scholarly journals Amiodarone-Related Sinoatrial Node Dysfunction and Its Implications in the Treatment of Atrial Fibrillation

2013 ◽  
Vol 77 (9) ◽  
pp. 2240-2241
Author(s):  
Masaomi Chinushi
Heart Rhythm ◽  
2010 ◽  
Vol 7 (1) ◽  
pp. 88-95 ◽  
Author(s):  
Boyoung Joung ◽  
Shien-Fong Lin ◽  
Zhenhui Chen ◽  
Patrick S. Antoun ◽  
Mitsunori Maruyama ◽  
...  

2011 ◽  
Vol 52 (2) ◽  
pp. 211 ◽  
Author(s):  
Boyoung Joung ◽  
Peng-Sheng Chen ◽  
Shien-Fong Lin

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

2019 ◽  
Vol 20 (13) ◽  
pp. 3224 ◽  
Author(s):  
Chao-Shun Chan ◽  
Yung-Kuo Lin ◽  
Yao-Chang Chen ◽  
Yen-Yu Lu ◽  
Shih-Ann Chen ◽  
...  

Heart failure (HF) frequently coexists with atrial fibrillation (AF) and dysfunction of the sinoatrial node (SAN), the natural pacemaker. HF is associated with chronic adrenergic stimulation, neurohormonal activation, abnormal intracellular calcium handling, elevated cardiac filling pressure and atrial stretch, and fibrosis. Pulmonary veins (PVs), which are the points of onset of ectopic electrical activity, are the most crucial AF triggers. A crosstalk between the SAN and PVs determines PV arrhythmogenesis. HF has different effects on SAN and PV electrophysiological characteristics, which critically modulate the development of AF and sick sinus syndrome. This review provides updates to improve our current understanding of the effects of HF in the electrical activity of the SAN and PVs as well as therapeutic implications for AF.


2019 ◽  
Vol 9 (7) ◽  
pp. 976-981
Author(s):  
Sun Juan ◽  
Wang Kun ◽  
Ailiman Mahemuti

Objective: To investigate the changes of Notch-1 protein expression and the changes of Notch-1 and NICD contents in the sinoatrial node fat pad (SAN-FP) nerve plexus of canines with chronic atrial fibrillation in which atrial fibrillation of the left atrium was induced in chronic pacing canines, in order to elucidate the relationship between the Notch signaling pathway of the SAN-FP nerve plexus and the occurrence and development of atrial fibrillation. Methods: Healthy Beagle dogs weighing 18 ± 2.66 kg, aged 7 to 9 years were randomly divided into a sham operation (SO) group (n = 5) and an atrial fibrillation (AF) group (n = 5), respectively. Results: Atrial fibrillation was successfully induced in canines in the AF group by rapid pacing on the left atrium appendage. The scattered nerve plexus was observed in fat cells of the SAN-FP. In contrast with the SO group, Notch-1 protein expression in the AF group was significantly increased (P < 0.05). No significantly statistical differences were observed in the concentration of Notch-1 and NICD between the AF group and the SO group (P > 0.05). In addition, no statistical differences in baseline Notch-1 and NICD concentrations were observed between the AF group and the SO group (P > 0.05). After an 8-week study, the concentrations of Notch-1 and NICD in the AF group were significantly increased compared with the SO group (P < 0.05). Conclusion: During the occurrence and development of AF, Notch-1 was expressed in different phases in the SAN-FP nerve plexus. After combining with ligands, Notch-1 was activated as NICD to affect the downstream target genes.


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.


Circulation ◽  
2007 ◽  
Vol 116 (14) ◽  
pp. 1569-1576 ◽  
Author(s):  
Zahurul A. Bhuiyan ◽  
Maarten P. van den Berg ◽  
J. Peter van Tintelen ◽  
Margreet T.E. Bink-Boelkens ◽  
Ans C.P. Wiesfeld ◽  
...  

Background— Catecholaminergic polymorphic ventricular tachycardia is a disease characterized by ventricular arrhythmias elicited exclusively under adrenergic stress. Additional features include baseline bradycardia and, in some patients, right ventricular fatty displacement. The clinical spectrum is expanded by the 2 families described here. Methods and Results— Sixteen members from 2 separate families have been clinically evaluated and followed over the last 15 years. In addition to exercise-related ventricular arrhythmias, they showed abnormalities in sinoatrial node function, as well as atrioventricular nodal function, atrial fibrillation, and atrial standstill. Left ventricular dysfunction and dilatation was present in several affected individuals. Linkage analysis mapped the disease phenotype to a 4-cM region on chromosome 1q42-q43. Conventional polymerase chain reaction–based screening did not reveal a mutation in either the Ryanodine receptor 2 gene ( RYR2 ) or ACTN2 , the most plausible candidate genes in the region of interest. Multiplex ligation-dependent probe amplification and long-range polymerase chain reaction identified a genomic deletion that involved RYR2 exon-3, segregated in all the affected family members (n=16) in these 2 unlinked families. Further investigation revealed that the genomic deletion occurred in both families as a result of Alu repeat–mediated polymerase slippage. Conclusions— This is the first report on a large genomic deletion in RYR2 , which leads to extended clinical phenotypes (eg, sinoatrial node and atrioventricular node dysfunction, atrial fibrillation, atrial standstill, and dilated cardiomyopathy). These features have not previously been linked to RYR2 .


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