Effect of β-adrenergic stimulation on the QRS duration of the signal-averaged electrocardiogram

Arnar, Davíð O.; Why, Kent J. Van; Gleed, Kent; Foreman, Blair; Hopson, James R.; Lee, Hon-Chi; Martins, James B.

doi:10.1016/s0002-8703(97)70072-3

Cited by 6 publications

(4 citation statements)

References 11 publications

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“…Previous studies have demonstrated that β-adrenergic agonists increase the inward sodium current in cardiomyocytes [27]–[29]. Because the sodium current is a major determinant of conduction, it is thus reasonable to speculate that enhanced cardiac sympathetic tone is responsible for the reduction in the duration of P wave (index of atrial activation interval), PQ segment (index of atrio-ventricular conduction) and QRS complex (index of ventricular activation) within the heart of FTO deficient mice.…”

Section: Discussionmentioning

confidence: 99%

Signs of Cardiac Autonomic Imbalance and Proarrhythmic Remodeling in FTO Deficient Mice

et al. 2014

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In humans, variants of the fat mass and obesity associated (FTO) gene have recently been associated with obesity. However, the physiological function of FTO is not well defined. Previous investigations in mice have linked FTO deficiency to growth retardation, loss of white adipose tissue, increased energy metabolism and enhanced systemic sympathetic activation. In this study we investigated for the first time the effects of global knockout of the mouse FTO gene on cardiac function and its autonomic neural regulation. ECG recordings were acquired via radiotelemetry in homozygous knockout (n = 12) and wild-type (n = 8) mice during resting and stress conditions, and analyzed by means of time- and frequency-domain indexes of heart rate variability. In the same animals, cardiac electrophysiological properties (assessed by epicardial mapping) and structural characteristics were investigated. Our data indicate that FTO knockout mice were characterized by (i) higher heart rate values during resting and stress conditions, (ii) heart rate variability changes (increased LF to HF ratio), (iii) larger vulnerability to stress-induced tachyarrhythmias, (iv) altered ventricular repolarization, and (v) cardiac hypertrophy compared to wild-type counterparts. We conclude that FTO deficiency in mice leads to an imbalance of the autonomic neural modulation of cardiac function in the sympathetic direction and to a potentially proarrhythmic remodeling of electrical and structural properties of the heart.

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Section: Discussionmentioning

confidence: 99%

Signs of Cardiac Autonomic Imbalance and Proarrhythmic Remodeling in FTO Deficient Mice

et al. 2014

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“…Our results demonstrated that isoprenaline increased the APA and V max of the action potentials, which explains the shortening of the QRS wave on ECG. It should be acknowledged, however, that a shortened QRS duration may also involve increased cellto-cell coupling, which has been shown to change with betaadrenergic stimulation [19,20] . As the sodium-channel current is mainly responsible for the formation of the QRS wave and the action potentials, the shortening of QRS duration and the increases in APA and V max both suggested that isoprenaline might increase the sodiumchannel current.…”

Section: Discussionmentioning

confidence: 99%

Beta-receptor activation increases sodium current in guinea pig heart

et al. 2009

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Aim: To study the influence of β-receptor activation on sodium channel current and the physiological significance of increased sodium current with regard to the increased cardiac output caused by sympathetic excitation. Methods: Multiple experimental approaches, including ECG, action potential recording with conventional microelectrodes, whole-cell current measurements, single-channel recordings, and pumping-force measurements, were applied to guinea pig hearts and isolated ventricular myocytes. Results: Isoprenaline was found to dose-dependently shorten QRS waves, increase the amplitude and the V max of action potentials, augment the fast sodium current, and increase the occurrence frequencies and open time constants of the long-open and burst modes of the sodium channel. Increased levels of membrane-permeable cAMP have similar effects. In the presence of a calcium channel blocker, TTX reversed the increased pumping force produced by isoprenaline. Conclusion: Beta-adrenergic modulation increases the inward sodium current and accelerates the conduction velocity within the ventricles by changing the sodium channel modes, which might both be conducive to the synchronous contraction of the heart and enhance its pumping function.

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“…Beta adrenergic stimulation could enhance conduction that determined by sodium current in the myocardium (24). Adenosine is known to inhibit membrane currents that are stimulated by beta adrenergic agonists (25).…”

Section: Discussionmentioning

confidence: 99%

Effects of adenosine receptor antagonists onamitriptyline-induced QRS prolongation in isolated rat hearts

Akgun

Kalkan

Hocaoğlu

et al. 2008

Clinical Toxicology

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Effect of β-adrenergic stimulation on the QRS duration of the signal-averaged electrocardiogram

Cited by 6 publications

References 11 publications

Signs of Cardiac Autonomic Imbalance and Proarrhythmic Remodeling in FTO Deficient Mice

Signs of Cardiac Autonomic Imbalance and Proarrhythmic Remodeling in FTO Deficient Mice

Beta-receptor activation increases sodium current in guinea pig heart

Effects of adenosine receptor antagonists onamitriptyline-induced QRS prolongation in isolated rat hearts

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