Repolarização ventricular em pacientes diabéticos: caracterização e implicações clínicas

Clemente, David; Pereira, Telmo; Ribeiro, Susana

doi:10.1590/s0066-782x2012005000095

Cited by 27 publications

(11 citation statements)

References 34 publications

(26 reference statements)

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“…They have been associated with the risk of arrhythmogenesis. They have also been shown to be prolonged in diabetic patients ( 17 , 18 ). The prevalence of prolonged QTc has been reported to be as high as 16% in type 1 diabetes ( 19 ) and 30.1% in T2DM ( 20 ).…”

Section: Discussionmentioning

confidence: 98%

The effect of 25-hydroxyvitamin D levels on QT interval duration and dispersion in type 2 diabetic patients

Yetkin¹,

Küçükkaya

Turhan

et al. 2015

Croat Med J

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AimTo assess the relationship between corrected QT (QTc) interval and vitamin 25-hydroxyvitamin D levels (25-OHD) deficiency in type 2 diabetic patients.MethodsThe study included 253 patients with type 2 diabetes and 170 age-matched controls treated between October and December 2013. QTc duration and QTc dispersion were measured on ECG recordings and 25-OHD, calcium, phosphorus, and blood glucose levels were determined.ResultsPatients with diabetes had significantly longer QTc duration and QTc dispersion than controls (P < 0.001 and P < 0.001 respectively). Diabetic patients with prolonged QTc duration were older and had longer diabetes duration and higher HbA1c levels than patients with normal QTc interval. They significantly more frequently had 25-OHD deficiency (P < 0.001), but had similar calcium and phosphorus levels. Diabetic patients with prolonged QTc dispersion were of similar age and had similar diabetes duration and HbA1c levels as patients with normal QTc dispersion. They significantly more frequently had 25-OHD deficiency (P = 0.010), but had similar calcium and phosphorus levels.ConclusionThis study showed prolonged QTc duration and QTc dispersion in patients with type 2 diabetes, especially those with 25-OHD deficiency.

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Section: Discussionmentioning

confidence: 98%

The effect of 25-hydroxyvitamin D levels on QT interval duration and dispersion in type 2 diabetic patients

Yetkin¹,

Küçükkaya

Turhan

et al. 2015

Croat Med J

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show abstract

“…The studies reached different conclusions regarding the association between QT parameters prolongation and cardiac end points. Previous study has evaluated the Tp-e interval and other QT parameters in patients with diabetes [ 36 ]. However, there has been a debate on dynamic changes in Tp-e interval like as QT interval so we measured also Tp-e/QT ratio and Tp-e/QTc ratio that is known to be relatively constant parameters and incorporation of these indices may have improved the accuracy of our study.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Tp-e Interval, Tp-e/QT Ratio and Tp-e/QTc Ratio in Patients with Type 2 Diabetes Mellitus

Tokatlı¹,

Kılıçaslan

Alis

et al. 2016

Endocrinol Metab

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BackgroundType 2 diabetes mellitus (T2DM) is associated with increased risk of malignant ventricular arrhythmias. Cardiac electrical inhomogeneity may be the leading cause of the increased arrhythmic risk in patients with T2DM. The peak and the end of the T wave (Tp-e) interval and associated Tp-e/QT ratio are promising measures of ventricular repolarization indicating transmural dispersion of repolarization. The aim of this study was to assess ventricular repolarization in patients with T2DM by using Tp-e interval, Tp-e/QT ratio and Tp-e/corrected QT interval (QTc) ratio.MethodsForty-three patients with T2DM and 43 healthy control subjects, matched by gender and age, were studied. All participants underwent electrocardiography (ECG) recording. PR, RR and QT intervals represents the ECG intervals. These are not abbreviations. In all literature these ECG intervals are written like in this text. Tp-e intervals were measured from 12-lead ECG. Rate QTc was calculated by using the Bazett's formula. Tp-e/QT ratio and Tp-e/QTc ratio were also calculated.ResultsMean Tp-e interval was significantly prolonged in patients with T2DM compared to controls (79.4±10.3, 66.4±8.1 ms, respectively; P<0.001). We also found significantly higher values of Tp-e/QT ratio and Tp-e/QTc ratio in patients with diabetes than controls (0.21±0.03, 0.17±0.02 and 0.19±0.02, 0.16±0.02, respectively; P<0.001). There was no difference in terms of the other ECG parameters between the groups.ConclusionTp-e interval, Tp-e/QT ratio and Tp-e/QTc ratio were prolonged in patients with T2DM. We concluded that T2DM leads to augmentation of transmural dispersion of repolarization suggesting increased risk for ventricular arrhythmogenesis.

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“…Given the evidence presented here, it is clear that increased ROS can lead to intracellular organelle dysfunction and arrhythmias in cardio-metabolic disorders such as diabetes mellitus and hypertension. It is therefore prudent that the at-risk population is identified, which would enable early intervention to reduce arrhythmic mortality (Cardoso et al, 2003 ; Salles et al, 2005 ; Stettler et al, 2007 ; Clemente et al, 2012 ; Tse, 2016a , c ; Tse and Yan, 2016a , b ).…”

Section: Clinical Relevance and Future Perspectivesmentioning

confidence: 99%

Reactive Oxygen Species, Endoplasmic Reticulum Stress and Mitochondrial Dysfunction: The Link with Cardiac Arrhythmogenesis

et al. 2016

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Background: Cardiac arrhythmias represent a significant problem globally, leading to cerebrovascular accidents, myocardial infarction, and sudden cardiac death. There is increasing evidence to suggest that increased oxidative stress from reactive oxygen species (ROS), which is elevated in conditions such as diabetes and hypertension, can lead to arrhythmogenesis.Method: A literature review was undertaken to screen for articles that investigated the effects of ROS on cardiac ion channel function, remodeling and arrhythmogenesis.Results: Prolonged endoplasmic reticulum stress is observed in heart failure, leading to increased production of ROS. Mitochondrial ROS, which is elevated in diabetes and hypertension, can stimulate its own production in a positive feedback loop, termed ROS-induced ROS release. Together with activation of mitochondrial inner membrane anion channels, it leads to mitochondrial depolarization. Abnormal function of these organelles can then activate downstream signaling pathways, ultimately culminating in altered function or expression of cardiac ion channels responsible for generating the cardiac action potential (AP). Vascular and cardiac endothelial cells become dysfunctional, leading to altered paracrine signaling to influence the electrophysiology of adjacent cardiomyocytes. All of these changes can in turn produce abnormalities in AP repolarization or conduction, thereby increasing likelihood of triggered activity and reentry.Conclusion: ROS plays a significant role in producing arrhythmic substrate. Therapeutic strategies targeting upstream events include production of a strong reducing environment or the use of pharmacological agents that target organelle-specific proteins and ion channels. These may relieve oxidative stress and in turn prevent arrhythmic complications in patients with diabetes, hypertension, and heart failure.

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Repolarização ventricular em pacientes diabéticos: caracterização e implicações clínicas

Abstract: We concluded that diabetes causes prolongation and spatial dispersion of repolarization, and it may contribute to a greater ventricular electrical instability, whose expected clinical expression may be malignant ventricular arrhythmias.

Cited by 27 publications

References 34 publications

The effect of 25-hydroxyvitamin D levels on QT interval duration and dispersion in type 2 diabetic patients

The effect of 25-hydroxyvitamin D levels on QT interval duration and dispersion in type 2 diabetic patients

Prolonged Tp-e Interval, Tp-e/QT Ratio and Tp-e/QTc Ratio in Patients with Type 2 Diabetes Mellitus

Reactive Oxygen Species, Endoplasmic Reticulum Stress and Mitochondrial Dysfunction: The Link with Cardiac Arrhythmogenesis

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