The ECG in Diabetes Mellitus

Stern, Shlomo; S, Sclarowsky

doi:10.1161/circulationaha.109.897496

Cited by 52 publications

(41 citation statements)

References 29 publications

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“…Prolonged QT interval is a cardiac electrical disorder that predicts late development of ventricular arrhythmias and sudden cardiac death (11). Long QT has been positively correlated with the body mass index (BMI) and occurs in early development of type 2 diabetes that occurs mostly in obese populations (14,17,25,29). The most recent report from the Multi-Ethnic Study of Atherosclerosis has provided strong evidence that, in addition to a positive correlation between QT interval and BMI, even a small increase in QT interval (10 ms) can impose a significant effect on future increased incidents of cardiovascular events, although the mechanism is presently unknown (3).…”

Section: Discussionmentioning

confidence: 99%

Leptin decreases heart rate associated with increased ventricular repolarization via its receptor

Lin

Huang

Hileman

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Leptin has been proposed to modulate cardiac electrical properties via ␤-adrenergic receptor activation. The presence of leptin receptors and adipocytes in myocardium raised a question as to whether leptin can directly modulate cardiac electrical properties such as heart rate and QT interval via its receptor. In this work, the role of local direct actions of leptin on heart rate and ventricular repolarization was investigated. We identified the protein expression of leptin receptors at cell surface of sinus node, atrial, and ventricular myocytes isolated from rat heart. Leptin at low doses (0.1-30 g/kg) decreased resting heart rate; at high doses (150 -300 g/kg), leptin induced a biphasic effect (decrease and then increase) on heart rate. In the presence of high-dose propranolol (30 mg/kg), high-dose leptin only reduced heart rate and sometimes caused sinus pauses and ventricular tachycardia. The leptin-induced inhibition of resting heart rate was fully reversed by leptin antagonist. Leptin also increased heart rate-corrected QT interval (QTc), and leptin antagonist did not. In isolated ventricular myocytes, leptin (0.03-0.3 g/ml) reversibly increased the action potential duration. These results supported our hypothesis that in addition to indirect pathway via sympathetic tone, leptin can directly decrease heart rate and increase QT interval via its receptor independent of ␤-adrenergic receptor stimulation. During inhibition of ␤-adrenergic receptor activity, high concentration of leptin in myocardium can cause deep bradycardia, prolonged QT interval, and ventricular arrhythmias.leptin; leptin receptor; resting heart rate; QT interval NEW & NOTEWORTHYLeptin is believed to increase heart rate via adrenergic receptor stimulation. We found evidence that leptin can exert local direct inhibition of heart rate and prolongation of QTc interval via its receptor. The findings offer better understanding of higher incidence of prolonged QT and sudden cardiac death in obesity.LEPTIN IS A 16-KDA ADIPOKINE released from adipocytes acting via its receptor. Detection of adipocytes in obese human heart (21, 30) and leptin receptors in human cardiac ventricles (19) has suggested that leptin can have autocrine and paracrine effects on cardiac functions.Leptin has been demonstrated to play an important role in cardiac contractility (19, 37), development of hypertrophy (12,19,37,39), and apoptosis (20). However, studies of leptin on cardiac electrical properties are rare and limited to indirect effects via adrenergic receptor stimulation. It has been widely accepted that leptin increases the heart rate through increasing sympathetic activity (5, 9, 10). Leptin-mediated increase in sympathetic activity can explain obese subjects with higher heart rate to meet the increased metabolic demands (25), but it cannot explain why many of them exhibit unchanged or decreased resting heart rate (2, 7).In heart failure patients, fatty infiltration of cardiomyocytes has been demonstrated. The percentage of fat in myocardium is positively correlat...

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Section: Discussionmentioning

confidence: 99%

Leptin decreases heart rate associated with increased ventricular repolarization via its receptor

Lin

Huang

Hileman

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…This further supports beneficial effect of MAO A inhibition in preventing excess accumulation of extracellular matrix proteins, which may impede LV contractility. Diabetes also affects electrical activity of the heart and ECG offers a non-invasive screen to assess these changes (38,39). QTc interval, an electrocardiographic parameter, is of particular clinical significance as it is a prominent predictor of stroke and mortality in patients with diabetes (40,41).…”

Section: Fig 5 Mao a Inhibition Prevents Diabetes-induced Myocardiamentioning

confidence: 99%

Monoamine oxidase-A is an important source of oxidative stress and promotes cardiac dysfunction, apoptosis, and fibrosis in diabetic cardiomyopathy

Umbarkar

Singh

Arkat

et al. 2015

Free Radical Biology and Medicine

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Oxidative stress is closely associated with the pathophysiology of diabetic cardiomyopathy (DCM). The mitochondrial flavoenzyme monoamine oxidase A (MAO-A) is an important source of oxidative stress in the myocardium. We sought to determine whether MAO-A plays a major role in modulating DCM. Diabetes was induced in Wistar rats by single intraperitoneal injection of streptozotocin (STZ). To investigate the role of MAO-A in the development of pathophysiological features of DCM, hyperglycemic and age-matched control rats were treated with or without the MAO-A-specific inhibitor clorgyline (CLG) at 1 mg/kg/day for 8 weeks. Diabetes upregulated MAO-A activity; elevated markers of oxidative stress such as cardiac lipid peroxidation, superoxide dismutase activity, and UCP3 protein expression; enhanced apoptotic cell death; and increased fibrosis. All these parameters were significantly attenuated by CLG treatment. In addition, treatment with CLG substantially prevented diabetes-induced cardiac contractile dysfunction as evidenced by decreased QRS, QT, and corrected QT intervals, measured by ECG, and LV systolic and LV end-diastolic pressure measured by microtip pressure transducer. These beneficial effects of CLG were seen despite the persistent hyperglycemic and hyperlipidemic environments in STZ-induced experimental diabetes. In summary, this study provides strong evidence that MAO-A is an important source of oxidative stress in the heart and that MAO-A-derived reactive oxygen species contribute to DCM.

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“…However, in clinical practice a 12-lead ECG provides more information compared with a single lead ECG. For example, it is established that there is a relationship between diabetes mellitus (DM) and QT abnormalities [27][28][29]. QT prolongation and increased QT dispersion have been shown to predict cardiac death in Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus.…”

Section: Introductionmentioning

confidence: 99%

“…This paper describes the work done to estimate diabetic-related features from 12-lead ECG data. The other ECG parameters which are affected in diabetic patients are QTc and ST segment depression [28,29,31].…”

Section: Introductionmentioning

confidence: 99%

“…About one third of acute myocardial infarction patients have diabetes mellitus, the prevalence of which is steadily increasing [29]. In the 1960s, there were 2 million Americans with diabetes mellitus; in the year 2000, their number was 15 million [29], in 2007 it was 17.9 million [32] and in 2010 it increased to 25.6 million [33]. In the United Arab Emirates (UAE) 19% of the people over 20 years of age are diabetic.…”

Section: Introductionmentioning

confidence: 99%

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ECG feature extraction using principal component analysis for studying the effect of diabetes

Kalpana¹,

Hamde

Waghmare

2013

Journal of Medical Engineering & Technology

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The condition of cardiac health is given by Electrocardiogram (ECG). ECG analysis is one of the most important aspects of research in the field of Biomedical and healthcare. The precision in the identification of various parameters in ECG is of great importance. Many algorithms have been developed in the last few years for this purpose. Since diabetes is the major chronic illness prevailing today, recently there has been increasing interest in the study of the relationship between diabetes and cardiac health. This paper presents an algorithm based on Principal Component Analysis (PCA) for 12 lead ECG feature extraction and the estimation of diabetes-related ECG parameters. The data used for our purpose is acquired by XBio Aqulyser unit from TMI systems. The baseline wander is removed from the acquired data using the FFT approach and the signal is de-noised using wavelet transform and then the PCA method is employed to extract the R-wave. The other waves are then extracted using the window method. Later, using these primary features, the diabetes mellitus (DM)-related features like corrected QT interval (QTc), QT dispersion (QTd), P wave dispersion (PD) and ST depression (STd) are estimated. This study has taken 25 diabetic patients data for study.

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The ECG in Diabetes Mellitus

Cited by 52 publications

References 29 publications

Leptin decreases heart rate associated with increased ventricular repolarization via its receptor

Leptin decreases heart rate associated with increased ventricular repolarization via its receptor

Monoamine oxidase-A is an important source of oxidative stress and promotes cardiac dysfunction, apoptosis, and fibrosis in diabetic cardiomyopathy

ECG feature extraction using principal component analysis for studying the effect of diabetes

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