Recruitment of bundle branches with permanent His bundle pacing in a patient with advanced conduction system disease: What is the mechanism?

Heart Rhythm ◽  
2016 ◽  
Vol 13 (2) ◽  
pp. 623-625 ◽  
Author(s):  
Parikshit S. Sharma ◽  
Jose Huizar ◽  
Kenneth A. Ellenbogen ◽  
Alex Y. Tan
EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
R Chattopadhyay ◽  
P Chousou ◽  
R Thomas ◽  
J O"brien ◽  
F Pierres ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Pacing-Induced Cardiomyopathy (PICM) can lead to significant morbidity, requiring treatment by device upgrade procedures. The risk of occurrence is directly related to the burden of right ventricular pacing, which can be reduced by careful device programming. When frequent ventricular stimulation cannot be avoided, pacing the conduction system may offer an alternative to myocardial pacing and reduce the risk of PICM. The most recent international pacing guidelines recommend that His-bundle pacing should be considered among 1) patients with EF 36-50% and expected to require >40% ventricular pacing (Vp > 40%) (class IIa); and 2) patients requiring pacing who have block at the level of the AV node (class IIb). Purpose This study sought to determine how many patients undergoing bradycardia pacing would have fulfilled those criteria. Methods This was a single-centre retrospective study over a 5 year period to the end of April 2020. Demographic and clinical details of patients receiving device implants were obtained from the Pacing Service Database, along with the indication for pacing, electrocardiographic and echocardiographic data. A cardiology consultant with a special interest in pacing reviewed each case with regards to the likelihood of requiring >40% ventricular pacing. Heart block at the level of the AV node was considered present if patients presented with a narrow QRS in conjunction with second or third degree heart block. Results 1,265 patients underwent pacemaker implant for bradycardia during the study period, 888 for conduction system disease (198 second degree block, 333 complete heart block), 349 for sinus node disease and 28 for other indication. Figure 1 gives a breakdown of patients with conduction system block according to i) level of block; ii) ejection fraction; iii) expectation or not of Vp > 40%.  In total, 166 patients had a class IIa indication for His-bundle pacing. 227 patients had block at the level of the AV node, of whom 36 also fulfilled the class IIa criteria for His-bundle pacing; 191 patients (16% of the total) had a sole class IIb indication for His-bundle pacing. Adjusting for the 176 patients who did not undergo echocardiography, up to an additional 45 patients may be expected to have an indication for His-bundle pacing Conclusion As many as 32% of patients in a bradycardia pacing population may be eligible for His-bundle pacing. This has significant implications for training and service provision. Abstract Figure 1. Flowsheet showing distribution


2001 ◽  
Vol 7 (3) ◽  
pp. 249-256 ◽  
Author(s):  
Petra M. Jakobs ◽  
Emily L. Hanson ◽  
Kathy A. Crispell ◽  
Warren Toy ◽  
Hugh Keegan ◽  
...  

2013 ◽  
Vol 19 (4) ◽  
pp. 233-239 ◽  
Author(s):  
Chad Brodt ◽  
Jill D. Siegfried ◽  
Mark Hofmeyer ◽  
Jose Martel ◽  
Evadnie Rampersaud ◽  
...  

2007 ◽  
Vol 292 (1) ◽  
pp. H399-H407 ◽  
Author(s):  
Zhu-Shan Zhang ◽  
Joseph Tranquillo ◽  
Valentina Neplioueva ◽  
Nenad Bursac ◽  
Augustus O. Grant

Some mutations of the sodium channel gene NaV1.5 are multifunctional, causing combinations of LQTS, Brugada syndrome and progressive cardiac conduction system disease (PCCD). The combination of Brugada syndrome and PCCD is uncommon, although they both result from a reduction in the sodium current. We hypothesize that slow conduction is sufficient to cause S-T segment elevation and undertook a combined experimental and theoretical study to determine whether conduction slowing alone can produce the Brugada phenotype. Deletion of lysine 1479 in one of two positively charged clusters in the III/IV inter-domain linker causes both syndromes. We have examined the functional effects of this mutation using heterologous expression of the wild-type and mutant sodium channel in HEK-293-EBNA cells. We show that ΔK1479 shifts the potential of half-activation, V1/2m, to more positive potentials ( V1/2m = −36.8 ± 0.8 and −24.5 ± 1.3 mV for the wild-type and ΔK1479 mutant respectively, n = 11, 10). The depolarizing shift increases the extent of depolarization required for activation. The potential of half-inactivation, V1/2h, is also shifted to more positive potentials ( V1/2h = −85 ± 1.1 and −79.4 ± 1.2 mV for wild-type and ΔK1479 mutant respectively), increasing the fraction of channels available for activation. These shifts are quantitatively the same as a mutation that produces PCCD only, G514C. We incorporated experimentally derived parameters into a model of the cardiac action potential and its propagation in a one dimensional cable (simulating endo-, mid-myocardial and epicardial regions). The simulations show that action potential and ECG changes consistent with Brugada syndrome may result from conduction slowing alone; marked repolarization heterogeneity is not required. The findings also suggest how Brugada syndrome and PCCD which both result from loss of sodium channel function are sometimes present alone and at other times in combination.


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