Sinus node dysfunction and atrial fibrillation: Which one dominates?

Amasyalı, Basri; Kilic, Ayhan; Kılıt, Celal

doi:10.1016/j.ijcard.2014.05.043

Cited by 18 publications

(12 citation statements)

References 12 publications

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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.…”

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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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

View full text Add to dashboard Cite

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“…68 In the cardiovascular health study, low heart rates were associated with an increased risk for AF in the elderly. 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.…”

Section: Bradycardia Predisposes To Afmentioning

confidence: 99%

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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“…Sinus bradycardia in sick sinus syndrome can strongly facilitate the conditions for atrial fibrillation occurrence by both increasing the atrial ectopy and dispersion of the refractoriness. 15 On the other hand, Chang et al showed that in patients with atrial fibrillation, van der HaerT and BLOMMaerT regional atrial remodeling near the sinus node area was associated with prolonged sinus node recovery time, a longer right atrial activation time, a lower voltage of the sinoatrial node area, and a slower conduction velocity, characteristics of sinus node dysfunction. 16 In a study from Hocini et al, ablation to cure atrial fibrillation resulted in a reverse modeling of sinus node function with an increase of the mean heart rate, maximal heart rate, and heart rate range and a decrease in the corrected sinus node recovery time.…”

Section: Discussionmentioning

confidence: 99%

“…Multiple studies have shown a relationship between sinus node dysfunction and atrial fibrillation. Sinus bradycardia in sick sinus syndrome can strongly facilitate the conditions for atrial fibrillation occurrence by both increasing the atrial ectopy and dispersion of the refractoriness . On the other hand, Chang et al showed that in patients with atrial fibrillation, regional atrial remodeling near the sinus node area was associated with prolonged sinus node recovery time, a longer right atrial activation time, a lower voltage of the sinoatrial node area, and a slower conduction velocity, characteristics of sinus node dysfunction .…”

Section: Discussionmentioning

confidence: 99%