The Sinoatrial Node and Its Dysfunction

1987 ◽  
pp. 107-135
Author(s):  
John D. Kugler
Keyword(s):  
Sinoatrial Node

scholarly journals Using the Sinoatrial Node to Induce Pulsatility in Mechanical Circulatory Support Devices

2021 ◽  
Vol 40 (4) ◽  
pp. S186
Author(s):  
S. Emmanuel ◽  
M. Stevens ◽  
G.M. Vazquez ◽  
M. Fetanat ◽  
A.Al Abed ◽  
...  
Keyword(s):  
Mechanical Circulatory Support ◽  
Sinoatrial Node ◽  
Circulatory Support ◽  
Mechanical Circulatory Support Devices ◽  
Support Devices

scholarly journals Assembly of the Cardiac Pacemaking Complex: Electrogenic Principles of Sinoatrial Node Morphogenesis

2021 ◽  
Vol 8 (4) ◽  
pp. 40
Author(s):  
Marietta Easterling ◽  
Simone Rossi ◽  
Anthony J Mazzella ◽  
Michael Bressan
Keyword(s):  
Cardiac Tissue ◽  
Sinoatrial Node ◽  
Cardiac Pacemaker ◽  
Tissue Level ◽  
Rhythmic Contraction ◽  
Entire Volume ◽  
Impulse Generation ◽  
Cardiac Pacemaking ◽  
Electrical Impulses ◽  
Sufficient Strength

Cardiac pacemaker cells located in the sinoatrial node initiate the electrical impulses that drive rhythmic contraction of the heart. The sinoatrial node accounts for only a small proportion of the total mass of the heart yet must produce a stimulus of sufficient strength to stimulate the entire volume of downstream cardiac tissue. This requires balancing a delicate set of electrical interactions both within the sinoatrial node and with the downstream working myocardium. Understanding the fundamental features of these interactions is critical for defining vulnerabilities that arise in human arrhythmic disease and may provide insight towards the design and implementation of the next generation of potential cellular-based cardiac therapeutics. Here, we discuss physiological conditions that influence electrical impulse generation and propagation in the sinoatrial node and describe developmental events that construct the tissue-level architecture that appears necessary for sinoatrial node function.

scholarly journals Intracellular Na+ Modulates Pacemaking Activity in Murine Sinoatrial Node Myocytes: An In Silico Analysis

2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Membrane Potential ◽  
In Silico ◽  
Sinoatrial Node ◽  
In Silico Analysis ◽  
Ankyrin B ◽  
Deficient Mice ◽  
Silico Analysis ◽  
Bursting Activity

Background: The mechanisms underlying dysfunction in the sinoatrial node (SAN), the heart’s primary pacemaker, are incompletely understood. Electrical and Ca2+-handling remodeling have been implicated in SAN dysfunction associated with heart failure, aging, and diabetes. Cardiomyocyte [Na+]i is also elevated in these diseases, where it contributes to arrhythmogenesis. Here, we sought to investigate the largely unexplored role of Na+ homeostasis in SAN pacemaking and test whether [Na+]i dysregulation may contribute to SAN dysfunction. Methods: We developed a dataset-specific computational model of the murine SAN myocyte and simulated alterations in the major processes of Na+ entry (Na+/Ca2+ exchanger, NCX) and removal (Na+/K+ ATPase, NKA). Results: We found that changes in intracellular Na+ homeostatic processes dynamically regulate SAN electrophysiology. Mild reductions in NKA and NCX function increase myocyte firing rate, whereas a stronger reduction causes bursting activity and loss of automaticity. These pathologic phenotypes mimic those observed experimentally in NCX- and ankyrin-B-deficient mice due to altered feedback between the Ca2+ and membrane potential clocks underlying SAN firing. Conclusions: Our study generates new testable predictions and insight linking Na+ homeostasis to Ca2+ handling and membrane potential dynamics in SAN myocytes that may advance our understanding of SAN (dys)function.

scholarly journals Phase resetting in central and peripheral sinoatrial node cell models

2005 ◽  
Author(s):  
D.G. Tsalikakis ◽  
H.G. Zhang ◽  
D.I. Fotiadis ◽  
G.P. Kremmydas
Keyword(s):  
Sinoatrial Node ◽  
Phase Resetting ◽  
Cell Models ◽  
Sinoatrial Node Cell

scholarly journals An anatomical approach to determine the location of the sinoatrial node during catheter ablation

2021 ◽  
Author(s):  
Keiko Shimamoto ◽  
Kenichiro Yamagata ◽  
Kenzaburo Nakajima ◽  
Tsukasa Kamakura ◽  
Mitsuru Wada ◽  
...  
Keyword(s):  
Catheter Ablation ◽  
Sinoatrial Node

scholarly journals Quantification of Cardiomyocyte Beating Frequency Using Fourier Transform Analysis

Photonics ◽  
2018 ◽  
Vol 5 (4) ◽  
pp. 39 ◽  
Author(s):  
Allison Reno ◽  
Andrew Hunter ◽  
Yang Li ◽  
Tong Ye ◽  
Ann Foley
Keyword(s):  
Fourier Transform ◽  
Fast Fourier Transform ◽  
Sinoatrial Node ◽  
Frequency Data ◽  
True Rate ◽  
Video Clips ◽  
Organoid Culture ◽  
Cholinergic Signaling ◽  
Beating Frequency

Pacemaker cardiomyocytes of the sinoatrial node (SAN) beat more rapidly than cells of the working myocardium. Beating in SAN cells responds to β-adrenergic and cholinergic signaling by speeding up or slowing, respectively. Beat rate has traditionally been assessed using voltage or calcium sensitive dyes, however these may not reflect the true rate of beating because they sequester calcium. Finally, in vitro differentiated cardiomyocytes sometimes briefly pause during imaging giving inaccurate beat rates. We have developed a MATLAB automation to calculate cardiac beat rates directly from video clips based on changes in pixel density at the edges of beating areas. These data are normalized to minimize the effects of secondary movement and are converted to frequency data using a fast Fourier transform (FFT). We find that this gives accurate beat rates even when there are brief pauses in beating. This technique can be used to rapidly assess beating of cardiomyocytes in organoid culture. This technique could also be combined with field scanning techniques to automatically and accurately assess beating within a complex cardiac organoid.

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