Ectopic Pacemaker Activity

2013 ◽  
pp. 1105-1105
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Sunil Jit R. J. Logantha ◽  
Sanjay R. Kharche ◽  
Yu Zhang ◽  
Andrew J. Atkinson ◽  
Guoliang Hao ◽  
...  

2014 ◽  
Vol 18 (4) ◽  
pp. 341 ◽  
Author(s):  
Han-Yi Jiao ◽  
Dong Hyun Kim ◽  
Jung Suk Ki ◽  
Kwon Ho Ryu ◽  
Seok Choi ◽  
...  

2021 ◽  
Vol 108 (Supplement_7) ◽  
Author(s):  
Armin Fardanesh ◽  
Jamie Powell ◽  
Maitham Al-Whouhayb

Abstract Introduction Roux-en-Y Gastric bypass (REYGB) amounts for a third of surgical bariatric interventions. Small bowel obstruction (SBO) is a long-term complication in REYGB and can be caused by intussusception of bowel, in approximately 0.5% of procedures.  Intussusception in REYBG is mostly attributed to dysmotility. This report demonstrates a rare case of intussusception in REYGB secondary to a benign polyp.  Case description A 45 year old female, three years post REYGB, presented to A&E with acute, extreme upper abdominal pain, with three days absolute constipation. She was tender on examination with normal blood tests. CT scan demonstrated small bowel intussusception. Initial concerns were of intussusception of the jejuno-jejunostomy anastomosis causing SBO.  She had an exploratory laparotomy, which confirmed intussusception, however this was 20cm distal to the jejuno-jejunostomy. Bowel was gently reduced, and deemed viable. On thorough run-through, a small segment at the transition point, was considered abnormal on palpation. This region was resected and a 1x1cm intraluminal polyp was identified as the causative lead point. The patient did well postoperatively.  Discussion Small bowel intussusception in adults is typically attributed to pathological lead point, such as benign or malignant lesions. Intussusception in REYBG is a rare but well-documented cause of intestinal obstruction, usually attributed to dysmotility, secondary to ectopic pacemaker cells particularly around anastomoses. In this case, the intussusception was caused by an unusual pathology separate from the jejuno-jejunal anastomosis. We recommend thorough examination of all adjacent bowel to exclude lesions, in this case a polyp, which could result in recurrence. 


1991 ◽  
Vol 260 (5) ◽  
pp. H1507-H1514 ◽  
Author(s):  
G. J. Rozanski

Effects of vagal nerve activity on atrial ectopic pacemaker foci were studied in vitro in strips of rabbit tricuspid valve. Transmembrane potentials were recorded from pacemaker and working atrial fibers superfused with Tyrode solution containing propranolol. Tissues were paced from the atrial muscle end at cycle lengths of 90, 70, or 50% of the intrinsic pacemaker cycle, and postganglionic vagal nerve endings were stimulated with brief trains of pulses (200 Hz; 100-200 microseconds) through a second electrode near the pacemaker. Vagal trains scanning diastole hyperpolarized pacemaker and surrounding fibers to a maximum membrane potential of -74.7 +/- 1.8 mV (normal maximum diastolic potential = -75.5 +/- 1.6 mV) and elicited a period of inexcitability lasting 217.9 +/- 27.3 ms (drive cycle = 90% of pacemaker cycle). Inexcitability was evident at critical diastolic intervals where vagal input prevented atrial impulses from activating the pacemaker allowing spontaneous discharges to occur, i.e., escape, late in diastole. Besides inexcitability, incidence and timing of escape impulses were determined by cumulative effects of drive cycle length, vagal stimulus, and subthreshold electrotonic input on intrinsic pacemaker cycle. These data suggest that phasic vagal stimuli may transiently protect atrial ectopic pacemaker foci from conducted sinus impulses by rendering pacemaker and surrounding fibers inexcitable. In the setting of a long sinus (drive) cycle length, phasic vagal activity may result in spontaneous discharges manifest as late atrial premature beats.


2020 ◽  
Vol 472 (12) ◽  
pp. 1733-1742
Author(s):  
Nadine Erlenhardt ◽  
Olaf Kletke ◽  
Franziska Wohlfarth ◽  
Marlene A. Komadowski ◽  
Lukas Clasen ◽  
...  

AbstractThe hyperpolarization-activated cation current If is a key determinant for cardiac pacemaker activity. It is conducted by subunits of the hyperpolarization-activated cyclic nucleotide–gated (HCN) channel family, of which HCN4 is predominant in mammalian heart. Both loss-of-function and gain-of-function mutations of the HCN4 gene are associated with sinus node dysfunction in humans; however, their functional impact is not fully understood yet. Here, we sought to characterize a HCN4 V759I variant detected in a patient with a family history of sick sinus syndrome. The genomic analysis yielded a mono-allelic HCN4 V759I variant in a 49-year-old woman presenting with a family history of sick sinus syndrome. This HCN4 variant was previously classified as putatively pathogenic because genetically linked to sudden infant death syndrome and malignant epilepsy. However, detailed electrophysiological and cell biological characterization of HCN4 V759I in Xenopus laevis oocytes and embryonic rat cardiomyocytes, respectively, did not reveal any obvious abnormality. Voltage dependence and kinetics of mutant channel activation, modulation of cAMP-gating by the neuronal HCN channel auxiliary subunit PEX5R, and cell surface expression were indistinguishable from wild-type HCN4. In good agreement, the clinically likewise affected mother of the patient does not exhibit the reported HCN4 variance. HCN4 V759I resembles an innocuous genetic HCN channel variant, which is not sufficient to disturb cardiac pacemaking. Once more, our work emphasizes the importance of careful functional interpretation of genetic findings not only in the context of hereditary cardiac arrhythmias.


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