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 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