The inducibility and reproducibility of ventricular tachycardia were evaluated in 97 dogs after myocardial infarction produced by single stage coronary artery ligation. Arrhythmia induction was performed with use of an endocardial electrode catheter positioned at the right ventricular apex before each study. An aggressive protocol of programmed stimulation was used, employing up to seven extrastimuli and three attempts at arrhythmia induction in each study. Electrophysiologic study was performed in individual dogs at the following times after infarction: 1) 7.7 ± 0.3 and 15 ± 0.2 days (34 consecutive dogs); 2) 14 ± 0.6 and 26 ± 1.7 days (24 selected dogs); 3) 19 ± 2 and 43 ± 3 days (12 selected dogs); 4) 36 ± 2 and 60 ± 6 days (8 selected dogs); and 5) 59 ± 12 and 130 ± 10 days (3 selected dogs). Inducibility of ventricular tachycardia decreased significantly from 74% 1 week after infarction to 41% 2 weeks after infarction. Thus, early reproducibility was low (48%). Reproducibility increased thereafter, with 88% of the dogs having reproducible ventricular tachycardia between 2 and 4 weeks (p < 0.025) and 100% having reproducibly inducible ventricular tachycardia between 4 weeks and 4 months after infarction. Dogs with no inducible arrhythmia early after infarction did not develop inducible ventricular tachycardia or fibrillation at later studies. Twelve dogs developed spontaneous ventricular tachycardia or sudden arrhythmic death late after infarction. Overall, 22% of dogs with inducible ventricular tachycardia with a cycle length >140 ms developed spontaneous ventricular tachycardia or sudden death. Arrhythmia induction decreases significantly during the 1st 2 weeks after myocardial infarction, but long-term reproducibility of ventricular tachycardia induced ≥2 weeks after infarction is very high. This canine model of long-term, reliably inducible ventricular tachycardia is suitable for investigation of antiarrhythmic drugs, surgery and other interventions.
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