TY - JOUR
T1 - Effects of catheter-delivered electrical discharges near the tricuspid anulus in dogs
AU - Ruder, Michael A.
AU - Davis, Jesse C.
AU - Eldar, Michael
AU - Finkbeiner, Walter
AU - Scheinman, Melvin M.
N1 - Funding Information:
From the Department of Medicine. Cardiovascular Research Institute and Department of Pathology. University of California, San Francisco. California. Dr. Ruder was partially supported by a Fellowship Grant from the North American Society of Pacing and ,Electrophysiology Wellesley Hills, Massachusetts. This study was supported by Grant from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. Manuscript received September 15, 1986; revised manuscript received February 18, 1987, accepted March 10, 1987. Address for reprints: Melvin Scheinman, MD, Room Hospital, University of California, San Francisco, California
PY - 1987
Y1 - 1987
N2 - The possibility of using electrical discharges to ablate right free wall accessory pathways by delivering a series of catheter shocks near the tricuspid anulus was assessed in a canine model. Before the shock, the amplitudes of the atrial and ventricular electrograms recorded from the distal electrodes were compared (A/V ratio), and the atrial pacing threshold was determined. To assess effects on function and arrhythmogenicity, right heart pressures were measured and programmed ventricular stimulation was performed before the shock and prior to sacrifice 7 to 10 days after the shock. Nine dogs received a total of 24 discharges at varying energies (50 to 400 J). Nonsustained ventricular tachycardia occurred with 13 shocks (62%) and transient atrioventricular block with 9 shocks (43%). There was no worsening in cardiac or valvular function as determined by right heart pressure measurements or right ventriculography. Programmed ventricular stimulation performed before the shocks and repeated before sacrifice Tailed to induce ventricular arrhythmias. The endocardial lesion produced by the shock was roughly circular and its area correlated with both the magnitude of the shock as well as the atrial pacing threshold. Transmural necrosis always occurred at the anulus when the A/V ratio was between 1.00 and 1.50 and preshock atrial pacing threshold suggested adequate wall contact (<1.5 mA). There was mild inflammation of the adventitia of the right coronary artery near two discharge sites (both 200 J) and inflammation of the media near one discharge site (400 J); no intimai involvement was seen. There was no evidence of tricuspid regurgitation, right heart failure or inducible ventricular arrhythmias before sacrifice of the animals. The location of the lesions suggests that this technique may prove adaptable to interrupting right free wall accessory pathways in humans.
AB - The possibility of using electrical discharges to ablate right free wall accessory pathways by delivering a series of catheter shocks near the tricuspid anulus was assessed in a canine model. Before the shock, the amplitudes of the atrial and ventricular electrograms recorded from the distal electrodes were compared (A/V ratio), and the atrial pacing threshold was determined. To assess effects on function and arrhythmogenicity, right heart pressures were measured and programmed ventricular stimulation was performed before the shock and prior to sacrifice 7 to 10 days after the shock. Nine dogs received a total of 24 discharges at varying energies (50 to 400 J). Nonsustained ventricular tachycardia occurred with 13 shocks (62%) and transient atrioventricular block with 9 shocks (43%). There was no worsening in cardiac or valvular function as determined by right heart pressure measurements or right ventriculography. Programmed ventricular stimulation performed before the shocks and repeated before sacrifice Tailed to induce ventricular arrhythmias. The endocardial lesion produced by the shock was roughly circular and its area correlated with both the magnitude of the shock as well as the atrial pacing threshold. Transmural necrosis always occurred at the anulus when the A/V ratio was between 1.00 and 1.50 and preshock atrial pacing threshold suggested adequate wall contact (<1.5 mA). There was mild inflammation of the adventitia of the right coronary artery near two discharge sites (both 200 J) and inflammation of the media near one discharge site (400 J); no intimai involvement was seen. There was no evidence of tricuspid regurgitation, right heart failure or inducible ventricular arrhythmias before sacrifice of the animals. The location of the lesions suggests that this technique may prove adaptable to interrupting right free wall accessory pathways in humans.
UR - http://www.scopus.com/inward/record.url?scp=0023267079&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(87)80214-0
DO - 10.1016/S0735-1097(87)80214-0
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AN - SCOPUS:0023267079
SN - 0735-1097
VL - 10
SP - 693
EP - 701
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 3
ER -