Key result
A complex model of the sinus node with discrete exit sites and specialized pathways provides a framework for understanding the mechanisms underlying various clinical atrial arrhythmias.
Understanding the complex structure and function of the sinus node, including discrete exit sites and specialized pathways, provides a framework for explaining the mechanisms of clinical atrial arrhythmias.
May refine arrhythmia mechanism interpretation; leaves open prospective validation before clinical adoption.
To understand abnormal sinus node function in clinical atrial arrhythmias, it is essential to understand the normal function of the sinus node. Much of our understanding of the sinus node comes from work done in rabbits. In small animals, the node is a thin structure and can be modeled in two dimensions. However, in canines and humans, the node is a more complex structure completely surrounded by myocytes. Recent data suggest that the node may be insulated from the surrounding atrial myocytes, except at a limited number of exit sites. A model of the node with discrete exit sites explains how atrial activation can be initiated from multiple sites simultaneously. Within the node there may exist specialized pathways that explain the complex conduction within the node. Multiple cell types, with different intrinsic rates, combined with the nonuniform distribution of autonomic receptors, provide a basis for understanding the dynamics of heart rate control and the initiation of atrial activation. In addition, this model of the sinus node provides a framework to propose novel mechanisms underlying various atrial arrhythmias, such as atrial premature depolarizations or sinus node reentry.
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Richard B. Schuessler (2003) conducted a review in Clinical atrial arrhythmias. A complex model of the sinus node with discrete exit sites and specialized pathways provides a framework for understanding the mechanisms underlying various clinical atrial arrhythmias.
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