Background. Elevated cardiac troponin in acute stroke in absence of acute coronary syndrome (ACS) has unclear long-term outcomes. Methods. Retrospective analysis of 566 patients admitted to Temple University Hospital from 2008 to 2010 for acute stroke was performed. Patients were included if cardiac troponin I was measured and had no evidence of ACS and an echocardiogram was performed. Of 200 patients who met the criteria, baseline characteristics, electrocardiograms, and major adverse cardiovascular events (MACE) were reviewed. Patients were characterized into two groups with normal and elevated troponins. Primary end point was nonfatal myocardial infarction during follow-up period after discharge. The secondary end points were MACE and death from any cause. Results. For 200 patients, 17 patients had positive troponins. Baseline characteristics were as follows: age , 64% African Americans, 78% with hypertension, and 22% with previous CVA. During mean follow-up of 20.1 months, 7 patients (41.2%) in elevated troponin and 6 (3.3%) patients in normal troponin group had nonfatal myocardial infarction (). MACE (41.2% versus 14.2%, ) and death from any cause (41.2% versus 14.5%, ) were significant in the positive troponin group. Conclusions. Elevated cardiac troponin in patients with acute stroke and no evidence of ACS is strong predictor of long-term cardiac outcomes. 1. Background The relationship between acute stroke and coronary artery disease is complex, and they are related to each other in multiple ways. Acute stroke confers a significant increase in adverse cardiac outcomes during short- and long-term follow-up [1]. A subset of patients with stroke might be at higher risk of long-term adverse cardiovascular outcomes. Identifying these patients, ideally with a simple test or biomarker, can help to reduce their long-term risk of adverse events. Troponin is a highly sensitive and specific marker for myocardial necrosis that is used in the diagnosis and prognosis of patients with acute coronary syndrome. However, troponin elevation has been documented in multiple clinical settings in the absence of ACS [2, 3]. Increase in troponin has been documented in all types of stroke including ischemic stroke and subarachnoid hemorrhage [4]. In a meta-analysis of 15 studies involving 2,901 patients, elevated troponins were documented in 18.1% patients with stroke that included patients with EKG changes suggestive of myocardial ischemia [3]. Troponin elevation has also been documented in acute stroke without any evidence of acute coronary syndrome [5]. While some
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