scholarly journals Snaring a Newly Placed His-Bundle Lead to Prevent Dislodgement after Superiorly Performed Atrioventricular Node Ablation

Author(s):  
Kamal Kotak ◽  
Ravi Mandapati ◽  
Jalaj Garg ◽  
Tahmeed Contractor
1980 ◽  
Vol 239 (1) ◽  
pp. H22-H30 ◽  
Author(s):  
S. J. Kopp ◽  
M. Perry ◽  
T. Glonek ◽  
M. Erlanger ◽  
E. F. Perry ◽  
...  

Female Long-Evans hooded rats received 0 or 5 parts per million Cd, Pb, or Cd + Pb in the drinking water from weaning to 20 mo. Growth, measured as body weight, and organ weights were comparable among heavy metal and control animals. Indirect blood pressure responses measured trimonthly are discussed. Analysis of His bundle electrograms (HBE) and electrocardiograms recorded in sodium pentobarbital-anesthetized animals at 20 mo demonstrated that Cd selectively depressed conduction system excitability proximal to the common His bundle (atrioventricular node region), whereas Pb and Pb + Cd impaired conductivity distal to the common His bundle (His-Purkinje system). Perchloric acid extracts of liquid N2-freeze-clamped isolated perfused hearts, derived from a subpopulation of control and Cd-fed rats in which HBE analyses were not performed, were analyzed by phosphorus-31 nuclear magnetic resonance (31P-NMR) spectroscopic techniques to quantitate [31P]phosphate metabolite profiles. Cardiac active tension and atrioventricular node excitability were depressed in the Cd group. High-energy phosphate and glycerol 3-phosphorylcholine concentrations were depressed. Results demonstrate potentially significant pathophysiological changes within cardiovascular tissues that develop in the absence of overt heavy metal toxicity manifestations.


1982 ◽  
Vol 243 (5) ◽  
pp. H754-H760 ◽  
Author(s):  
T. Mazgalev ◽  
L. S. Dreifus ◽  
J. Bianchi ◽  
E. L. Michelson

Atrial fibrillation was induced in 15 superfused rabbit atrial-atrioventricular nodal preparations in which surface bipolar electrograms were recorded simultaneously from the crista terminalis, interatrial septum, and His bundle along with microelectrode action potentials from cells in the atrionodal (AN), nodal (N), and nodal-His (NH) regions of the atrioventricular node. Effective engagement of the atrioventricular node with propagation to the His bundle was critically dependent on the relative timing of activation at the crista terminalis and interatrial septal input regions of the atrioventricular node. Conduction through the AN and N regions appeared dependent on the relative timing of activation wave fronts emerging from the two input regions. Asynchronous engagement of AN and N regions resulted in both distortion of action potentials and concealed conduction, with delayed conduction and block to the NH region and His bundle. Successful engagement of the NH region always produced a 1:1 NH-to-His bundle relationship. It is concluded that during atrial fibrillation 1) activation of the AN region occurs as a result of the variable interaction of inputs from the crista terminalis and interatrial septum; 2) predictably, effective synchronous engagement of the AN and consequently the N region is responsible for conduction to the NH and His bundle regions; 3) conversely, asynchronous activation inputs from the crista terminalis and interatrial septum result in fragmented, asynchronous as well as concealed conduction within the AN and N regions with block in the atrioventricular node and variable conduction to the His bundle.


2011 ◽  
Vol 27 (Supplement) ◽  
pp. PE3_030
Author(s):  
Muhammad Munawar ◽  
Dian Andina ◽  
Dian Larasati ◽  
Jimmy Pambudi

2018 ◽  
Vol 27 ◽  
pp. S167
Author(s):  
B. Abu Baker ◽  
C. Chow ◽  
P. Barlis ◽  
C. Eastwood ◽  
U. Mohamed

Author(s):  
Benzy J. Padanilam ◽  
Asim S. Ahmed ◽  
Brad A. Clark ◽  
Jasen L. Gilge ◽  
Parin J. Patel ◽  
...  

Background: Current maneuvers for differentiation of atrioventricular node reentry tachycardia (AVNRT) and atrioventricular reentry tachycardia (AVRT) lack sensitivity and specificity for AVRT circuits located away from the site of pacing. We hypothesized that a premature His complex (PHC) will always perturb AVRT because the His bundle is obligatory to the circuit. Further, AVNRT could not be perturbed by a late PHC (≤20 ms ahead of the His) due to the retrograde His conduction time. Earlier PHCs can advance the AVNRT circuit but only by a quantity less than the prematurity of the PHC. Methods: High-output pacing at the distal His location delivered PHCs. AVRT was predicted when late PHCs perturbed tachycardia or when earlier PHCs led to atrial advancement by an amount equal or greater than the degree of PHC prematurity. Results: Among the 73 supraventricular tachycardias, the test accurately predicted AVRT (n=29) and AVNRT (n=44) in all cases. Late PHC advanced the circuit in all 29 AVRTs and none of the AVNRTs (sensitivity and specificity, 100%). With earlier PHCs, the degree of atrial advancement was equal or greater than the PHC prematurity in 26/29 AVRTs and none of the AVNRTs (90% sensitivity and 100% specificity). The mean prematurity of the PHC required to perturb AVNRT was 48 ms (range, 28–70 ms) and the advancement less than the prematurity of the PHC (mean, 32 ms; range, 18–54 ms). Conclusions: The responses to PHCs distinguished AVRT and AVNRT with 100% specificity and sensitivity.


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