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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

Incidence of troponin elevation after adjusting the presence of Q‐waves or ST elevation on ECG (A and B) and incidence of QTc‐prolongation after adjusting the presence of †any drugs affecting QTc‐interval (C and D) according to the stroke severity, or the presence of insular cortical lesion. OR indicates odds ratio. *P<0.05 after adjusting for age, sex, heart rate, hypertension, diabetes mellitus, hyperlipidemia, smoking, and history of ischemic heart disease. †Any drugs affecting QTc‐interval are listed in Table S2.
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jah31815-fig-0002: Incidence of troponin elevation after adjusting the presence of Q‐waves or ST elevation on ECG (A and B) and incidence of QTc‐prolongation after adjusting the presence of †any drugs affecting QTc‐interval (C and D) according to the stroke severity, or the presence of insular cortical lesion. OR indicates odds ratio. *P<0.05 after adjusting for age, sex, heart rate, hypertension, diabetes mellitus, hyperlipidemia, smoking, and history of ischemic heart disease. †Any drugs affecting QTc‐interval are listed in Table S2.

Mentions: The incidence of troponin elevation was higher in patients with moderate‐to‐severe than mild neurological deficits (OR=1.76, 95% CI: 1.13–2.72) among those without Q‐waves or ST elevation on ECG, and higher in both patients with insular cortical lesion than those without insular cortical lesion (OR=2.66, 95% CI: 1.71–4.14 and OR=3.48, 95% CI: 1.34–9.00, respectively) regardless of the presence of Q‐wave or ST elevation on ECG, even after adjusting for covariables (Figure 2A and 2B).


Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke
Incidence of troponin elevation after adjusting the presence of Q‐waves or ST elevation on ECG (A and B) and incidence of QTc‐prolongation after adjusting the presence of †any drugs affecting QTc‐interval (C and D) according to the stroke severity, or the presence of insular cortical lesion. OR indicates odds ratio. *P<0.05 after adjusting for age, sex, heart rate, hypertension, diabetes mellitus, hyperlipidemia, smoking, and history of ischemic heart disease. †Any drugs affecting QTc‐interval are listed in Table S2.
© Copyright Policy - creativeCommonsBy-nc
Related In: Results  -  Collection

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

jah31815-fig-0002: Incidence of troponin elevation after adjusting the presence of Q‐waves or ST elevation on ECG (A and B) and incidence of QTc‐prolongation after adjusting the presence of †any drugs affecting QTc‐interval (C and D) according to the stroke severity, or the presence of insular cortical lesion. OR indicates odds ratio. *P<0.05 after adjusting for age, sex, heart rate, hypertension, diabetes mellitus, hyperlipidemia, smoking, and history of ischemic heart disease. †Any drugs affecting QTc‐interval are listed in Table S2.
Mentions: The incidence of troponin elevation was higher in patients with moderate‐to‐severe than mild neurological deficits (OR=1.76, 95% CI: 1.13–2.72) among those without Q‐waves or ST elevation on ECG, and higher in both patients with insular cortical lesion than those without insular cortical lesion (OR=2.66, 95% CI: 1.71–4.14 and OR=3.48, 95% CI: 1.34–9.00, respectively) regardless of the presence of Q‐wave or ST elevation on ECG, even after adjusting for covariables (Figure 2A and 2B).

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&#8208;lead electrocardiography within 24&nbsp;hours of symptom onset. However, patients with well&#8208;known troponin&#8208;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&nbsp;mg/mL. Multivariable analysis identified electrocardiography abnormalities such as QTc&#8208;prolongation (odds ratio [OR]: 1.52, 95% CI: 1.02&ndash;2.28), left ventricular hypertrophy (OR: 2.14, 95% CI 1.43&ndash;3.19), Q&#8208;wave (OR: 2.53, 95% CI: 1.48&ndash;4.32), and ST elevation (OR: 2.74, 95% CI: 1.12&ndash;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&ndash;1.07) and insular cortical lesions (OR: 2.78, 95% CI: 1.85&ndash;4.19) as neurological variables associated with troponin elevation. Incidence of troponin elevation as well as QTc&#8208;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