scholarly journals The Role of the Calcium and the Voltage Clocks in Sinoatrial Node Dysfunction

2011 ◽  
Vol 52 (2) ◽  
pp. 211 ◽  
Author(s):  
Boyoung Joung ◽  
Peng-Sheng Chen ◽  
Shien-Fong Lin
2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  

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.


Circulation ◽  
2007 ◽  
Vol 115 (10) ◽  
pp. 1178-1179 ◽  
Author(s):  
Haris M. Haqqani ◽  
Jonathan M. Kalman

2011 ◽  
Vol 109 (8) ◽  
pp. 848-857 ◽  
Author(s):  
Yue-Kun Ju ◽  
Jie Liu ◽  
Bon Hyang Lee ◽  
Donna Lai ◽  
Elizabeth A. Woodcock ◽  
...  

2000 ◽  
Vol 7 (2) ◽  
pp. 100-113 ◽  
Author(s):  
Hengtao Zhang ◽  
Mario Vassalle
Keyword(s):  

2017 ◽  
Vol 35 (5_suppl) ◽  
pp. 132-132
Author(s):  
Yushen Qian ◽  
Sara Aileen Dudley ◽  
Kiran Kumar ◽  
Aadel Chaudhuri ◽  
Alexander Chin ◽  
...  

132 Background: Sinoatrial node (SAN) injury following stereotactic ablative radiation therapy (SABR) in the chest has not been reported in the literature. We report SAN dysfunction as a potential toxicity of SABR in the chest. Methods: We examined the clinical courses and SABR plans of 47 patients treated for T1 or T2 non-small cell lung cancer of the right upper lobe, middle lobe, lower lobe, or hilum. After developing a contouring atlas for the SAN, based upon the junction between the superior vena cava and the right atrium, dose to the SAN was retrospectively determined for each patient. We identified 13 patients whose treatment imparted significant dose to the SAN, as defined by the SAN encompassed within the 10% prescription isodose (IDL) line. Biologically effective doses (BED), acute and chronic, were correlated with SAN toxicity. Results: Patients underwent SABR to the right lung to a dose of 40-50 Gy in 4 or 5 fractions, with mean acute BED (alpha/beta ratio = 10) of 100.2 Gy and late BED (alpha/beta ratio = 3) of 222.7 Gy. Mean volume of the GTV and PTV were 26.1 and 75.1 mL, respectively. Mean follow-up was 25.5 months. The mean volume of the SAN was 0.37 mL. Average max dose and mean dose to the SAN were 24.7 and 70.7 Gy, respectively. Of the 13 patients whose treatment imparted significant dose to the SAN, one patient without prior arrhythmia developed symptomatic SAN dysfunction requiring pacemaker placement at 6 months after completion of treatment. The sinoatrial node of the patient received a maximum dose of 44.8 Gy in 4 fractions, correlated with an acute BED (alpha/beta ratio = 10) of 90 Gy and late BED (alpha/beta ratio = 3) of 194.1 Gy, and a mean dose of 35.5 Gy in 4 fractions, correlated with an acute BED (alpha/beta ratio = 10) of 71 Gy and late BED (alpha/beta ratio = 3) of 153.8 Gy. This was the third highest max dose and second highest mean dose to SAN in the cohort. Conclusions: We report sinoatrial node dysfunction as a potential toxicity of SABR in the chest for non-small cell lung cancer. Caution is advised when treatment imparts significant dose to the sinoatrial node.


2008 ◽  
Vol 96 (1-3) ◽  
pp. 294-304 ◽  
Author(s):  
Jie Liu ◽  
Penelope J. Noble ◽  
Guosheng Xiao ◽  
Mohamed Abdelrahman ◽  
Halina Dobrzynski ◽  
...  

2014 ◽  
Vol 41 (5) ◽  
pp. 499-501 ◽  
Author(s):  
Sowmya Ramanan ◽  
Navaneetha Sasikumar ◽  
Soman Rema Krishna Manohar ◽  
Kotturathu Mammen Cherian

The Warden procedure for the correction of a right-sided partial anomalous pulmonary venous connection to the high superior vena cava is well established. It has the advantages of avoiding sinoatrial node dysfunction and pulmonary and systemic venous obstruction. In the case related here, a 3-year-old girl presented with a superior vena cava type of sinus venosus atrial septal defect and an anomalously draining right upper pulmonary vein, with bilateral superior venae cavae. Our approach to the Warden procedure was through a right posterolateral thoracotomy, which provided additional advantages.


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