Ischemic, genetic and pharmacological origins of cardiac arrhythmias: The contribution of the Quebec Heart Institute

Drolet, Benoît; Simard, Chantale; Gailis, L; Daleau, Pascal

doi:10.1016/s0828-282x(07)71006-1

Cited by 5 publications

(6 citation statements)

References 85 publications

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“…The augmented systemic oxidative stress is associated with cardiac electrical and structural remodelling [ 26 – 28 ], and reactive oxygen species may impair Na, K, Ca channels and Na-Ca exchanger activity, leading to gap junction remodelling, decreasing the action potential amplitude and duration, and increasing the incidence of cardiac arrhythmias in animal models [ 15 ]. In fact, oxidative stress results in decreased hERG protein levels, accelerated activation and deactivation of hERG, increased in current amplitude of hERG and hKv1.5, allowing a greater amount of K ions to flow through these channels in the phase 3 of the action potential, down regulation of Ito (transient outward potassium current) responsible for the rapid repolarization phase, and increased the channel opening probability of Ik1 (inward rectifying channel) [ 27 , 28 ].…”

Section: Resultsmentioning

confidence: 99%

Metabolic syndrome is associated with a poor outcome in patients affected by outflow tract premature ventricular contractions treated by catheter ablation

Sardu

Carreras²,

Katsanos

et al. 2014

BMC Cardiovasc Disord

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BackgroundThe purpose of this study was to investigate the impact of metabolic syndrome (MS) on outcome of catheter ablation (CA) for treatment of frequent premature ventricular contraction beats (PVCs) originating from right ventricular outflow tract (RVOT), left ventricular outflow tract (LVOT) or coronary cusps (CUSPs), in patients with normal ventricular systolic function and absence of cardiac structural disease.MethodsIn this multicentre prospective study we evaluated 90 patients with frequent PVCs originating from RVOT (n = 68), LVOT (n = 19) or CUSPs (n = 3), treated with CA. According to baseline diagnosis they were divided in patients with MS (n = 24) or without MS (n = 66). The study endpoint was a composite of recurrence of acute or delayed outflow tract ventricular arrhythmia: acute spontaneous or inducible outflow tract ventricular arrhythmia recurrence or recurrence of outflow tract PVCs in holter monitoring at follow up.ResultsPatients with MS compared to patients without MS showed a higher acute post-procedural recurrence of outflow tract PVCs (n = 8, 66.6%, vs. n = 6, 9.0%, p = 0.005). At a mean follow up of 35 (17-43) months survival free of recurrence of outflow tract PVCs was lower in patients with baseline MS compared to patients without MS diagnosis (log-rank test, p < 0.001). In cox regression analysis, only MS was independently associated with study endpoint (HR = 9.655 , 95% CI 3.000-31.0.68 , p < 0.001).ConclusionsMS is associated with a higher recurrence rate of outflow tract PVCs after CA in patients without structural heart disease.

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Section: Resultsmentioning

confidence: 99%

Metabolic syndrome is associated with a poor outcome in patients affected by outflow tract premature ventricular contractions treated by catheter ablation

Sardu

Carreras²,

Katsanos

et al. 2014

BMC Cardiovasc Disord

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“…Obese subjects exhibit increased systemic oxidative stress, enhanced by abdominal adiposity and associated with adiponectin deficiency [135]. Recent clinical and experimental evidence demonstrated the involvement of oxidative stress in cardiac electrical and structural remodeling [23,136,137]. Reactive oxygen species may impair Na, K and Ca channels, Na-Ca exchanger activity, may be implicated in gap junction remodeling, decrease the action potential amplitude and duration, and increase the incidence of cardiac arrhythmias in animal models [136][137][138][139][140].…”

Section: Oxidative Stress and Arrhythmogenesismentioning

confidence: 99%

“…Oxidative stress results in decreased hERG protein levels, accelerated activation and deactivation of hERG, and increase in current amplitude of hERG and hKv1.5, allowing a greater amount of K ions to flow through these channels in the phase 3 of the action potential, downregulation of Ito (responsible for the rapid repolarization phase), and increases the channel opening probability of Ik1 (inward rectifying channel) [136,137].…”

Section: Oxidative Stress and Arrhythmogenesismentioning

confidence: 99%

Arrhythmia Risk and Obesity

Mozoş¹

2014

J Mol Genet Med

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“…The AGEs/RAGE axis can elicit mitochondrial dysfunction and generate reactive oxygen species (ROS), which in turn activate a nuclear factor kappa B (NFκB) cascade (Gloire et al, 2006 ; Wang et al, 2015 ; Wautier et al, 2001 ; Yamagishi et al, 2015 ). Augmented systemic oxidative stress is associated with cardiac electrical and structural remodeling, which may impair Na + , potassium (K + ), and calcium (Ca 2+ ) channels and Na–Ca exchanger (NCX) activity, thus leading to gap junction remodeling, decreased action potential (AP) amplitude (APA) and AP duration (APD), and increased incidence of cardiac arrhythmia in animal models (Dong & Ren, 2014 ; Drolet et al, 2007 ; Jeong et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Advanced glycation end products modulate electrophysiological remodeling of right ventricular outflow tract cardiomyocytes: A novel target for diabetes‐related ventricular arrhythmogenesis

Chen

et al. 2022

Physiological Reports

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Diabetes mellitus is associated with cardiovascular disease and cardiac arrhythmia. Accumulation of advanced glycation end products closely correlates with cardiovascular complications through mitochondrial dysfunction or oxidative stress and evoke proliferative, inflammatory, and fibrotic reactions, which might impair cardiac electrophysiological characteristics and increase the incidence of cardiac arrhythmia. This study examined the mechanisms how advanced glycation end products may contribute to arrhythmogenesis of right ventricular outflow tract—a unique arrhythmogenic substrate. A whole‐cell patch clamp, conventional electrophysiological study, fluorescence imaging, Western blot, and confocal microscope were used to study the electrical activity, and Ca 2+ homeostasis or signaling in isolated right ventricular outflow tract myocytes with and without advanced glycation end products (100 μg/ml). The advanced glycation end products treated right ventricular outflow tract myocytes had a similar action potential duration as the controls, but exhibited a lower L‐type Ca 2+ current, higher late sodium current and transient outward current. Moreover, the advanced glycation end products treated right ventricular outflow tract myocytes had more intracellular Na + , reverse mode Na + –Ca 2+ exchanger currents, intracellular and mitochondrial reactive oxygen species, and less intracellular Ca 2+ transient and sarcoplasmic reticulum Ca 2+ content with upregulated calcium homeostasis proteins and advanced glycation end products related signaling pathway proteins. In conclusions, advanced glycation end products modulate right ventricular outflow tract electrophysiological characteristics with larger late sodium current, intracellular Na + , reverse mode Na + –Ca 2+ exchanger currents, and disturbed Ca 2+ homeostasis through increased oxidative stress mediated by the activation of the advanced glycation end products signaling pathway.

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Ischemic, genetic and pharmacological origins of cardiac arrhythmias: The contribution of the Quebec Heart Institute

Cited by 5 publications

References 85 publications

Metabolic syndrome is associated with a poor outcome in patients affected by outflow tract premature ventricular contractions treated by catheter ablation

Metabolic syndrome is associated with a poor outcome in patients affected by outflow tract premature ventricular contractions treated by catheter ablation

Arrhythmia Risk and Obesity

Advanced glycation end products modulate electrophysiological remodeling of right ventricular outflow tract cardiomyocytes: A novel target for diabetes‐related ventricular arrhythmogenesis

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