Sinus Node Dysfunction and Atrial Fibrillation: A Reversible Phenomenon?

BACKGROUND: Symptomatic sinus node dysfunction (SND) consists of a variety of manifestations, including tachycardia-bradycardia syndrome. Atrial fibrillation (AF) is commonly associated with SND, which complicates the management of both conditions. This paper reviews the epidemiology, pathophysiology, and clinical trial data investigating therapeutic approaches for treatment of patients with both SND and AF. METHODS: The authors reviewed articles published in English describing the epidemiology, pathophysiology, and therapeutic approaches for patients with SND and AF. The search was conducted using PubMed. Keywords included: sick sinus syndrome, sinus node dysfunction, atrial fibrillation, pacing, and pulmonary vein isolation. RESULTS: SND affects up to one in five patients with AF. AF can lead to anatomical and electrophysiological remodeling in both atria, including the region of sinoatrial node. Changes including atrial fibrosis, altered calcium channel metabolism, and transformed gene expression have been demonstrated in patients with AF and SND. Nonrandomized clinical trial data have failed to demonstrate whether any pacing strategy can reduce the risk of AF. Pulmonary vein isolation appears to decrease episodes of tachybrady syndrome and sinus pauses. CONCLUSIONS: SND affects up to one in five patients with AF. The pathophysiological derangements in gene expression, ion channel metabolism, and alterations in myocardial architecture associated with AF may lead to anatomic and electrical changes in the region of the sinoatrial node. Ablation may improve symptoms associated with SND in patients with AF. Future randomized trials are needed to clarify the epidemiology and optimal management of patients with SND and AF.

Mecanismos de las arritmias cardiacas / Mechanisms of cardiac arrhythmias

En la especie humana, las arritmias cardiacas son muy prevalentes en todos los grupos de edad y pueden darse tanto en el contexto de una cardiopatía subyacente como en corazones estructuralmente normales. Aunque las formas de presentación clínica de las arritmias son muy diversas, en las células comparten propiedades electrofisiológicas comunes. Los 3 mecanismos principales de las arritmias cardiacas son las alteraciones en el automatismo, la actividad desencadenada y la reentrada. Aunque la identificación del mecanismo específico a veces pueda resultar difícil para el clínico y requerir un estudio electrofisiológico invasivo, diferenciar y comprender el mecanismo subyacente puede ser crucial para desarrollar una correcta estrategia diagnóstica y terapéutica (AU)

Cardiac arrhythmias are prevalent among humans across all age ranges and may occur in the setting of underlying heart disease as well as in structurally normal hearts. While arrhythmias are widely varied in their clinical presentations, they possess shared electrophysiologic properties at the cellular level. The 3 main mechanisms responsible for cardiac arrhythmias are automaticity, triggered activity, and reentry. Although identifying the specific mechanism may at times be challenging for the clinician and require invasive electrophysiologic study, differentiating and understanding the underlying mechanism may be critical to the development of an appropriate diagnosis and treatment strategy (AU)

Coronary sinus pacing prevents induction of atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is due to reentry, and its incidence has been shown to decrease after dual-site atrial or biatrial pacing. We investigated whether a simpler pacing approach via the distal coronary sinus (CSd) could eliminate AF inducibility by high right atrial (HRA) extrastimuli (APDs). We based our hypothesis on our previous observation that AF inducibility by HRA APDs was associated with conduction delays to the posterior triangle of Koch, whereas AF was never induced with CSd APDs, which were associated with minimal intra-atrial conduction delays. METHODS AND RESULTS: Programmed electrical stimulation was performed from the high right atrium and CSd, and bipolar recordings were obtained from the high right atrium, His bundle, posterior triangle of Koch, and coronary sinus. In 13 patients (age, 44+/-18 years), AF was reproducibly induced with a critically timed HRA APD (220+/-22 ms) delivered during HRA pacing. AF was not induced in any of the patients when HRA APDs were delivered during CSd pacing at the same critical coupling intervals. Coronary sinus APDs delivered during HRA pacing also were not associated with AF induction. The APD coupling interval measured at the posterior triangle of Koch during CSd pacing was significantly prolonged compared with the one measured during HRA pacing and AF induction (381+/-58 versus 263+/-37 ms; P<.0001). CONCLUSIONS: We propose that CSd pacing suppresses the propensity of HRA APDs to induce AF by limiting their prematurity at the posterior triangle of Koch and not allowing local conduction delay and local reentry to occur.

Catheter ablation of sinoatrial node reentrant tachycardia.

OBJECTIVES: This study evaluates 1) the safety and efficacy of catheter delivery of radiofrequency current to eliminate sustained sinoatrial node reentrant tachycardia; 2) the incidence of sinoatrial node reentrant tachycardia in the current group of patients undergoing electrophysiologic study for paroxysmal supraventricular tachycardia; and 3) the association of sinoatrial node reentrant tachycardia with other tachyarrhythmias. BACKGROUND: Sustained sinoatrial node reentrant tachycardia is an uncommon cause of paroxysmal supraventricular tachycardia that is reported to occur infrequently in conjunction with other arrhythmias. Although pharmacologic and surgical therapies are available, there is limited information with regard to catheter ablation of sinoatrial node reentrant tachycardia. METHODS: Ten patients with sustained sinoatrial node reentrant tachycardia underwent electrophysiologic study and radiofrequency current ablation. Patients were followed up for 9.2 +/- 6.0 months. RESULTS: Of 343 consecutive patients referred for electrophysiologic evaluation of paroxysmal supraventricular tachycardia, 11 (3.2%) were found to have inducible sustained sinoatrial node reentrant tachycardia. Nine of the 11 patients had other associated arrhythmias, including atrioventricular (AV) node reentrant tachycardia (6 patients), AV reciprocating tachycardia (2 patients), ectopic atrial tachycardia (2 patients) and bundle branch reentrant tachycardia (1 patient). In 10 patients, direct ablation of sinoatrial node reentrant tachycardia was attempted and was successful in all (confidence interval for failure 0-0.26). Sinoatrial node reentrant tachycardia was eliminated with a median of four radiofrequency current applications (range 1 to 10) at 20 to 30 W. Successful ablation site characteristics during sinoatrial node reentrant tachycardia included 1) atrial activation > or = 35 ms (mean 44 +/- 8 ms) before the onset of the surface P wave, 2) atrial activation > or = 20 ms (mean 28 +/- 6 ms) before the onset of high right atrial activation, and 3) significantly prolonged and fractionated electrograms (mean duration 87 +/- 21 ms). No complications were encountered, and there have been no recurrences of sinoatrial node reentrant tachycardia. CONCLUSIONS: Sinoatrial node reentrant tachycardia may be effectively and safely treated with radiofrequency current ablation at the site of earliest atrial activation.