Minimizing right ventricular pacing: A new paradigm for cardiac pacing in sinus node dysfunction

Abstract

Sinus node dysfunction (SND) was first described as a clinical entity in 1968, although Wenckebach reported the electrocardiographic manifestation of SND in 1923. Sinus node dysfunction refers to a broad array of abnormalities in sinus node and atrial impulse formation and propagation. These include persistent sinus bradycardia and chronotropic incompetence without identifiable causes, paroxysmal or persistent sinus arrest with replacement by subsidiary escape rhythms in the atrioventricular (AV) junction or ventricular myocardium, and paroxysmal or persistent atrial fibrillation (AF). The frequent association of paroxysmal AF and sinus bradycardia or sinus inertia, which may oscillate suddenly from one to the other, usually accompanied by symptoms, is termed btachy-bradyQ syndrome. Sinus node dysfunction is primarily a disease of the elderly and is presumed to be due to senescence of the sinus node and atrial muscle. Collected data from 28 different studies on atrial-only (AAIR) pacing for SND showed a mean annual incidence of complete AV block (AVB) of 0.6% (0%-4.5%) with a total prevalence of 2.1% (0%-11.9%). This suggests that the degenerative process also affects the specialized conduction system, although the rate of progression is slow and does not dominate the clinical course of disease. Sinus node dysfunction is typically diagnosed in the sixth and seventh decade of life, which is also the average age at enrollment in clinical trials of pacemaker therapy for SND. Sinus node dysfunction may arise at any time in life as a secondary phenomenon of any condition that results in destruction of sinus node cells, such as ischemia, inflammation, or cardiac surgery. The clinical manifestations of SND are diverse, reflecting the range of typical sinoatrial rhythm disturbances. The most dramatic presentation is syncope. The mechanism of syncope is a sudden pause in sinus impulse formation, either spontaneously or after the termination of an atrial tachyarrhythmia, causing cerebral hypoperfusion. The pause in sinus node activity is