Prolongation of QTc and Risk of Stroke

Soliman, Elsayed Z.; Howard, George; Cushman, Mary; Kissela, Brett M.; Kleindorfer, Dawn; Le, Anh; Judd, Suzanne E.; McClure, Leslie A.; Howard, Virginia J.

doi:10.1016/j.jacc.2012.01.025

Cited by 87 publications

(42 citation statements)

References 27 publications

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Ahn

Kim

Shin

et al. 2016

JAHA

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BackgroundTroponin 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 ResultsWe 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.ConclusionsCertain 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.

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Section: Discussionmentioning

confidence: 99%

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

Ahn

Kim

Shin

et al. 2016

JAHA

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“…Recently, Soliman and colleagues reported a strong association between the QT interval and incident stroke among 27,411 participants in the REGARDS study (7). The results of REGARDS are in full agreement with our findings.…”

Section: Discussionmentioning

confidence: 99%

“…Aside from its direct association with arrhythmia and sudden death, QT interval prolongation, perhaps through other mediating factors, is associated with mortality in high-risk individuals (2–5) and in the general population (6–11). Prolongation of the QT interval is also associated with incident stroke (7). However, the association of QT interval duration with incident cardiovascular events in healthy individuals has not been investigated.…”

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confidence: 99%

The QT Interval Is Associated With Incident Cardiovascular Events

Beinart

Zhang

Lima

et al. 2014

Journal of the American College of Cardiology

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Background Prolonged heart rate-corrected QT interval on the electrocardiogram (ECG) is associated with increased risk of myocardial infarction and cardiovascular disease (CVD)-related death in patients with prevalent coronary heart disease (CHD). Objectives We sought to examine the prognostic association between the baseline QT interval and incident cardiovascular events in individuals without known prior CVD. Methods The corrected baseline 12-lead ECG QT interval duration (QTcorr) was determined by adjustment for age, sex, race/ethnicity, and RR interval duration in 6,273 participants in the Multi-Ethnic Study of Atherosclerosis (MESA). Cox proportional hazards models adjusting for demographic and clinical risk factors were used to examine the association of baseline QTcorr with incident cardiovascular events. Results The mean age at enrollment was 61.7 ± 10 years, and 53.4% of participants were women. Cardiovascular events occurred in 291 participants over a mean follow-up of 8.0 ± 1.7 years. Each 10 ms increase in the baseline QTcorr was associated with incident heart failure (HR, 95% confidence interval (CI): 1.25 [1.14 to 1.37]), CVD events (HR, 95% CI: 1.12 [1.05 to 1.20]), and stroke (HR, 95% CI: 1.19 [1.07 to 1.32]) after adjustment for CVD risk factors and potential confounders. There was no evidence of interaction with sex or ethnicity. Conclusion The QT interval is associated with incident cardiovascular events in middle-aged and older adults without prior cardiovascular disease.

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“…QT-interval prolongation is an electrophysiologic phenomenon associated with sudden cardiac death. Prolongation of QT is associated with a significantly increased risk of incident stroke independent of traditional stroke risk factors [31]. Thus, it seems plausible that this SNP may interact with drug treatment to effect stroke risk.…”

Section: Discussionmentioning

confidence: 99%

Pharmacogenetic effects of ‘candidate gene complexes’ on stroke in the GenHAT study

Sørensen

Vázquez

Irvin

et al. 2014

Pharmacogenetics and Genomics

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Objective The goal of this study was to investigate whether there is a genotype by treatment interaction in patients experiencing stroke and treated with one of three antihypertensive drugs, i.e. chlorthalidone, amlodipine and lisinopril. Methods A population of 436 African Americans and 539 whites that have experienced stroke in the GenHAT study were genotyped for 768 single nucleotide polymorphisms in 280 candidate genes. To detect a genotype by treatment interaction we used the Pearson's chi-square test to assess if the genotype frequencies differed at the single SNP level for the three drug treatment groups. From these single SNP analyses we derived a summary statistic for the degree of association at the gene and gene complex levels. This was done by grouping SNPs using information on gene locations and defining gene complexes based on protein-protein interactions. To assess the statistical significance of the observed test statistic we derived an empirical p-value by simulating data under the null hypothesis. Results We found that, in patients that have experienced stroke, there is a significant genetic difference between hypertension drug treatment groups. In African Americans SNP rs12143842 showed significant association (p < 0.001) with drug treatment. At gene-level HNRNPA1P4 and NOS1AP in African Americans and PRICKLE1 and NINJ2 in non-Hispanic whites were significantly associated (p < 0.01) to drug treatment, while none of the gene-complexes tested showed significance. Conclusions Based on the genetic differences between drug treatment groups, we conclude that there may be an interaction between certain genotypes and antihypertensive treatment in stroke patients. This needs to be replicated in other studies.

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Prolongation of QTc and Risk of Stroke

Cited by 87 publications

References 27 publications

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

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

The QT Interval Is Associated With Incident Cardiovascular Events

Pharmacogenetic effects of ‘candidate gene complexes’ on stroke in the GenHAT study

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