Abstract

Introduction: Elevated cardiac troponin (cTn) in acute ischemic stroke (AIS) is common, and associated with increased risk of death. Whether this association depends on the cause of the cTn elevation is unclear. We examined whether etiology of elevated cTN after AIS modulates the risk of death using a large population-based study in the Greater Cincinnati Northern Kentucky (GCNK) region. Methods: Using well-validated methods, all hospitalized AIS cases in the GCNK region were collected and adjudicated in 2015. Cases with a positive cTN underwent retrospective review by cardiologists using the Fourth Universal Definition of Myocardial Infarction (MI). Date/cause of death were obtained from the National Death Index. Kaplan Meier estimates of 3-year cardiac and all-cause death were generated, stratified into the following three categories: Acute MI (Type I/Type II), elevated troponin without acute MI, and nonelevated troponin. Estimates were then compared with a Log Rank test. Results: There were 2096 AIS patients during the study period in which a cTN was obtained; cTN was elevated in 464 (22.1%). Among AIS patients with elevated cTN, 107 (23%) had an acute MI, and the remaining 357 (77%) had elevated cTN without MI. At 3 years, cardiac/all cause deaths were more common in patients with elevated cTN when compared with patients without elevated cTN regardless of cause (P<0.01, Figure). Among patients with elevated cTN, death rates were not significantly higher in patients with acute MI (P=0.44 all cause, p=0.67 cardiac). Discussion: Elevated cTN after AIS is associated with a higher risk of death at 3 years, regardless of whether an MI occurred. Interventions targeting patients with elevated cTN could improve long-term outcome after AIS.

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