Hyperglycemia Is Associated With Corrected QT Prolongation and Mortality in Acutely Ill Patients

Pickham, David; Flowers, Elena; Drew, Barbara J.

doi:10.1097/jcn.0b013e31827f174c

Cited by 35 publications

(27 citation statements)

References 31 publications

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“…[8][9][10][11] In addition, a fundamental role of inflammation has been established in all stages of atherosclerosis from initiation through progression and many cardiovascular events. 48 A postulated mechanism underlying the glucose-QTc interval relationship is parasympathetic tone, namely heart rate variability. 8 Consistent with these findings, in the present study, we found that hs-CRP levels and WBC count were significantly higher in the patients with an abnormal QTc interval than in those with a normal QTc interval and hs-CRP level, WBC count and QTc interval were negatively correlated with levels of albumin.…”

Section: Discussionmentioning

confidence: 99%

“…Pickham et al showed that hyperglycaemia is linked with QTc prolongation. 48 A postulated mechanism underlying the glucose-QTc interval relationship is parasympathetic tone, namely heart rate variability. 49 In our study, we also found that the QTc interval was negatively associated with eGFR and albumin level.…”

Section: Despite the Strong Evidence Showing The Effect Of Serum Albumentioning

confidence: 99%

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Serum albumin level and abnormal corrected QT interval in patients with coronary artery disease and chronic kidney disease

et al. 2018

Internal Medicine Journal

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Section: Discussionmentioning

confidence: 99%

Section: Despite the Strong Evidence Showing The Effect Of Serum Albumentioning

confidence: 99%

Serum albumin level and abnormal corrected QT interval in patients with coronary artery disease and chronic kidney disease

et al. 2018

Internal Medicine Journal

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“…Besides insulin, glucose levels are also associated with the QTc interval prolongation, in non‐diabetic patients, T1D and in patients with insulin resistance . Although not all prolongations bear the same CV risk, hyperglycaemia has been attributed to high‐risk QTc prolongation, as well as with increased risk of death .…”

Section: The Hypothesismentioning

confidence: 99%

The role of glucagon in the possible mechanism of cardiovascular mortality reduction in type 2 diabetes patients

Skelin

Javor²,

Lucijanić

et al. 2018

Int J Clin Pract

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Aim: Type 2 diabetes (T2D) is one of the major public health issues worldwide. The main cause of mortality and morbidity among T2D patients are cardiovascular (CV) causes. Various antidiabetics are used in T2D treatment, but until recently they lacked clear evidence of the reduction in CV mortality and all-cause mortality as independent study end-points. The aim of this article was to present and critically evaluate potential mechanisms behind the remarkable results documented in trials with new antidiabetics for the treatment of T2D.Methods: Relevant data were collected using the MEDLINE, PubMed, EMBASE, Web of Science, Science Direct, and Scopus databases with the key words: "type 2 diabetes," "mortality," "glucagon," "empagliflozin," "liraglutide," "insulin" and "QTc."Searches were not limited to specific publication types or study designs. Results:The EMPA-REG OUTCOME trial with empagliflozin and LEADER trial with liraglutide presented remarkable results regarding the reduction in mortality in T2D treatment. However, the potential mechanism for those beneficial effects is difficult to determine. It is not likely that improvements in classic CV risk factors are responsible for the observed effect. A potential mechanism may be caused by the elevation of postprandial (PP) glucagon concentrations that can be seen with an empagliflozin and liraglutide therapy, which could have beneficial effects considering the myocardial electrical stability in T2D patients. Conclusion: This hypothesis throws new light upon possible mechanisms of reduction in mortality in T2D patients. How to cite this article: Skelin M, Javor E, Lucijanić M, Lucijanić T, Jakupović L, Rahelić D. The role of glucagon in the possible mechanism of cardiovascular mortality reduction in type 2 diabetes patients. Int J Clin Pract. 2018;72:e13274.

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“…Some studies have also described electrolytic imbalances, including hypokalemia, as TDP facilitators. Hyperglycemia has also been frequently associated with QTc prolongation in patient suffering acute illnesses [5]. This two conditions should be managed immediately but carefully since treatment of hyperglycemia can result as hypokalemia as well and excessive correction of hypokalemia can lead to another malignant arrythmia.…”

Section: Figure 4: Basal Electrocardiographymentioning

confidence: 99%

Bradycardia-Induced Recurrent Torsade de Pointes: When Serenity Turns into Chaosity

Agusta¹,

Riswati²,

Akbar³

et al. 2018

ijcp

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Torsade De Pointes is typical form of polymorphic ventricular tachycardia. It was in the setting of bradycardia when first described. We present a case of patient coming to emergency room with torsade de pointes development who was found to have bradycardia on basal electrocardiography record. In fact, bradycardia has been shown as a cause of acquired long QT syndrome that can lead to torsade de pointes. The inverse relationship between heart rate and repolarization time primarily accounts for QT prolongation. Finally, proper treatment considering electrophysiology mechanism is essential to prevent mortality.

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Hyperglycemia Is Associated With Corrected QT Prolongation and Mortality in Acutely Ill Patients

Cited by 35 publications

References 31 publications

Serum albumin level and abnormal corrected QT interval in patients with coronary artery disease and chronic kidney disease

Serum albumin level and abnormal corrected QT interval in patients with coronary artery disease and chronic kidney disease

The role of glucagon in the possible mechanism of cardiovascular mortality reduction in type 2 diabetes patients

Bradycardia-Induced Recurrent Torsade de Pointes: When Serenity Turns into Chaosity

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