Electrocardiographic abnormalities and risk of complete atrioventricular block

Watanabe, Hiroshi; Makita, Naomasa; Tanabe, Naohito; Watanabe, Tôru; Aizawa, Yoshifusa

doi:10.1016/j.ijcard.2011.12.028

Cited by 6 publications

(5 citation statements)

References 25 publications

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“…Depression of I CaL activity via reduced trafficking to the membrane, or altered channel kinetics, will decrease AVN conduction velocity, and can therefore induce ECG changes, including first to third degree AV block (Watanabe ; Watanabe et al. ). There is also evidence to suggest that AV block can initiate the development of QT prolongation and of Torsade de pointes (Tsuji et al.…”

Section: Discussionmentioning

confidence: 99%

“…I CaL is responsible for the action potential upstroke in AVN myocytes, and is therefore fundamental to conduction through the region. Depression of I CaL activity via reduced trafficking to the membrane, or altered channel kinetics, will decrease AVN conduction velocity, and can therefore induce ECG changes, including first to third degree AV block (Watanabe 1981; Watanabe et al 2012). There is also evidence to suggest that AV block can initiate the development of QT prolongation and of Torsade de pointes (Tsuji et al 2002), which can result in sudden cardiac death.…”

Section: Clinical Significance and Conclusionmentioning

confidence: 99%

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Characterization of L-type calcium channel activity in atrioventricular nodal myocytes from rats with streptozotocin-induced Diabetes mellitus

2015

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Cardiovascular complications are common in patients with Diabetes mellitus (DM). In addition to changes in cardiac muscle inotropy, electrical abnormalities are also commonly observed in these patients. We have previously shown that spontaneous cellular electrical activity is altered in atrioventricular nodal (AVN) myocytes, isolated from the streptozotocin (STZ) rat model of type-1 DM. In this study, utilizing the same model, we have characterized the changes in L-type calcium channel activity in single AVN myocytes. Ionic currents were recorded from AVN myocytes isolated from the hearts of control rats and from those with STZ-induced diabetes. Patch-clamp recordings were used to assess the changes in cellular electrical activity in individual myocytes. Type-1 DM significantly altered the cellular characteristics of L-type calcium current. A reduction in peak ICaL density was observed, with no corresponding changes in the activation parameters of the current. L-type calcium channel current also exhibited faster time-dependent inactivation in AVN myocytes from diabetic rats. A negative shift in the voltage dependence of inactivation was also evident, and a slowing of restitution parameters. These findings demonstrate that experimentally induced type-1 DM significantly alters AVN L-type calcium channel cellular electrophysiology. These changes in ion channel activity may contribute to the abnormalities in cardiac electrical function that are associated with high mortality levels in patients with DM.

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Section: Discussionmentioning

confidence: 99%

Section: Clinical Significance and Conclusionmentioning

confidence: 99%

Characterization of L-type calcium channel activity in atrioventricular nodal myocytes from rats with streptozotocin-induced Diabetes mellitus

2015

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“…A population-based cohort study demonstrated that older age, previous myocardial infarction, male sex, suboptimal blood pressure, and fasting glucose levels were associated with the development of atrioventricular block [ 18 ]. Baseline ECG findings, such as first-degree atrioventricular block, bundle branch block, and prolonged QRS duration have also been associated with cardiovascular events [ 19 ]. These background factors should be considered before initiating ICI therapy.…”

Section: Discussionmentioning

confidence: 99%

Two Cases of Immune Checkpoint Inhibitor-Induced Myocarditis With Complete Atrioventricular Block

Kondo¹,

Kirigaya²,

Matsuzawa³

et al. 2023

Cureus

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Immune checkpoint inhibitor-induced myocarditis (ICIM) has been reported to be complicated by a complete atrioventricular block. Even though steroids are used in the treatment thereof, there is no standard protocol for their use. We report two cases of ICIM with a complete atrioventricular block with different outcomes. In the first case, the complete atrioventricular block did not recover. In contrast, in the second case, the complete atrioventricular block did recover. We discuss the different courses and outcomes of the two cases in relation to steroid use.

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“…This is shown in the ECG as an increase in QRS duration. Reduced expression of HCN4, connexin, and ion channels was also identified in various regions of the cardiac conduction system (CCS) in the STZ model of T1DM [37]. Moreover, in a study on hearts of T1DM rats, it was reported that the dysfunction of the CCS plays an integral role in developing cardiac arrhythmias due to increases in RR interval, PR interval and QRS complex duration of the ECG [38].…”

Section: Diabetes Mellitus Induces Changes In the Conduction System O...mentioning

confidence: 95%

Effects of Diabetes Mellitus on the Conduction System of the Heart: Mini-Review

Smail¹,

Rupee²,

Rupee³

et al. 2024

New Insights on Cardiomyopathy

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Diabetes mellitus can induce substantial damage to the conduction system of the heart, especially the sinoatrial node. This is due to hyperglycemia leading to bradyarrhythmia. DM, via the elevation of HG, generates the production of a number of insulting agents in the myocardium known as reactive oxygen species and reactive carbonyl species, which elicit direct damage to neuro-filament-M and β2-adrenergic receptors in the conducting system as well as a number of cardiac contractile, cation transporting and channel proteins. One cation channel protein is the hyperpolarization-activated cyclic nucleotide-gated potassium channel. It encodes the protein responsible for the hyperpolarizing-activated current or the “funny current” that participates in spontaneous diastolic membrane depolarization in sinoatrial node cells. Gene expression of these proteins and their physiological functions are decreased in the diabetic heart, which affects the generation of electrical impulses or action potentials resulting in increases in RR and PR intervals and QRS complex duration of the electrocardiogram. The heart rate and force of contraction of the myocardium are decreased leading to bradyarrhythmia and sudden cardiac death. This review attempts to explain the cellular mechanism(s) involved in diabetes-induced bradyarrhythmia with emphasis on cation-transporting proteins, especially the hyperpolarization-activated cyclic nucleotide-gated channels pacemaker current channels.

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Electrocardiographic abnormalities and risk of complete atrioventricular block

Cited by 6 publications

References 25 publications

Characterization of L-type calcium channel activity in atrioventricular nodal myocytes from rats with streptozotocin-induced Diabetes mellitus

Characterization of L-type calcium channel activity in atrioventricular nodal myocytes from rats with streptozotocin-induced Diabetes mellitus

Two Cases of Immune Checkpoint Inhibitor-Induced Myocarditis With Complete Atrioventricular Block

Effects of Diabetes Mellitus on the Conduction System of the Heart: Mini-Review

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