Sick sinus syndrome and atrial fibrillation in older persons - A view from the sinoatrial nodal myocyte

J Mol Cell Cardiol. 2015 Jun;83:88-100. doi: 10.1016/j.yjmcc.2015.02.003. Epub 2015 Feb 7.


Sick sinus syndrome remains a highly relevant clinical entity, being responsible for the implantation of the majority of electronic pacemakers worldwide. It is an infinitely more complex disease than it was believed when first described in the mid part of the 20th century. It not only involves the innate leading pacemaker region of the heart, the sinoatrial node, but also the atrial myocardium, predisposing to atrial tachydysrhythmias. It remains controversial as to whether the dysfunction of the sinoatrial node directly causes the dysfunction of the atrial myocardium, or vice versa, or indeed whether these two aspects of the condition arise through some related underlying pathological mechanism, such as extracellular matrix remodeling, i.e., fibrosis. This review aims to shed new light on the myriad possible contributing factors in the development of sick sinus syndrome, with a particular focus on the sinoatrial nodal myocyte. This article is part of a Special Issue entitled CV Aging.

Keywords: Arrhythmia; Atrial fibrillation; Calcium handling; Ion channels; Pacemaking; Sinoatrial node.

Publication types

  • Review

MeSH terms

  • Aged
  • Aging / metabolism*
  • Aging / pathology
  • Animals
  • Atrial Fibrillation / genetics
  • Atrial Fibrillation / metabolism*
  • Atrial Fibrillation / pathology
  • Bradycardia / genetics
  • Bradycardia / metabolism*
  • Bradycardia / pathology
  • Connexins / genetics
  • Connexins / metabolism
  • Gene Expression Regulation
  • Heart Atria / metabolism*
  • Heart Atria / pathology
  • Humans
  • Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels / genetics
  • Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels / metabolism
  • Ion Transport
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology
  • NAV1.5 Voltage-Gated Sodium Channel / genetics
  • NAV1.5 Voltage-Gated Sodium Channel / metabolism
  • Receptors, Purinergic P1 / genetics
  • Receptors, Purinergic P1 / metabolism
  • Renin-Angiotensin System / genetics
  • Sinoatrial Node / metabolism*
  • Sinoatrial Node / pathology


  • Connexins
  • Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
  • MicroRNAs
  • NAV1.5 Voltage-Gated Sodium Channel
  • Receptors, Purinergic P1
  • SCN5A protein, human