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

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus

Suggested explanation of troponin elevation in acute stage of ischemic stroke. Troponin elevation may be synergistically induced by a combination of provocative cerebrogenic stress (eg, after insular cortical lesion [major or minor involvement; A and B] or severe stroke) and vulnerable heart (eg, hypertrophic or damaged myocardium). QTc‐prolongation may be a composite marker for reflecting both predisposed and newly provoked prolongation due to the underlying cardiac problems and provocative cerebrogenic stress.
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jah31815-fig-0004: Suggested explanation of troponin elevation in acute stage of ischemic stroke. Troponin elevation may be synergistically induced by a combination of provocative cerebrogenic stress (eg, after insular cortical lesion [major or minor involvement; A and B] or severe stroke) and vulnerable heart (eg, hypertrophic or damaged myocardium). QTc‐prolongation may be a composite marker for reflecting both predisposed and newly provoked prolongation due to the underlying cardiac problems and provocative cerebrogenic stress.

Mentions: We found that QTc‐prolongation was the most common ECG abnormality and one of the cardiac factors associated with troponin elevation. In addition, QTc‐prolongation was closely associated with both cardiac and neurological factors the same as troponin elevation (Figures 1 and 2). QTc‐prolongation represents a ventricular repolarization delay and is related to diverse etiologies including LVH, ischemic heart disease, certain drugs, dyselectrolytemia, hypertension, diabetes mellitus, and stroke.25 Neuromediated autonomic dysregulation has also been suggested as a potential mechanism of QTc‐prolongation in stroke similarly to troponin elevation.24 Therefore, QTc‐prolongation is a composite cardiac marker reflecting both neurological and cardiac conditions. Taken together, our findings point to 2 different clinical implications of troponin elevation and ECG abnormalities in the acute stage of ischemic stroke as representing (1) primary changes by predisposed cardiac problems and (2) secondary changes superimposed on the primary changes before and after stroke (Figure 4).


Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke
Suggested explanation of troponin elevation in acute stage of ischemic stroke. Troponin elevation may be synergistically induced by a combination of provocative cerebrogenic stress (eg, after insular cortical lesion [major or minor involvement; A and B] or severe stroke) and vulnerable heart (eg, hypertrophic or damaged myocardium). QTc‐prolongation may be a composite marker for reflecting both predisposed and newly provoked prolongation due to the underlying cardiac problems and provocative cerebrogenic stress.
© Copyright Policy - creativeCommonsBy-nc
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5121511&req=5

jah31815-fig-0004: Suggested explanation of troponin elevation in acute stage of ischemic stroke. Troponin elevation may be synergistically induced by a combination of provocative cerebrogenic stress (eg, after insular cortical lesion [major or minor involvement; A and B] or severe stroke) and vulnerable heart (eg, hypertrophic or damaged myocardium). QTc‐prolongation may be a composite marker for reflecting both predisposed and newly provoked prolongation due to the underlying cardiac problems and provocative cerebrogenic stress.
Mentions: We found that QTc‐prolongation was the most common ECG abnormality and one of the cardiac factors associated with troponin elevation. In addition, QTc‐prolongation was closely associated with both cardiac and neurological factors the same as troponin elevation (Figures 1 and 2). QTc‐prolongation represents a ventricular repolarization delay and is related to diverse etiologies including LVH, ischemic heart disease, certain drugs, dyselectrolytemia, hypertension, diabetes mellitus, and stroke.25 Neuromediated autonomic dysregulation has also been suggested as a potential mechanism of QTc‐prolongation in stroke similarly to troponin elevation.24 Therefore, QTc‐prolongation is a composite cardiac marker reflecting both neurological and cardiac conditions. Taken together, our findings point to 2 different clinical implications of troponin elevation and ECG abnormalities in the acute stage of ischemic stroke as representing (1) primary changes by predisposed cardiac problems and (2) secondary changes superimposed on the primary changes before and after stroke (Figure 4).

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus