Dataset Information

Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke.

ABSTRACT:

Background

Troponin elevation with electrocardiography changes is not uncommon in patients with acute ischemic stroke; however, it is still unclear whether the mechanism of these changes is due to cardiac problems or neurally mediated myocytic damage. Thus, we investigated cardiac and neurological predictors of troponin elevation in those patients.

Methods and results

We retrospectively analyzed medical data of the prospectively registered ischemic stroke patients on stroke registry who were admitted and underwent a serum cardiac troponin I and 12-lead electrocardiography within 24 hours of symptom onset. However, patients with well-known troponin-elevating comorbidities were excluded from the analysis. Among 1404 ischemic stroke patients, 121 (8.7%) had elevated troponin, which was defined as more than 0.04 mg/mL. Multivariable analysis identified electrocardiography abnormalities such as QTc-prolongation (odds ratio [OR]: 1.52, 95% CI: 1.02-2.28), left ventricular hypertrophy (OR: 2.14, 95% CI 1.43-3.19), Q-wave (OR: 2.53, 95% CI: 1.48-4.32), and ST elevation (OR: 2.74, 95% CI: 1.12-6.72) as cardiac variables associated with troponin elevation, and higher National Institutes of Health Stroke Scale score (OR: 1.04, 95% CI: 1.01-1.07) and insular cortical lesions (OR: 2.78, 95% CI: 1.85-4.19) as neurological variables associated with troponin elevation. Incidence of troponin elevation as well as QTc-prolongation was increased further in combination with cardiac and neurological factors.

Conclusions

Certain cardiac and neurological conditions in acute ischemic stroke may contribute to troponin elevation. The proposed concept of cardiac vulnerability to cerebrogenic stress can be a practical interpretation of troponin elevation and electrocardiography abnormalities in stroke patients.

SUBMITTER: Ahn SH

PROVIDER: S-EPMC5121511 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature

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Publications

Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke.

Ahn Sung-Ho SH Kim Young-Hak YH Shin Chol-Ho CH Lee Ji-Sung JS Kim Bum-Joon BJ Kim Yeon-Jung YJ Noh Sang-Mi SM Kim Seung-Min SM Kang Hyun-Goo HG Kang Dong-Wha DW Kim Jong S JS Kwon Sun U SU

Journal of the American Heart Association 20161006 10

<h4>Background</h4>Troponin elevation with electrocardiography changes is not uncommon in patients with acute ischemic stroke; however, it is still unclear whether the mechanism of these changes is due to cardiac problems or neurally mediated myocytic damage. Thus, we investigated cardiac and neurological predictors of troponin elevation in those patients.<h4>Methods and results</h4>We retrospectively analyzed medical data of the prospectively registered ischemic stroke patients on stroke regist ...[more]

PMID: 27792642

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Project description:Background. Cardiac morbidities account for 20% of deaths after ischemic stroke and is the second commonest cause of death in acute stroke population. Elevation of cardiac troponin has been regarded as a prognostic biomarker of poor outcome in patients with acute stroke. Methods. This retrospective study enrolled 871 patients with acute ischemic stroke from August 2010 to March 2015. Data included vital signs, laboratory parameters collected in the emergency department, and clinical features during hospitalization. National Institutes of Health Stroke Scale (NIHSS), Barthel index, and modified Rankin Scale (mRS) were used to assess stroke severity and outcome. Results. Elevated troponin I (TnI) > 0.01 µg/L was observed in 146 (16.8%) patients. Comparing to patients with normal TnI, patients with elevated TnI were older (median age 77.6 years vs. 73.8 years), had higher median heart rates (80 bpm vs. 78 bpm), higher median white blood cells (8.40 vs. 7.50 1,000/m(3)) and creatinine levels (1.40 mg/dL vs. 1.10 mg/dL), lower median hemoglobin (13.0 g/dL vs. 13.7 g/dL) and hematocrit (39% vs. 40%) levels, higher median NIHSS scores on admission (11 vs. 4) and at discharge (8 vs. 3), higher median mRS scores (4 vs3) but lower Barthel index scores (20 vs. 75) at discharge (p < 0.001). Multivariate analysis revealed that age ? 76 years (OR 2.25, CI [1.59-3.18]), heart rate ? 82 bpm (OR 1.47, CI [1.05-2.05]), evidence of clinical deterioration (OR 9.45, CI [4.27-20.94]), NIHSS score ? 12 on admission (OR 19.52, CI [9.59-39.73]), and abnormal TnI (OR 1.98, CI [1.18-3.33]) were associated with poor outcome. Significant factors for in-hospital mortality included male gender (OR 3.69, CI [1.45-9.44]), evidence of clinical deterioration (OR 10.78, CI [4.59-25.33]), NIHSS score ? 12 on admission (OR 8.08, CI [3.04-21.48]), and elevated TnI level (OR 5.59, CI [2.36-13.27]). C-statistics revealed that abnormal TnI improved the predictive power of both poor outcome and in-hospital mortality. Addition of TnI > 0.01 ug/L or TnI > 0.1 ug/L to the model-fitting significantly improved c-statistics for in-hospital mortality from 0.887 to 0.926 (p = 0.019) and 0.927 (p = 0.028), respectively. Discussion. Elevation of TnI during acute stroke is a strong independent predictor for both poor outcome and in-hospital mortality. Careful investigation of possible concomitant cardiac disorders is warranted for patients with abnormal troponin levels.

Project description:Levels of the cardiac muscle regulatory protein troponin T (cTnT) are frequently elevated in patients with acute ischemic stroke and elevated cTnT predicts poor outcome and mortality. The pathomechanism of troponin release may relate to co-morbid coronary artery disease and myocardial ischemia or, alternatively, to neurogenic cardiac damage due to autonomic activation after acute ischemic stroke. Therefore, there is uncertainty about how acute ischemic stroke patients with increased cTnT levels should be managed regarding diagnostic and therapeutic workup.The primary objective of the prospective observational trial TRELAS (TRoponin ELevation in Acute ischemic Stroke) is to investigate the frequency and underlying pathomechanism of cTnT elevation in acute ischemic stroke patients in order to give guidance for clinical practice. All consecutive patients with acute ischemic stroke admitted within 72 hours after symptom onset to the Department of Neurology at the Campus Benjamin Franklin of the University Hospital Charité will be screened for cTnT elevations (i.e. ? 0.05 ?g/l) on admission and again on the following day. Patients with increased cTnT will undergo coronary angiography within 72 hours. Diagnostic findings of coronary angiograms will be compared with age- and gender-matched patients presenting with Non-ST-Elevation myocardial infarction to the Department of Cardiology. The primary endpoint of the study will be the occurrence of culprit lesions in the coronary angiogram indicating underlying co-morbid obstructive coronary artery disease. Secondary endpoints will be the localization of stroke in the cerebral imaging and left ventriculographic findings of wall motion abnormalities suggestive of stroke-induced global cardiac dysfunction.TRELAS will prospectively determine the frequency and possible etiology of troponin elevation in a large cohort of ischemic stroke patients. The findings are expected to contribute to clarify pathophysiologic concepts of co-morbid cardiac damage in ischemic stroke patients and also to provide a basis for clinical recommendations for cardiac workup of such patients.clinicaltrials.gov NCT01263964.

Project description:The measurement of cardiac troponin is crucial in the diagnosis of myocardial infarction. The performance of troponin measurement is most conveniently monitored by external quality assessment (EQA) programs. The commutability of EQA samples is often unknown and the effectiveness of EQA programs is limited.Commutability of possible EQA materials was evaluated. Commercial control materials used in an EQA program, human serum pools prepared from patient samples, purified analyte preparations, swine sera from model animals and a set of patient samples were measured for cTnI with 4 assays including Abbott Architect, Beckman Access, Ortho Vitros and Siemens Centaur. The measurement results were logarithm-transformed, and the transformed data for patient samples were pairwise analyzed with Deming regression and 95% prediction intervals were calculated for each pair of assays. The commutability of the materials was evaluated by comparing the logarithmic results of the materials with the limits of the intervals. Matrix-related biases were estimated for noncommutable materials. The impact of matrix-related bias on EQA was analyzed and a possible correction for the bias was proposed.Human serum pools were commutable for all assays; purified analyte preparations were commutable for 2 of the 6 assay pairs; commercial control materials and swine sera were all noncommutable; swine sera showed no reactivity to Vitros assay. The matrix-related biases for noncommutable materials ranged from -83% to 944%. Matrix-related biases of the EQA materials caused major abnormal between-assay variations in the EQA program and correction of the biases normalized the variations.Commutability of materials has major impact on the effectiveness of EQA programs for cTnI measurement. Human serum pools prepared from patient samples are commutable and other materials are mostly noncommutable. EQA programs should include at least one human serum pool to allow proper interpretation of EQA results.

Dataset Information

Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke.

Background

Methods and results

Conclusions

Publications

Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke.

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