Sick sinus syndrome is an abnormality involving the generation of the action potential by the sinus node and is characterized by an atrial rate inappropriate for physiological requirements. Manifestations include severe sinus bradycardia, sinus pauses or arrest, sinus node exit block, chronic atrial tachyarrhythmias, alternating periods of atrial bradyarrhythmias and tachyarrhythmias, and inappropriate responses of heart rate during exercise or stress.1 Although its incidence increases in an exponential-like manner with age,1 it can occur at all ages, including in the newborn.2 The mean age of patients with the syndrome is 68 years, with both genders being affected in approximately equal proportion.2 The syndrome occurs in 1 of every 600 cardiac patients older than 65 years and accounts for approximately half of implantations of pacemakers in the United States.2 The syndrome is a collection of conditions, with a variety of causes intrinsic or extrinsic relative to the node.2 Age-dependent degenerative fibrosis of the tissues of the node has been suggested to be a common cause,2 although this is disputed.1 Clinical aspects of the syndrome have been reviewed many times.1–3 In this review, coinciding with the centenary of the discovery of the node, we offer new insights into intrinsic causes that come from an understanding of the mechanisms underlying pacemaking.

It is now exactly 100 years since Arthur Keith (Figure 1A) performed the work that introduced the world to the location of the sinus node.4,5 Keith had been intrigued by the actions of the musculature of the heart and was anxious to establish any muscular mechanisms involved in closure of the great caval veins as the right atrium contracted to deliver its load to the ventricles.5 He was aware of the work of James Mackenzie, then a medical practitioner working …

New Insights Into Pacemaker Activity Promoting Understanding of Sick Sinus Syndrome

All the myocytes within the heart have the capacity to conduct the cardiac impulse. A population of myocytes is specialized so as to generate the cardiac impulse and then to conduct it from the atrial to the ventricular chambers. This population has become known as the conduction system. Anatomists who seek to demonstrate the location of the components of this system must contend with the fact that the components of the system cannot be distinguished from the working myocardial elements by gross dissection. In important presentations to the German Pathological Society in 1910, rules were suggested for the histological distinction of these conducting cells. These rules proposed that the myocytes, to be considered as part of the conduction system, should be histologically discrete, traceable from section to section in serially prepared material, and if to be considered as tracts, should be insulated by fibrous tissue from the adjacent myocytes. Immunohistochemical techniques have now been developed that better demonstrate the distinction between the cells specialized to conduct from working myocytes. These new techniques, for the most part, confirm the accuracy of the initial descriptions. They also reveal additional areas with the characteristics of conduction tissues. These additional areas are located in a paranodal area adjacent to the sinus node, in the vestibules of both atrioventricular valvar orifices, and in a partial ring around the aortic root. In this review, we describe all these features, emphasizing the relationship of the newly recognized components to the established parts of the cardiac conduction system, and how the new findings need to be assessed in the light of the old criteria.

The anatomy of the cardiac conduction system.

Objective: To study the architecture of the human sinus node to facilitate understanding of mapping and ablative procedures in its vicinity

Methods: The sinoatrial region was examined in 47 randomly selected adult human hearts by histological analysis and scanning electron microscopy

Results: The sinus node, crescent-like in shape, and 135 (25) mm long, was not insulated by a sheath of fibrous tissue Its margins were irregular, with multiple radiations interdigitating with ordinary atrial myocardium The distances from the node to endocardium and epicardium were variable In 72% of the hearts, the whole nodal body was subepicardial and in 13 specimens (28%) the inner aspect of the nodal body was subendocardial The nodal body cranial to the sinus nodal artery was more subendocardial than the remaining nodal portion, which was separated from the endocardium by the terminal crest In 50% of hearts, the most caudal boundaries of the body of the node were at least 35 mm from the endocardium When the terminal crest was > 7 mm thick (13 hearts, 28%), the tail was subepicardial or intramyocardial and at least 3 mm from the endocardium

Conclusions: The length of the node, the absence of an insulating sheath, the presence of nodal radiations, and caudal fragments offer a potential for multiple breakthroughs of the nodal wavefront The very extensive location of the nodal tissue, the cooling effect of the nodal artery, and the interposing thick terminal crest caudal to this artery have implications for nodal ablation or modification with endocardial catheter techniques

https://heart.bmj.com/content/heartjnl/91/2/189.full.pdf

Sinus node revisited in the era of electroanatomical mapping and catheter ablation

The sinoatrial node is the primary pacemaker of the heart. Nodal dysfunction with aging, heart failure, atrial fibrillation, and even endurance athletic training can lead to a wide variety of pathological clinical syndromes. Recent work utilizing molecular markers to map the extent of the node, along with the delineation of a novel paranodal area intermediate in characteristics between the node and the surrounding atrial muscle, has shown that pacemaker tissue is more widely spread in the right atrium than previously appreciated. This can explain the phenomenon of a "wandering pacemaker" and concomitant changes in the P-wave morphology. Extensive knowledge now exists regarding the molecular architecture of the node (in particular, the expression of ion channels) and how this relates to pacemaking. This review is an up-to-date summary of the current state of our appreciation of the above topics.

http://www.cardresp.fmed.edu.uy/Boyett_2010_review.pdf

The Anatomy and Physiology of the Sinoatrial Node—A Contemporary Review

Background—We correlated the electrophysiologic (EP) effects of adenosine with tachycardia mechanisms in patients with supraventricular tachycardias (SVT). Methods and Results—Adenosine was administered to 229 patients with SVTs during EP study: atrioventricular (AV) reentry (AVRT; n=59), typical atrioventricular node reentry (AVNRT; n=82), atypical AVNRT (n=13), permanent junctional reciprocating tachycardia (PJRT; n=12), atrial tachycardia (AT; n=53), and inappropriate sinus tachycardia (IST; n=10). There was no difference in incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine, but patients with AVRT showed increases in the ventriculoatrial (VA) intervals (13%) compared with typical AVNRT (0%), P<0.005. Changes in atrial, AV, or VA intervals after adenosine did not predict the mode of termination of long R-P tachycardias. For patients with AT, there was no correlation with location of the atrial focus and adenosine response. AV block after adenosine was o...

Electrophysiologic Effects of Adenosine in Patients With Supraventricular Tachycardia

The exact location of the sinus node was determined in 25 infant hearts using reconstructive techniques. The sinus node was found to lie on the lateral aspect of the superior cavo-atrial junction in the great majority (22 hearts). In only 3 hearts was it found to straddle the summit of the crest of the right atrial appendage where it is popularly believed to be located. In the majority of instances a single artery supplied the node (in 11 hearts the artery approached posteriorly, and in 10 the artery approached anteriorly), though there was considerable variation in the exact anatomy of the arterial supply. Connections between the sinus node and atrial myocardium were diffuse and abundant but in no instances were tracts of specialised cells observed leaving the node and traversing any distance through the atrial wall. These findings are relevant to the sinus node dysfunction that may follow cardiac surgical procedures.

https://heart.bmj.com/content/heartjnl/41/1/28.full.pdf

S Y Ho

Papers

Location and vascular supply of sinus node in human heart.