Sinus Node and Atrial Arrhythmias

Abstract

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...

Aging Modulates the Substrate and Triggers Remodeling in Atrial Fibrillation

“…70 Low heart rates (HR) are associated with an increased risk of AF in elderly people. 71 HR is reduced whereas SAN recovery time, a direct measure of SAN function, is prolonged in the aged human or animal.…”

Skin sympathetic nerve activity precedes the onset and termination of paroxysmal atrial tachycardia and fibrillation

“…Additionally, sick sinus syndrome is a commonly associated with atria tachyarrhythmias. 13 Because reverse remodeling of sinoatrial node (SAN) function may occur after catheter ablation of AF, 14 AT and AF may play an important role in the pathogenesis of sinus node dysfunction. Abnormal response of superior SAN to sympathetic stimulation is a characteristic finding in patients with AF and symptomatic bradycardia.…”

Sick sinus syndrome - a case report of paroxysmal supraventricular tachycardia due to atrioventricular node re-entry

“…Thus, the treatment strategy will vary according to the predominant disease phenotype. Ablation alone may improve symptoms associated with sinus node dysfunction in patients with atrial fibrillation, without the need of permanent cardiac pacing, but future randomized trials are needed to clarify the epidemiology and optimal management of patients with sinus node dysfunction and atrial fibrillation [13,14]. This could indicate towards new management strategies in AVNRT, in which slow pathway ablation has been a very effective treatment, with success rates of over 99% [15].…”