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Joung B, Chen PS. Function and dysfunction of human sinoatrial node. Korean Circ J. 2015;45(3):184-91doi: 10.4070/kcj.2015.45.3.184.
Joung, B., & Chen, P. S. (2015). Function and dysfunction of human sinoatrial node. Korean circulation journal, 45(3), 184-91. https://doi.org/10.4070/kcj.2015.45.3.184
Joung, Boyoung, and Chen, Peng-Sheng. "Function and dysfunction of human sinoatrial node." Korean circulation journal vol. 45,3 (2015): 184-91. doi: https://doi.org/10.4070/kcj.2015.45.3.184
Joung B, Chen PS. Function and dysfunction of human sinoatrial node. Korean Circ J. 2015 May;45(3):184-91. doi: 10.4070/kcj.2015.45.3.184. Epub 2015 May 27. PMID: 26023305; PMCID: PMC4446811.
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Korean Circ J. 2015 May;45(3):184-91. doi: 10.4070/kcj.2015.45.3.184. Epub 2015 May 27.

Function and dysfunction of human sinoatrial node.

Korean circulation journal

Boyoung Joung, Peng-Sheng Chen

Affiliations

  1. Division of Cardiology, Department of Medicine, Yonsei University College of Medicine, Seoul, Korea.
  2. The Krannert Institute of Cardiology and the Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.

PMID: 26023305 PMCID: PMC4446811 DOI: 10.4070/kcj.2015.45.3.184

Abstract

Sinoatrial node (SAN) automaticity is jointly regulated by a voltage (cyclic activation and deactivation of membrane ion channels) and Ca(2+) clocks (rhythmic spontaneous sarcoplasmic reticulum Ca(2+) release). Using optical mapping in Langendorff-perfused canine right atrium, we previously demonstrated that the β-adrenergic stimulation pushes the leading pacemaker to the superior SAN, which has the fastest activation rate and the most robust late diastolic intracellular calcium (Cai) elevation. Dysfunction of the superior SAN is commonly observed in animal models of heart failure and atrial fibrillation (AF), which are known to be associated with abnormal SAN automaticity. Using the 3D electroanatomic mapping techniques, we demonstrated that superior SAN served as the earliest atrial activation site (EAS) during sympathetic stimulation in healthy humans. In contrast, unresponsiveness of superior SAN to sympathetic stimulation was a characteristic finding in patients with AF and SAN dysfunction, and the 3D electroanatomic mapping technique had better diagnostic sensitivity than corrected SAN recovery time testing. However, both tests have significant limitations in detecting patients with symptomatic sick sinus syndrome. Recently, we reported that the location of the EAS can be predicted by the amplitudes of P-wave in the inferior leads. The inferior P-wave amplitudes can also be used to assess the superior SAN responsiveness to sympathetic stimulation. Inverted or isoelectric P-waves at baseline that fail to normalize during isoproterenol infusion suggest SAN dysfunction. P-wave morphology analyses may be helpful in determining the SAN function in patients at risk of symptomatic sick sinus syndrome.

Keywords: Adrenergic beta-agonists; Biological pacemaker; Calcium; Sick sinus syndrome; Sinoatrial node

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