Sinoatrial node electrical activity modulates pulmonary vein arrhythmogenesis

Chen, Yao Chang; Lu, Yen Yu; Cheng, Chen Chuan; Lin, Yung‐Kuo; Chen, Shih A.; Chen, Yi‐Jen

doi:10.1016/j.ijcard.2014.03.009

Cited by 36 publications

(32 citation statements)

References 35 publications

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“…69 An intriguing experimental study using isolated rabbit atrial sections that incorporated the SN and pulmonary veins suggested an interaction between SN tissue, atrial myocardium, and pulmonary vein tissue. 70 When the connection between SN and the pulmonary vein were interrupted in this preparation, pulmonary venous musculature demonstrated more burst firing and early after-depolarizations in response to provocative agents in comparison with control rabbits with intact connections. Thus, the loss of SN overdrive modulation on subsidiary pace-making cells likely facilitates the generation of ectopic arrhythmias.…”

Section: Bradycardia Predisposes To Afmentioning

confidence: 74%

Sinus Node and Atrial Arrhythmias

2016

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Sinus node dysfunction (SND) and atrial arrhythmias frequently coexist and interact to initiate and perpetuate each other. Atrial arrhythmias are present in 40% to 70% of patients at the time of diagnosis of SND.1,2 However, the complex relationship between the 2 remains ill defined. The documented degenerative changes in atrial myocardial structure relating to SND are primarily right atrial. Yet, the majority of triggers and substrates for atrial fibrillation (AF) originate from the left atrium. Although progressive biatrial fibrosis is a feature in patients with structural heart disease and in senescence, paroxysmal AF that occurs in patients with no structural heart disease may have a different pathophysiology. SND associated with this latter condition is likely to be primarily a result of electric remodeling and potentially reversible. The time course of the progression of SND and AF 3 and their individual clinical manifestations also vary depending on the underlying pathology. The purpose of this review is to summarize the state of our knowledge of sinus node (SN) function in both health and disease, and to understand the complex relationship between SN disease and atrial arrhythmias. Structure and Functional Components of the Sinus NodeIn the adult human heart, the SN is a crescent-shaped structure 1 to 2 cm long and 0.5 cm wide that lies at the junction of the superior vena cava with the right atrium and lies along the sulcus terminalis. The node itself is composed of clusters of pacemaker myocytes arranged in parallel rows with short digitations that frequently anastomose with the surrounding atrial tissue. The specialized pacemaker cells are interspersed with nerves and capillaries and scaffolded by dense connective tissue to form the SN pacemaker complex. The caudal portion fragments to merge with the atrial myocardium. The lack of a distinct encapsulation and the radiating sinoatrial connections explains the lack of a single breakthrough of the sinus impulse. The position of the leading pacemaker site shifts within the node and varies with sympathetic and vagal stimulation. 3The SN pacemaker cells are interspersed with interstitial collagen that varies in extent as a function of older age. 4 Collagen content increases from 24% in the infant to 70% in the adult heart.5 The fibrous matrix with surrounding fatty insulation of the SN together with distinct electrophysiological properties (see below) provides insulation and prevents the depression of pacemaker automaticity from the hyperpolarizing electric load of the surrounding atrial myocardium. 6 Multiple currents are involved in the activation of the SN. The predominant inward current in the center of the node is I CaL . Action potentials with slow upstrokes initiated in the center spreads peripherally and into the musculature of the terminal crest. However, in the periphery of the node, I Na is operative and is necessary for providing sufficient inward current to depolarize the larger mass of atrial tissue. Delayed rectifier potassium currents facili...

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Section: Bradycardia Predisposes To Afmentioning

confidence: 74%

Sinus Node and Atrial Arrhythmias

2016

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“…Bradycardia per se might stimulate atrial ectopic beats and enhance greater dispersion of atrial refractoriness, and both are vital factors for initiating AF 16. An experimental study also found that interrupted electrical connection between the sinoatrial node and pulmonary veins might facilitate burst firing of the pulmonary veins and occurrence of AF 17. Therefore, up to 50% of sick sinus syndrome patients with long pauses are accompanied by paroxysmal supraventricular tachycardia, and most of them were AF 18, 19.…”

Section: Discussionmentioning

confidence: 99%

Intermediate Pause at Daytime Is Associated With Increased Cardiovascular Risk and Mortality: An 8‐Year Cohort Study

Liu

Lin

Chang

et al. 2018

JAHA

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BackgroundLong‐term cardiovascular risk in patients with intermediate pauses remains unclear. Whether asymptomatic patients with intermediate pauses have increased future cardiovascular events remains unknown. We hypothesize that intermediate pause is associated with increased cardiovascular risk and mortality.Methods and ResultsWe retrospectively analyzed 5291 patients who have pauses of <3 seconds on 24‐hour Holter monitoring. Patients with pauses of 2 to 3 seconds constitute the intermediate pause patients, who are further divided into daytime pause (8:00 am–8:00 pm), nighttime pause (8:00 pm–8:00 am), and daytime plus nighttime pause groups depending on the occurring time of the pauses. The rest of the patients (pause <2 seconds) are the no pause group. The multivariate Cox hazards regression model was used to assess the hazard ratio for mortality (primary outcome) and adverse cardiovascular events (secondary outcome). There were 4859 (91.8%) patients in no pause, 248 (4.7%) in nighttime pause, 103 (1.9%) in daytime pause, and 81 (1.5%) in daytime plus nighttime pause groups. After a follow‐up of 8.8±1.7 years’ follow‐up, 343 (6.5%) patients died. The risk for adverse cardiovascular events, including all‐cause hospitalization, cardiovascular‐cause hospitalization, pacemaker implantation, new‐onset atrial fibrillation/heart failure, and transient ischemic attack, were higher in daytime pause and nighttime pause patients than those in the no pause group. Daytime pause (hazard ratio, 2.35; P=0.008) and daytime plus nighttime pause (hazard ratio, 2.26; P=0.016) patients have a higher mortality rate than that in nighttime pause.ConclusionsPatients with intermediate pause are associated with increased cardiovascular risk. Intermediate pauses occurring at daytime have a higher mortality rate than that at nighttime during long‐term follow‐up.

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“…Intact electrical connections between the SAN and PVs is crucial for preventing arrhythmogenesis, as demonstrated by experiments in which rabbits with disrupted electrical connections between the SAN and PVs demonstrated more burst firing and EAD in response to Anemonia sulcata toxin (ATX)-II ( Figure 5). 75 However, the reverse view is also supported by clinical observation that longstanding AF and other supraventricular tachycardias cause remodeling of the SAN, leading to its dysfunction and subsequent bradycardias, which might recover after ablation of the tachyarrhythmias.…”

Section: Aging Increases Oxidative Stress and Inflammationmentioning

confidence: 99%

Aging Modulates the Substrate and Triggers Remodeling in Atrial Fibrillation

Lin

Chen

Lee

et al. 2018

Circ J

Self Cite

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how aging and AF are connected and highlight the potential role of aging in AF substrate and triggered remodeling. Effects of Aging on Structural RemodelingStructural remodeling is characterized by histopathological changes, such as cellular hypertrophy, apoptosis, or myocardial fibrosis, and anatomical changes, such as chamber dilatation. 5 Anatomical Changes With Dilation of PV and Atria in AgingThe left atrium (LA) anteroposterior diameter and wall thickness increase with aging, and the 4 PVs become dilated in patients older than 50 years (Figure 1), 3 which suggests mechanical effects of aging on AF triggers and substrates. 3 Clinical data indicate that PV size correlates with PV arrhythmogenesis. Therefore, larger PVs may correlate with a higher PV arrhythmogenesis resulting in AF. Histopathological Changes With AgingBoth animal and human studies had shown that loss of cardiomyocytes by apoptosis and necrosis produces compensatory cellular hypertrophy, which may represent the structural basis of the aged heart, and contribute to cardiac dysfunction in the elderly. 5 Aging increases the rate of ventricular cardiomyocyte death caused by enhanced vulnerability to stress such as oxidative stress. 6 These histopathological changes at the microscopic level potentially T he prevalence and severity of arrhythmias increase with age. Advancing age is independently associated with the prevalence of atrial fibrillation (AF). 1 Aging and aging-related underlying diseases frequently result in structural remodeling as cardiac morphological changes either grossly or at the histological and ultrastructural levels, or they induce electrophysiological remodeling with changes in cardiac electrical properties in response to a functional insult, or as a result of a structural alteration. Aging-associated cardiac anatomical and functional remodeling may enhance the occurrence or the persistence of AF.Ectopic impulses generated from the pulmonary veins (PVs) play a key role in the genesis and maintenances of AF. 2 Elimination of PV arrhythmogenic foci or targeting atrial substrate abnormalities reduces the AF burden or cures AF. 2 PVs contain complex electrical activity because of their distinctive anatomical and physiological characteristics. 3 Aging-associated electrophysiological or structural changes in the atria or PVs may facilitate AF occurrence. 3 Age is an independent predictor of AF recurrence in lone AF patients after undergoing the first circumferential PV isolation. 4 AF may coexist with cardiovascular disorders, which may potentiate its occurrence, and these are also more prevalent with increased age. Together with agingrelated myocardial degeneration or anatomical changes, both inflammation and oxidative stress, as consequences of aging, enhance the occurrence and maintenance of AF. The aim of this review is to update the understanding of Aging plays a critical role in the genesis of atrial fibrillation (AF) and also increases the risks of cardiac dysfunction and stroke in AF patients. AF is caused by increased AF t...

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Sinoatrial node electrical activity modulates pulmonary vein arrhythmogenesis

Cited by 36 publications

References 35 publications

Sinus Node and Atrial Arrhythmias

Sinus Node and Atrial Arrhythmias

Intermediate Pause at Daytime Is Associated With Increased Cardiovascular Risk and Mortality: An 8‐Year Cohort Study

Aging Modulates the Substrate and Triggers Remodeling in Atrial Fibrillation

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