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From the Baylor College of Medicine (S.L.), Houston, TX; School of Public Health (S.L.Z.) and School of Medicine (J.A.C.L., S.N.G., I.S.W.), Johns Hopkins University, Baltimore, MD; and New Jersey Neuroscience Institute (S.M.O.), Edison, NJ.
Address correspondence and reprint requests to Dr. Stephen Oppenheimer, 101 Wendover Road, Baltimore, MD 21218; e-mail: soppenh{at}hotmail.com
Background: After stroke, 10% of patients have adverse cardiac outcomes. Left insular damage may contribute to this by impairing sympathovagal balance (associated with cardiac structural damage and arrhythmias).
Methods: The authors conducted a prospective study of 32 patients with left insular stroke (Group 1) and 84 patients with non-insular stroke/TIA (Group 2). Adverse cardiac outcomes (cardiac death, myocardial infarction, angina, and heart failure) were assessed over 1 year. Myocardial wall motion was investigated with transesophageal echocardiography.
Results: Group 1’s cardiac outcome relative risk (RR) compared with Group 2 was 1.75 (95% CI: 1.02, 3.00, p = 0.05). Left insular stroke remained an independent predictor of cardiac outcome in multivariate analyses. Sensitivity analysis excluding TIA and angina showed similar results. For Group 1 patients without symptomatic coronary artery disease (SCAD), cardiac outcome RR = 4.06 (95% CI: 1.83, 9.01, p = 0.002). For Group 1 with SCAD, RR = 0.36 (95% CI: 0.06, 2.13, p = 0.14). Cardiac wall motion impairment was also associated with left insular stroke independent of CAD or nonischemic heart disease. Right insular stroke was not associated with adverse cardiac outcomes or cardiac wall motion impairment.
Conclusions: Left insular stroke is associated with an increased risk of adverse cardiac outcome and decreased cardiac wall motion compared to stroke in other locations and TIA. This was particularly marked in patients without symptomatic coronary artery disease (SCAD). In patients with SCAD, the cardioprotective effect of medications, especially beta-blockers alone or combined with ischemic preconditioning, may explain the lack of association in this subgroup.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the February 28 issue to find the title link for this article.
Commentary, see page 463
Funded by PHS grants NS R01-33770 and RR-00052 (S.M.O.).
Disclosure: The authors report no conflicts of interest.
Received January 24, 2005. Accepted in final form December 28, 2005.
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Neurology 2006 66: 463.
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