Comparison of ion channel distribution and expression in cardiomyocytes of canine pulmonary veins versus left atrium

Melnyk, Peter; Ehrlich, Joachim R.; Pourrier, Marc; Villeneuve, Louis; Cha, Tae-Joon; Nattel, Stanley

doi:10.1016/j.cardiores.2004.08.014

Cited by 94 publications

(88 citation statements)

References 38 publications

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“…Podoplanin knockout embryos have a significant smaller SV and SAN myocardial volume (*P Ͻ 0.05) compared with WT embryos. sion patterns of molecular and immunohistochemical markers (Blom et al, 1999;Jongbloed et al, 2004;Melnyk et al, 2005). In the current study, we observed HCN4 expression in the sinoatrial node and in the myocardium of the wall of the cardinal veins and the pulmonary vein.…”

Section: Discussionmentioning

confidence: 99%

Podoplanin deficient mice show a rhoa‐related hypoplasia of the sinus venosus myocardium including the sinoatrial node

Mahtab

Vicente‐Steijn

Hahurij

et al. 2008

Developmental Dynamics

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We investigated the role of podoplanin in development of the sinus venosus myocardium comprising the sinoatrial node, dorsal atrial wall, and primary atrial septum as well as the myocardium of the cardinal and pulmonary veins. We analyzed podoplanin wild-type and knockout mouse embryos between embryonic day 9.5-15.5 using immunohistochemical marker podoplanin; sinoatrial-node marker HCN4; myocardial markers MLC-2a, Nkx2.5, as well as Cx43; coelomic marker WT-1; and epithelial-to-mesenchymal transformation markers E-cadherin and RhoA. Three-dimensional reconstructions were made and myocardial morphometry was performed. Podoplanin mutants showed hypoplasia of the sinoatrial node, primary atrial septum, and dorsal atrial wall. Myocardium lining the wall of the cardinal and pulmonary veins was thin and perforated. Impaired myocardial formation is correlated with abnormal epithelial-tomesenchymal transformation of the coelomic epithelium due to up-regulated E-cadherin and downregulated RhoA, which are controlled by podoplanin. Our results demonstrate an important role for podoplanin in development of sinus venosus myocardium.

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Section: Discussionmentioning

confidence: 99%

Podoplanin deficient mice show a rhoa‐related hypoplasia of the sinus venosus myocardium including the sinoatrial node

Mahtab

Vicente‐Steijn

Hahurij

et al. 2008

Developmental Dynamics

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“…The pulmonary vein cardiomyocytes have shorter action potential duration, less negative resting membrane potential, and smaller maximum upstroke velocity than those in the left atrium in dogs (8). These characteristics can be explained by lower density of inward rectifier K + current (I K1 ) and L-type Ca 2+ current (I Ca ) and higher density of the delayed rectifier K + current (I K ) in the pulmonary vein myocardial cells than in the atrial ones, whereas there is no significant difference in the density of Na + current (I Na ) between the two regions (8,11).…”

Section: Electrical Conduction In the Pulmonary Veinmentioning

confidence: 95%

Pulmonary Vein Myocardium as a Possible Pharmacological Target for the Treatment of Atrial Fibrillation

et al. 2014

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Abstract. The pulmonary vein has a unique electrophysiological property showing an autonomic electrical activity, and this phenomenon has been further focused on as a source of triggers of atrial fibrillation. The pulmonary vein cardiomyocytes have shorter action potential duration, less negative resting membrane potential, and smaller maximum upstroke velocity than those in the left atrium, whose underlying cellular mechanisms may generate arrhythmogenic substrates such as abnormal automaticity and triggered activity. In diseased conditions including sustained atrial tachycardia or chronic volume overload, its arrhythmogenic profile can be further modified through abbreviation of action potential duration of the pulmonary vein myocardium, which may become a cause of reentry. Recently, antiarrhythmic effects of various drugs have been extensively investigated in isolated pulmonary vein preparations. The present review article highlights the recent advances in our understanding of electrophysiological and pharmacological profiles of the pulmonary vein.

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“…functional conduction block. 47,48 After a waiting period of 30-60 minutes, a slow hyperpolarisation can be observed leading to spontaneous PV reconnection, called DC. 49 The difference between dormant and nondormant PVs lies primarily in the degree of RF-induced depolarisation.…”

Section: Adenosinementioning

confidence: 99%

Pharmacological Tests in Atrial Fibrillation Ablation

Gourraud

Andrade

Macle

et al. 2016

Arrhythmia &Amp; Electrophysiology Review

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Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia observed in clinical practice, occurring in approximately 2 % of the general population.1-3 A progressive increase in both the prevalence and incidence of AF has been demonstrated in recent years, defining AF as a major economic and public health issue. 1 The identification of sites of AF initiation and/or maintenance within the pulmonary veins (PVs) has led to the development of percutaneous procedures to electrically isolate the PVs from the left atrium (LA). 4 Large observational studies and multiple randomised-controlled trials have demonstrated that catheter ablation is universally superior to anti-arrhythmic drugs (AADs) for the maintenance of sinus rhythm (66-89 % versus 9-58 %, respectively) and results in a greater improvement in arrhythmia-related symptoms, exercise capacity and quality of life.1,2,5-8 As a result, catheter ablation has become the 'standard of care' for the maintenance of sinus rhythm in symptomatic patients in whom drugs are ineffective or poorly tolerated.While the results of ablation are unequivocally superior to medical therapy, they are unfortunately not flawless: approximately 30 % of paroxysmal AF patients will experience arrhythmia recurrence after a single ablation procedure.8 As most recurrences are in association with PV reconnection or as a result of non-PV triggers, several pharmacological challenges have been proposed to improve outcomes. [9][10][11][12] This article reviews the pathophysiological background and evidence for the use of pharmacological challenges during catheter ablation procedures. Pathophysiology of Atrial Fibrillation and Atrial Fibrillation Catheter AblationDespite decades of progress, there is no comprehensive pathophysiological explanation of AF. Early hypotheses postulated that AF resulted from the co-existence of multiple independent wavelets propagating randomly throughout the left and right atria (the 'multiple wavelet hypothesis'). 13,14 This hypothesis suggested that as long as the atria had a sufficient electrical mass, and an adequately short refractory period, AF could be initiated and indefinitely perpetuated. 15 Based on this theory, the early surgical interventions for AF were designed to reduce the excitable mass of atrial tissue by compartmentalising the atria into smaller regions incapable of sustaining a critical number of circulating wavelets. 16 Unfortunately this strategy has proved to be of limited efficacy and has been associated with a substantial risk of major complications. 17In the late 1990s, Haïssaguerre and colleagues demonstrated that AF is a triggered arrhythmia initiated by rapid repetitive discharges, predominantly from the proximal aspect of the PVs. 4 This discovery led to the development of percutaneous procedures to directly eliminate spontaneous focal ectopic activity within the PVs. However, early AF recurrences from the targeted and other nontargeted PVs led to modification of the ablation strategy to electrically isolate all of the PV...

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Comparison of ion channel distribution and expression in cardiomyocytes of canine pulmonary veins versus left atrium

Cited by 94 publications

References 38 publications

Podoplanin deficient mice show a rhoa‐related hypoplasia of the sinus venosus myocardium including the sinoatrial node

Podoplanin deficient mice show a rhoa‐related hypoplasia of the sinus venosus myocardium including the sinoatrial node

Pulmonary Vein Myocardium as a Possible Pharmacological Target for the Treatment of Atrial Fibrillation

Pharmacological Tests in Atrial Fibrillation Ablation

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