Circulation, Vol 69, 1006-1012, Copyright © 1984 by American Heart Association
BB Lerman, JL Weiss, BH Bulkley, LC Becker and ML Weisfeldt
Although electrical ablation of ventricular tachycardia via percutaneous
catheters has been recently accomplished in human beings, little is known
of its pathologic or arrhythmogenic effects. We studied 21 open-chest
anesthetized dogs in which an endocardial electrode catheter was
percutaneously introduced into the left ventricle. Direct current (DC)
shock was delivered by a standard defibrillator through the distal
electrode to a back paddle. Cross-sectional two-dimensional
echocardiographic studies were performed in the plane of the catheter
(confirmed by epicardial metal beads), and blood flow was determined by the
microsphere technique before DC shock and when the animals were killed 2 to
8 days later. Of 11 dogs receiving a total of 100 to 400 J, only three
survived 48 hr compared with nine of 10 receiving 50 J and all three
control dogs. Holter monitoring demonstrated sustained ventricular
tachycardia (VT) (greater than or equal to 30 sec) in all 11 dogs monitored
(six received greater than or equal to 100 J), beginning within 5 hr of the
DC shock; three control dogs had no VT. Two dogs that died suddenly while
being monitored showed ventricular fibrillation. Histologic examination
revealed hemorrhagic contraction band necrosis in the shock zone, a type of
injury similar to that observed in reperfusion necrosis. Necrosis of the
left ventricle was 0.5% to 5%. There was no significant difference in
necrosis between dogs receiving 100 J or more and those receiving 50 J (2.5
vs 1.7 g; p greater than .10). Percent systolic thickening determined in
eight equally divided regions around the left ventricle showed no
difference between the shock zone, perishock zone, or remote normal zone in
dogs receiving 50 J.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Myocardial injury and induction of arrhythmia by direct current shock delivered via endocardial catheters in dogs
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