G. Related Collections All Cerebrovascular disease/Stroke Infarction Cardiac

Neuroanatomic correlates of stroke-related myocardial injury

From the A.A. Martinos Center for Biomedical Imaging (H.A., T.B., M.G.V., C.M., E.M.A., M.Z., A.G.S.) and GCRC Biomedical Imaging Core (M.G.V.), Department of Radiology, and Stroke Service (H.A., W.J.K., C.A, L.H.S.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, and Division of Health Sciences and Technology (A.G.S.), Harvard–MIT, Boston, MA.

Address correspondence and reprint requests to Dr. H. Ay, A.A. Martinos Center for Biomedical Imaging and Stroke Service, Departments of Neurology and Radiology, Massachusetts General Hospital, CNY149-2301, Charlestown, MA 02129; e-mail: hay{at}partners.org

Background: Myocardial injury can occur after ischemic stroke in the absence of primary cardiac causes. The neuroanatomic basis of stroke-related myocardial injury is not well understood.

Objective: To identify regions of brain infarction associated with myocardial injury using a method free of the bias of an a priori hypothesis as to any specific location.

Methods: Of 738 consecutive patients with acute ischemic stroke, the authors identified 50 patients in whom serum cardiac troponin T (cTnT) elevation occurred in the absence of any apparent cause within 3 days of symptom onset. Fifty randomly selected, age- and sex-matched patients with ischemic stroke without cTnT elevation served as controls. Diffusion-weighted images with outlines of infarction were co-registered to a template, averaged, and then subtracted to find voxels that differed between the two groups. Voxel-wise p values were determined using a nonparametric permutation test to identify specific regions of infarction that were associated with cTnT elevation.

Results: The study groups were well balanced with respect to stroke risk factors, history of coronary artery disease, infarction volume, and frequency of right and left middle cerebral artery territory involvement. Brain regions that were a priori associated with cTnT elevation included the right posterior, superior, and medial insula and the right inferior parietal lobule. Among patients with right middle cerebral artery infarction, the insular cluster was involved in 88% of patients with and 33% without cTnT elevation (odds ratio: 15.00; 95% CI: 2.65 to 84.79).

Conclusions: Infarctions in specific brain regions including the right insula are associated with elevated serum cardiac troponin T level indicative of myocardial injury.

This article was previously published in electronic format as an Expedited E-Pub on March 8, 2006, at www.neurology.org.

Supported in part by the Agency for Health Research and Quality grant R01-HS11392-02 (W.J.K.) and NIH grants R01-NS38477-04 and P41-RR14075 (A.G.S.).

Disclosure: The authors report no conflicts of interest.

Received August 9, 2005. Accepted in final form January 17, 2006.

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