scholarly journals Sinus Node Syndrome in a critical COVID-19 patient

2021 ◽  
Vol 40 (12) ◽  
pp. 987-988
Author(s):  
Juliana Elices-Teja ◽  
Álvaro Bueno-Sacristán ◽  
Olga Durán-Bobin ◽  
Ana María Ferreiro-González ◽  
Carlos Gonzalez-Juanatey
Keyword(s):  
Sinus Node

P.2.4 Evaluation of theophylline influence on sinus node function

EP Europace ◽  
2003 ◽  
Vol 4 ◽  
pp. A40
Author(s):  
A PIETRUCHA
Keyword(s):  
Sinus Node

COVID-19-associated multisystem inflammatory syndrome in children presenting uniquely with sinus node dysfunction in the setting of shock

2021 ◽  
pp. 1-3
Author(s):  
Lesya G. Tomlinson ◽  
Mitchell I. Cohen ◽  
Rebecca E. Levorson ◽  
Megan B. Tzeng
Keyword(s):  
Inflammatory Process ◽  
Myocardial Dysfunction ◽  
Sinus Node ◽  
Qtc Prolongation ◽  
Mild Disease ◽  
Abnormal Immune Response ◽  
Idioventricular Rhythm ◽  
Inflammatory Syndrome ◽  
Electrocardiographic Abnormalities ◽  
Post Infectious

Abstract SARS-CoV-2, which causes the disease COVID-19, generally has a mild disease course in children. However, a severe post-infectious inflammatory process known as multisystem inflammatory syndrome in children has been observed in association with COVID-19. This inflammatory process is a result of an abnormal immune response with similar clinical features to Kawasaki disease. It is well established that multisystem inflammatory syndrome in children is associated with myocardial dysfunction, coronary artery dilation or aneurysms, and occasionally arrhythmias. The most common electrocardiographic abnormalities seen include premature atrial or ventricular ectopy, variable degrees of atrioventricular block, and QTc prolongation, and rarely, haemodynamically significant arrhythmias necessitating extracorporeal membrane oxygenation support. However, presentation with fever, hypotension, and relative bradycardia with a left axis idioventricular rhythm has not been previously reported. We present a case of a young adolescent with multisystem inflammatory syndrome in children with myocarditis and a profoundly inappropriate sinus node response to shock with complete resolution following intravenous immunoglobulin.

Partial Anomalous Pulmonary Venous Connection: Forty-Six Years of Follow-Up

2021 ◽  
Vol 12 (1) ◽  
pp. 70-75
Author(s):  
Anne Kathrine M. Nielsen ◽  
Vibeke E. Hjortdal
Keyword(s):  
Superior Vena Cava ◽  
Superior Vena ◽  
Sinus Node ◽  
Vena Cava ◽  
Node Disease ◽  
Sinus Node Disease ◽  
Patch Technique ◽  
Anomalous Pulmonary Venous Connection

Background: Surgical repair of partial anomalous pulmonary venous connection (PAPVC) may disturb the electrical conduction in the atria. This study documents long-term outcomes, including the late occurrence of atrial tachyarrhythmia and bradyarrhythmia. Methods: This retrospective study covers all PAPVC operations at Aarhus University Hospital between 1970 and 2010. Outcome measures were arrhythmias, sinus node disease, pacemaker implantation, pathway stenosis (pulmonary vein(s), intra-atrial pathway, and/or superior vena cava), and mortality. Data were collected from databases, surgical protocols, and hospital records until May 2018. Results: A total of 83 patients were included with a postoperative follow-up period up to 46 years. Average age at follow-up was 43 ± 21 years. During follow-up, new-onset atrial fibrillation or atrial flutter appeared in four patients (5%). Sinus node disease was present in nine patients (11%). A permanent pacemaker was implanted in seven patients (8%) at an average of 12.7 years after surgery. Pulmonary venous and/or superior vena cava obstruction was seen in five patients (6%). Stenosis was most prevalent in the two-patch technique, and arrhythmia was most prevalent in the single-patch technique. Sixty-seven (81%) of 83 patients had neither bradyarrhythmias nor tachyarrhythmias or pacemaker need. Conclusions: This study contributes important long-term data concerning the course of patients who have undergone repair of PAPVC. It confirms that PAPVC can be operated with low postoperative morbidity. However, late-onset stenosis, bradyarrhythmias and tachyarrhythmias, and need for pacemaker call for continued follow-up.

scholarly journals Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation

2008 ◽  
Vol 295 (2) ◽  
pp. H691-H698 ◽  
Author(s):  
Alex Y. Tan ◽  
Shengmei Zhou ◽  
Byung Chun Jung ◽  
Masahiro Ogawa ◽  
Lan S. Chen ◽  
...  
Keyword(s):  
Pulmonary Vein ◽  
Sinus Node ◽  
Periodic Acid ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Atrial Arrhythmias ◽  
Periodic Acid Schiff ◽  
Stellate Ganglia ◽  
Ectopic Beats

The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein ( n = 11), right atrium ( n = 5), left atrium ( n = 2), and the vein of Marshall ( n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells ( P < 0.05) and sympathetic nerves ( P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

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