Serum Cardiac Troponin I in Acute Stroke Is Related to Serum Cortisol and TNF-α

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Abstract
Serum cardiac troponin I (cTnI) is a specific marker of myocardial injury related to in-patient fatality and cardiac injury in acute stroke. We investigated whether cTnI in acute stroke is related to serum cortisol, acute inflammatory response, and insular damage. We also investigated whether cTnI predicted outcome at 3 months. The study was based on 155 patients with CT-confirmed acute cerebral infarction and study inclusion within 24 h (50% within 12 h) of stroke onset. Blood samples were obtained on inclusion. Stroke severity was assessed by the Scandinavian Stroke Scale (SSS) and outcome was assessed by the modified Rankin Scale (mRS), death or dependency was defined as mRS > or =3 three months after stroke. 35% of all patients and 63% of patients who died within 3 months were troponin positive. Tumor necrosis factor-alpha (TNF-alpha) and cortisol were independently related to detection of cTnI: TNF-alpha(+100 pg/ml) OR 1.5 (CI 95% 1.1-2.2), cortisol(+100 nmol/l) OR 1.1 (CI 95% 1.01-1.2). SSS and age were also included in this model and did not reach significance. cTnI positivity was, together with age, stroke severity and prestroke mRS, but not s-cortisol, an independent explanatory variable of outcome at 3 months (death or dependency) with OR 4.1 (CI 95% 1.1-14.5). cTnI did not relate to insular involvement. In this study, cortisol and TNF-alpha were independently related to cTnI, which was predictive of 3-month prognosis.