Canine Model of Ischemia-Induced Ventricular Tachycardia

Abstract

Introduction: Despite advances in antiarrhythmia therapies, ventricular tachycardia (VT) is a leading cause of sudden cardiac death. Investigation into the characteristics and new treatments for this arrhythmia is required to improve outcomes and a reproducible model of VT would be useful in these endeavors. We therefore created a canine model of ischemia-induced VT.

Materials and methods: A pacing lead was implanted in the right ventricle in canines (n = 13) and the left anterior descending artery was occluded in two locations for 2 h and subsequently released to create an ischemia-reperfusion injury. In the 10 dogs that survived the first 48 h following the initial study, a terminal study was conducted 4-7 d later and VT was induced using premature stimulation or burst pacing through the right ventricle lead. The arrhythmia was terminated using either antitachycardia pacing or a defibrillatory shock. Multiple inductions into sustained VT were attempted.

Results: Sustained VT was induced in eight of 10 dogs with an average cycle length of 335 ± 70 bpm. Multiple episodes of VT were induced. Episodes of VT exhibited different electrocardiogram morphologies and cycle lengths in individual animals.

Conclusions: This canine model provides a consistent technique for inducing multiple episodes of sustained VT. It may be useful for investigating VT mechanisms and testing novel therapeutics and treatments for patients with VT.

Keywords: Canine model; Ischemia-reperfusion; Ventricular tachycardia.

Fig. 1 –

Tissue discoloration following occlusion. We observed cyanotic tissue color change in the region between the two occlusions to confirm creation of ischemic region.

Fig. 2 –

ECG throughout study duration. (A) Sinus rhythm observed approximately 1 hour after ischemia-induced injury. (B) Accelerated idioventricular rhythm observed approximately 24 h after infarct study. (C) Sinus rhythm observed approximately 72 h after infarct study. ECGs shown from one representative animal with 25 mm/s chart speed.

Fig. 3 –

VT wave morphologies. Episodes of VT with distinct rates and waveforms were inducible in an individual animal using S1-S2 pacing.

Fig. 4 –

Adverse outcomes. (A) Non-sustained VT induced by S1-S2 pacing. (B) Ventricular fibrillation induced by S1-S2 pacing.