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Anatomy and electrophysiology of the sinoatrial node

INTRODUCTION

The sinoatrial (SA) node is normally the most rapid pacemaker. However, what we call the SA node is actually the integrated activity of pacemaker cells in a compact region of the right atrium [1,2]. These several thousand cells depolarize and produce action potentials almost synchronously. They seem to be influencing each other through cell-to-cell coupling, a process that has been called mutual entrainment [3,4]. The location of the primary pacemaker may move among groups of cells within the region of the SA node. It is estimated that only about 1 percent of the cells in the SA node act as the leading pacemaker [5].

BLOOD SUPPLY

Past studies have suggested that over 90 percent of hearts have only one arterial branch to the SA node [6], and common wisdom was that the right coronary artery supplied the SA node in about 55 percent of hearts. More recent data, however, suggest that the SA nodal artery may take one of six different routes, and two or more branches to the node may be present in about 54 percent of hearts studied morphologically [6]. This suggests that collateral blood supplies are common and perhaps explains the rarity of infarction of the SA node.

ANATOMY

The sinus node is located at the junction of the high right atrium at the junction of the crista terminalis, a thick band of atrial muscle at the border of the atrial appendage, and the superior vena cava. The sinus node is located beneath the epicardial surface of the crista terminalis; there is a layer of atrial muscle between the node and the endocardium so that it does not occupy the entire thickness of the atrial myocardium.

A characteristic feature of the sinus node is extensive connective tissue, mainly collagen and fibroblasts. In the center of the node are the characteristic "P" cells, which are the leading pacemaker cells. There is a gradual transition in cell type over several millimeters from the center in all directions to the periphery of the node. Perinodal cells, sometimes called transitional or (T) cells, transmit the electrical impulse from the SA node to the right atrium. SA nodal dysfunction may result from abnormalities in impulse generation by the P cells or in conduction across the T cells. (See "Manifestations and causes of the sick sinus syndrome" and "Sinoatrial nodal pause; arrest; and exit block".)

The conduction velocity within the sinus node is very slow compared to non-nodal atrial tissue. This is a result of poor electrical coupling arising from the relative paucity of gap junctions in the center of the node compared to the periphery [2]. These gap junctions may result in preferential conduction pathways for the propagation of the action potential from the center to the atrial muscle and might provide the structural substrate for the transitional zone, enabling the sinus node to drive the surrounding atrial muscle without being suppressed by this tissue [7].

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References Top
  1. Bleeker, WK, Mackaay, AJ, Masson-Pevet, M, et al. Functional and morphological organization of the rabbit sinus node. Circ Res 1980; 46:11.
  2. Boyett, MR, Honjo, H, Kodama, I. The sinoatrial node, a heterogeneous pacemaker structure. Cardiovasc Res 2000; 47:658.
  3. Winfree, AT. The geometry of biological time. Springer-Verlag, New York 1980.
  4. Jalife, J. Mutual entrainment and electrical coupling as mechanisms for synchronous firing of rabbit sino-atrial pacemaker cells. J Physiol (Lond) 1984; 356:221.
  5. Boyett, MR, Dobrzynski, H, Lancaster, MK, et al. Sophisticated architecture is required for the sinoatrial node to perform its normal pacemaker function. J Cardiovasc Electrophysiol 2003; 14:104.
  6. Kawashima, T, Sasaki, H. The morphological significance of the human sinuatrial nodal branch (artery). Heart Vessels 2003; 18:213.
  7. Joyner, RW, van Capelle, FJ. Propagation through electrically coupled cells. How a small SA node drives a large atrium. Biophys J 1986; 50:1157.
  8. Perez-Lugones, A, McMahon, JT, Ratliff, NB, et al. Evidence of specialized conduction cells in human pulmonary veins of patients with atrial fibrillation. J Cardiovasc Electrophysiol 2003; 14:803.
  9. Jalife, J. Synchronization of pacemaker cells in the sinus node. In: Atrial Arrhythmias: Current Concepts and Management. Touboul, P, Waldo, AL (Eds), Mosby Year Book, St Louis 1990. p.69.
  10. Veldkamp, MW, Wilders, R, Baartscheer, A, et al. Contribution of sodium channel mutations to bradycardia and sinus node dysfunction in LQT3 families. Circ Res 2003; 92:976.
  11. Nof, E, Luria, D, Brass, D, et al. Point mutation in the HCN4 cardiac ion channel pore affecting synthesis, trafficking, and functional expression is associated with familial asymptomatic sinus bradycardia. Circulation 2007; 116:463.
  12. Du, Y, Huang, X, Wang, T, et al. Downregulation of neuronal sodium channel subunits Nav1.1 and Nav1.6 in the sinoatrial node from volume-overloaded heart failure rat. Pflugers Arch 2007; 454:451.
  13. Schuessler, RB. Abnormal sinus node function in clinical arrhythmias. J Cardiovasc Electrophysiol 2003; 14:215.
  14. Sanders, P, Morton, JB, Davidson, NC, et al. Electrical remodeling of the atria in congestive heart failure: electrophysiological and electroanatomic mapping in humans. Circulation 2003; 108:1461.
  15. Morton, JB, Sanders, P, Vohra, JK, et al. Effect of chronic right atrial stretch on atrial electrical remodeling in patients with an atrial septal defect. Circulation 2003; 107:1775.
  16. Hocini, M. Sanders P, Deisenhofer, I et al, Reverse remodeling of sinus node function after catheter ablation of atrial fibrillation in patients with prolonged sinus pauses. Circulation 2003; 108:1172.
  17. Sparks, PB, Jayaprakash, S, Vohra, JK, et al. Electrical remodeling of the atria associated with paroxysmal and chronic atrial flutter. Circulation 2000; 102:1807.
  18. Daoud, EG, Weiss, R, Augostini, RS, et al. Remodeling of sinus node function after catheter ablation of right atrial flutter. J Cardiovasc Electrophysiol 2002; 13:20.
  19. Hadian, D, Zipes, DP, Olgin, JE, Miller, JM. Short-term rapid atrial pacing produces electrical remodeling of sinus node function in humans. J Cardiovasc Electrophysiol 2002; 13:584.
  20. Sparks, PB, Mond, HG, Vohra, JK, et al. Electrical remodeling of the atria following los of atrioventricular synchrony: a long-term study in humans. Circulation 1999; 100:1894.
  21. Sanders, P, Kistler, PM, Morton, JB, et al. Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve. Circulation 2004; 110:897.
  22. Randall, W. Arrhythmogenesis and neural control of the atria. In: Atrial Arrhythmias: Current Concepts and Management. Touboul, P, Waldo, AL (Eds), Mosby Year Book, St Louis 1990. p.81.
  23. Levy, MN. Neural and reflex control of the circulation. In: Current Concepts in Cardiovascular Physiology. Garfein, O (Ed), Academic Press, New York 1990. p.133.
  24. Pappano, AJ, Mubagwa, K. Actions of muscarinic agents and adenosine on the heart. In: The Heart and Cardiovascular System. Fozzard, HA, et al (Eds), Raven Press, New York 1992. p.1765.
  25. Zaza, A, Rocchetti, M, DiFrancesco,D. Modulation of the hyperpolarization-activated current (If) by adenosine in rabbit sinoatrial myocytes. Circulation 1996; 94:734.
  26. Susanni, EE, Vatner, DE, Homcy, CJ. Beta-adrenergic receptor/adenylyl cyclase system. In: The Heart and Cardiovascular System. Fozzard, HA, et al (Eds), Raven Press, New York 1992. p.1685.
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