This chapter examines the pathophysiology of various clinical forms of conduction system disturbances and sinus node dysfunction (SND) (see Fuster and Hurst’s Central Illustration). The conduction system serves as the “translator” between the autonomic nervous system’s various demands for heart rate and coordinates electrical activation to provide efficient excitation–contraction coupling. Dysfunction can occur at any level of the electrical system, sinus node, atrioventricular (AV) conduction axis (AV node/His bundle), and intraventricular conduction (right and left bundle branches), with variable clinical effects. Many disease processes affect the electrical system, but the most prominent are aging and concomitant structural heart disease. Genetic disorders, although rare, are important to discover because they may be syndromic and can affect other family members. AV block caused by surgical trauma, particularly during transcatheter aortic valve procedures, is increasing in incidence and often requires complex decision making. Treatment primarily involves pacemaker implantation when appropriate, and the indications for pacing are reviewed. Novel technologies, including leadless pacing, conduction system pacing, and the promise of biological pacing, are also discussed.
The sinus node serves as the dominant pacemaker of the heart. Its role is to provide adequate rates at rest as well as increased rate during periods of exercise or other metabolic stressors (chronotropic competence). The function of the sinus node is modulated by unique anatomic features, rich autonomic nervous system innervation, and distinctive aspects of its cellular electrophysiology. Failure of the sinus node may be due to abnormalities in impulse formation or conduction block, as will be discussed in this chapter. Incident sinus node dysfunction (SND) occurs in approximately 0.8 per 1000 person-years and is highly age-related, representing an indication for more than 50% of pacemakers implanted in the United States. SND and atrial fibrillation (AF) commonly coexist (“tachy-brady syndrome”), with a lifetime incidence of AF in patients with SND as high as 50%.
There are several unique anatomic features of the sinus node that relate to its function. The sinus node is a “tadpole-shaped” structure, 8 mm to 22 mm in length, located subepicardially within the sulcus terminalis (Fig. 38–1).1 It receives blood from the sinus node artery, which arises from the right (60%) or left circumflex (40%) coronary artery. It is relatively electrically insulated anatomically (fibrosis, fat, blood vessels) and functionally (limited connexins), linked by a finite number of sinoatrial conduction pathways to surrounding atrial myocytes.2 This isolation is thought to be important, to protect hyperpolarization of the sinus node cells by the larger atrial mass (with more negative resting potential), allowing the smaller “source” to activate the larger “sink.”2,3 The location of impulse generation is in the superior portion of the sinus node during faster rates and more inferior during slower rates.3 A related concept ...