Susceptibility of infarcted canine hearts to digitalis-toxic ventricular tachycardia

The susceptibility to the toxic arrhythmogenic effects of digitalis was studied in 10 normal dogs (group 1) and in 15 dogs with healed myocardial infarction (group 2) 26 ± 5 days after coronary artery ligation. The dose of ouabain required to cause stable digitalis-toxic ventricular tachycardia was...

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Published inJournal of the American College of Cardiology Vol. 2; no. 1; pp. 45 - 51
Main Authors Iesaka, Yoshito, Aonuma, Kazutaka, Gosselin, Arthur J., Pinakatt, Teresa, Stanford, William, Benson, Jerome, Sampsell, Ronald, Rozanski, John J., Lister, John W.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.07.1983
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Abstract The susceptibility to the toxic arrhythmogenic effects of digitalis was studied in 10 normal dogs (group 1) and in 15 dogs with healed myocardial infarction (group 2) 26 ± 5 days after coronary artery ligation. The dose of ouabain required to cause stable digitalis-toxic ventricular tachycardia was 25% less in the group 2 dogs than in the group 1 control dogs (70 ± 21 versus 93 ± 16 μg/kg, probability [p] < 0.01). The average cycle length of the digitalis-toxic ventricular tachycardia was significantly shorter in group 2 than in group 1 (337 ± 47 versus 400 ± 59 ms, p < 0.01). During stable digitalis-toxic ventricular tachycardia, the heart was mapped from 14 to 28 (average 18) preselected endocardial sites and from 15 to 30 (average 21) preselected epicardial ventricular sites. In 12 of the 15 dogs from group 2, the site of origin of the digitalis-toxic ventricular tachycardia was localized to the infarcted or peri-infarcted area of the left ventricular free wall. Furthermore, in five of these, the site of origin of the tachycardia was further confirmed by pace mapping. In contrast, in none of the 10 control dogs was the site of the ventricular tachycardia located in the left ventricular free wall. In five of these dogs, the left ventricle was mapped by catheter and the site of origin of the ventricular tachycardia was found to be in the left ventricular septum. These findings are consistent with healed infarcted myocardium serving as a site of predilection for the origin of digitalis-toxic ventricular tachycardia. Our observations add to a growing body of information suggesting that hearts with healed myocardial infarction have an enhanced susceptibility to digitalis intoxication.
AbstractList The purpose of this study is to report on both the increased propensity to and the site of origin of digitalis-toxic ventricular arrhythmias in infarcted canine hearts. The susceptibility to the toxic arrhythmogenic effects of digitalis was studied in 10 normal dogs (group 1) and in 15 dogs with healed myocardial infarction (group 2). The dose of ouabain required to cause stable digitalis-toxic ventricular tachycardia was 25% less in group 2 dogs than in the group 1 control dogs. The average cycle length of the digitalis-toxic ventricular tachycardia was significantly shorter in group 2 than in group 1. In the dogs from group 2, the site of origin of the digitalis-toxic ventricular tachycardia was localized to the infarcted or peri-infarcted area of the left ventricular free wall. In contrast, in none of the 10 control dogs was the site of the ventricular tachycardia located in the left ventricular free wall. These findings are consistent with healed infarcted myocardium serving as a site of predilection for the origin of digitalis-toxic ventricular tachycardia.
The susceptibility to the toxic arrhythmogenic effects of digitalis was studied in 10 normal dogs (group 1) and in 15 dogs with healed myocardial infarction (group 2) 26 ± 5 days after coronary artery ligation. The dose of ouabain required to cause stable digitalis-toxic ventricular tachycardia was 25% less in the group 2 dogs than in the group 1 control dogs (70 ± 21 versus 93 ± 16 μg/kg, probability [p] < 0.01). The average cycle length of the digitalis-toxic ventricular tachycardia was significantly shorter in group 2 than in group 1 (337 ± 47 versus 400 ± 59 ms, p < 0.01). During stable digitalis-toxic ventricular tachycardia, the heart was mapped from 14 to 28 (average 18) preselected endocardial sites and from 15 to 30 (average 21) preselected epicardial ventricular sites. In 12 of the 15 dogs from group 2, the site of origin of the digitalis-toxic ventricular tachycardia was localized to the infarcted or peri-infarcted area of the left ventricular free wall. Furthermore, in five of these, the site of origin of the tachycardia was further confirmed by pace mapping. In contrast, in none of the 10 control dogs was the site of the ventricular tachycardia located in the left ventricular free wall. In five of these dogs, the left ventricle was mapped by catheter and the site of origin of the ventricular tachycardia was found to be in the left ventricular septum. These findings are consistent with healed infarcted myocardium serving as a site of predilection for the origin of digitalis-toxic ventricular tachycardia. Our observations add to a growing body of information suggesting that hearts with healed myocardial infarction have an enhanced susceptibility to digitalis intoxication.
Author Stanford, William
Rozanski, John J.
Gosselin, Arthur J.
Sampsell, Ronald
Pinakatt, Teresa
Benson, Jerome
Lister, John W.
Iesaka, Yoshito
Aonuma, Kazutaka
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Snippet The susceptibility to the toxic arrhythmogenic effects of digitalis was studied in 10 normal dogs (group 1) and in 15 dogs with healed myocardial infarction...
The purpose of this study is to report on both the increased propensity to and the site of origin of digitalis-toxic ventricular arrhythmias in infarcted...
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StartPage 45
SubjectTerms Animals
digitalis
Digitalis Glycosides - administration & dosage
Disease Models, Animal
Disease Susceptibility
Dogs
Dose-Response Relationship, Drug
Electrophysiology
Heart Septum - physiopathology
Heart Ventricles - physiopathology
Myocardial Infarction - complications
Ouabain - administration & dosage
Tachycardia - chemically induced
Tachycardia - complications
Tachycardia - physiopathology
Title Susceptibility of infarcted canine hearts to digitalis-toxic ventricular tachycardia
URI https://dx.doi.org/10.1016/S0735-1097(83)80375-1
https://www.ncbi.nlm.nih.gov/pubmed/6853917
https://search.proquest.com/docview/13992562
Volume 2
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