J Stroke.  2023 Jan;25(1):141-150. 10.5853/jos.2022.02012.

Explanatory Power and Prognostic Implications of Factors Associated with Troponin Elevation in Acute Ischemic Stroke

Affiliations
  • 1Department of Neurology, Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Busan, Korea
  • 2Clinical Research Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
  • 3Division of Biostatistics, Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Busan, Korea
  • 4Department of Neurology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, Korea
  • 5Division of Cardiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
  • 6Division of Cardiology, Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Busan, Korea
  • 7Department of Neurology, Gangneung Asan Hospital, University of Ulsan, Gangneung, Korea

Abstract

Background and Purpose
We investigated the impact of comorbidity burden on troponin elevation, with separate consideration of neurological conditions, in patients with acute ischemic stroke (AIS).
Methods
This prospective, observational cohort study consecutively enrolled patients with AIS for 2 years. Serum cardiac troponin I was repeatedly measured, and disease-related biomarkers were collected for diagnosis of preassigned comorbidities, including atrial fibrillation (AF), ischemic heart disease (IHD), myocardial hypertrophy (MH), heart failure (HF), renal insufficiency (RI), and active cancer. The severity of neurological deficits and insular cortical ischemic lesions were assessed as neurological conditions. Adjusted associations between these factors and troponin elevation were determined using a multivariate ordinal logistic regression model and area under the receiver operating characteristic curve (AUC). Cox proportional hazards model was used to determine the prognostic significance of comorbidity beyond neurological conditions.
Results
Among 1,092 patients (66.5±12.4 years, 63.3% male), 145 (13.3%) and 335 (30.7%) had elevated (≥0.040 ng/mL) and minimally-elevated (0.040–0.010 ng/mL) troponin, respectively. In the adjusted analysis, AF, MH, HF, RI, active cancer, and neurological deficits were associated with troponin elevation. The multivariate model with six comorbidities and two neurological conditions exhibited an AUC of 0.729 (95% confidence interval [CI], 0.698–0.759). In Cox regression, AF, IHD, and HF were associated with adverse cardio-cerebrovascular events, whereas HF and active cancer were associated with mortality.
Conclusion
Troponin elevation in patients with AIS can be explained by the burden of comorbidities in combination with neurological status, which explains the prognostic significance of troponin assay.

Keyword

Troponin; Stroke; Comorbidity; Prognosis

Figure

  • Figure 1. Flow diagram of the study protocol. Process of patient selection and classification according to the troponin level and diagnosis of troponin elevation-related factors to assess their predictive value. AIS, acute ischemic stroke; ECG, electrocardiography; BNP, b-type natriuretic peptide; NIHSS, National Institutes of Health Stroke Scale; AF, atrial fibrillation; IHD, ischemic heart disease; MH, myocardial hypertrophy; HF, heart failure; RI, renal insufficiency; MACCE, major adverse cardiac and cerebrovascular event.

  • Figure 2. Diagnostic approach model for assessing troponin elevation in patients with AIS. Process for detecting the troponin elevation (red line) and etiological evaluation of troponin elevation (blue line), including the recommendation of the clinical process (blue box) and diagnosis of the troponin elevation-related factors (green box). AIS, acute ischemic stroke; CMI, cerebrogenic myocardial injury; NIHSS, National Institutes of Health Stroke Scale; ECG, electrocardiography; ACS, acute coronary syndrome; STEMI, ST-segment elevation myocardial infarction; NSTEMI, non-ST-segment elevation myocardial infarction; RI, renal insufficiency; SICMP, stress-induced cardiomyopathy; AF, atrial fibrillation; IHD, ischemic heart disease; MH, myocardial hypertrophy; HF, heart failure; RI, renal insufficiency; CT, computed tomography; LBBB, left bundle branch block. *ECG pattern, including (1) suspicious STEMI, which initially developed as an acute ischemic change (e.g., ST-segment elevation or LBBB), followed by newly developed Q-wave on serial ECG investigation; and (2) suspicious NSTEMI, which transiently/persistently developed as an acute ischemic change (e.g., ST-segment depression with or without T-wave inversion) on serial ECG investigation.


Reference

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