High-Sensitivity Cardiac Troponin T and Recurrent Vascular Events After First Ischemic Stroke

Abstract

Background Recent evidence suggests cardiac troponin levels to be a marker of increased vascular risk. We aimed to assess whether levels of high-sensitivity cardiac troponin T (hs-cTnT) are associated with recurrent vascular events and death in patients with first-ever, mild to moderate ischemic stroke. Methods and Results We used data from the PROSCIS-B (Prospective Cohort With Incident Stroke Berlin) study. We computed Cox proportional hazards regression analyses to assess the association between hs-cTnT levels upon study entry (Roche Elecsys, upper reference limit, 14 ng/L) and the primary outcome (composite of recurrent stroke, myocardial infarction, and all-cause death). A total of 562 patients were analyzed (mean age, 67 years [SD 13]; 38.6% women; median National Institutes of Health Stroke Scale=2; hs-cTnT above upper reference limit, 39.2%). During a mean follow-up of 3 years, the primary outcome occurred in 89 patients (15.8%), including 40 (7.1%) recurrent strokes, 4 (0.7%) myocardial infarctions, and 51 (9.1%) events of all-cause death. The primary outcome occurred more often in patients with hs-cTnT above the upper reference limit (27.3% versus 10.2%; adjusted hazard ratio, 2.0; 95% CI, 1.3-3.3), with a dose-response relationship when the highest and lowest hs-cTnT quartiles were compared (15.2 versus 1.8 events per 100 person-years; adjusted hazard ratio, 4.8; 95% CI, 1.9-11.8). This association remained consistent in sensitivity analyses, which included age matching and stratification for sex. Conclusions Hs-cTnT is dose-dependently associated with an increased risk of recurrent vascular events and death within 3 years after first-ever, mild to moderate ischemic stroke. These findings support further studies of the utility of hs-cTnT for individualized risk stratification after stroke. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT01363856.

Keywords: epidemiology; ischemic stroke; mortality/survival; troponin; vascular disease.

Conflict of interest statement

Dr Scheitz reports grants from Corona‐Stiftung during the conduct of the study; personal fees from Stryker GmbH and CoKG, and personal fees from Bristol‐Myers Squibb outside the submitted work. P.S. Sperber reports personal fees from FAZIT‐Stiftung Gemeinnützige Verlagsgesellschaft mbH during the conduct of the study; and research grants from Center for Stroke Research Berlin outside the submitted work. Dr Nolte received research grants from the German Ministry of Research and Education, German Center for Neurodegenerative Diseases, and German Center for Cardiovascular Research. Dr Nolte received speaker and/or consultation fees from Boehringer Ingelheim, Bristol‐Myers Squibb, Pfizer Pharma, Abbott, and W.L. Gore and Associates, all outside the submitted work. Dr Endres reports grants from Bayer and fees paid to the Charité from Bayer, Boehringer Ingelheim, Bristol‐Myers Squibb, Daiichi Sankyo, Amgen, GlaxoSmithKline, Sanofi, Covidien, Novartis, and Pfizer, all outside the submitted work. Dr Audebert reports personal fees from Bayer Vital, personal fees from Boehringer Ingelheim, personal fees from Bristol‐Myers Squibb, personal fees from Novo Nordisk, personal fees from Pfizer, and personal fees from Sanofi, outside the submitted work. Dr Heuschmann reports grants from the German Ministry of Research and Education, German Research Foundation, European Union, Federal Joint Committee (G‐BA) within the Innovationfond, Charité–Universitätsmedizin Berlin, Berlin Chamber of Physicians, German Parkinson Society, University Hospital Würzburg, Robert Koch Institute, German Heart Foundation, University Göttingen (within FIND‐AF randomized, supported by an unrestricted research grant to the University Göttingen from Boehringer‐Ingelheim), University Hospital Heidelberg (within RASUNOA‐prime, supported by an unrestricted research grant to the University Hospital Heidelberg from Bayer, Bristol‐Myers Squibb, Boehringer‐Ingelheim, and Daiichi Sankyo); and grants from Charité–Universitätsmedizin Berlin (within Mondafis, supported by an unrestricted research grant to the Charité from Bayer), outside the submitted work. S. Huo reports grants from the Sonnenfeld Foundation doctoral scholarship outside of the submitted work. The remaining authors have no disclosures to report.

Figures

Figure 1. Study recruitment.

eGFR indicates estimated glomerular filtration rate; hs‐cTnT, high‐sensitivity cardiac troponin T; MI, myocardial infarction; NIHSS, National Institutes of Health Stroke Scale; and PROSCIS‐B, Prospective Cohort With Incident Stroke Berlin.

Figure 2. Kaplan–Meier curves of the combined end point within 3 years after first stroke according to hs‐cTnT.

A, Kaplan–Meier curves of dichotomous hs‐cTnT for the combined end point within 3 years after first stroke. B, Kaplan–Meier curves of hs‐cTnT quartiles* for the combined end point within 3 years after first stroke. hs‐cTnT indicates high‐sensitivity cardiac troponin T; and MI, myocardial infarction. *Quartile 1: hs‐cTnT <6.01 ng/L; Quartile 2: hs‐cTnT ≥6.01 and <11.30 ng/L; Quartile 3: hs‐cTnT ≥11.30 and <19.59 ng/L; Quartile 4: hs‐cTnT ≥19.59 ng/L. hs‐cTnT indicates high‐sensitivity cardiac troponin T.

Figure 3. Kaplan–Meier curves of recurrent stroke within 3 years after first stroke according to hs‐cTnT.

A, Kaplan–Meier curves of dichotomous hs‐cTnT for recurrent stroke within 3 years after first‐ever stroke. B, Kaplan–Meier curves of hs‐cTnT quartiles* for recurrent stroke within 3 years after first‐ever stroke. *Quartile 1: hs‐cTnT <6.01 ng/L; Quartile 2: hs‐cTnT ≥6.01 and <11.30 ng/L; Quartile 3: hs‐cTnT ≥11.30 and <19.59 ng/L; Quartile 4: hs‐cTnT ≥19.59 ng/L. hs‐cTnT indicates high‐sensitivity cardiac troponin T.