In vivo induction of "focal" triggered ventricular arrhythmias and responses to overdrive pacing in the canine heart

T Furukawa, S Kimura, A Catstellanos, A L Bassett, R J Myerburg
1990 Circulation  
Delayed afterdepolarizations and triggered activity were evoked in focal areas of myocardium in vivo by local exposure of endocardium to ouabain by means of a catheter electrode system capable of recording monophasic action potentials (MAPs) and delivering ouabain to the recording site. MAPs were recorded from the septum and the posterior wall of the left ventricle with silver-silver chloride electrode catheters. Ouabain (10-'M) was infused through the MAP recording catheter onto the
more » ... surface of the septum. After infusion of 10 jug/kg ouabain, the amplitude of MAPs recorded from the septum (the site of ouabain infusion) decreased from 37.4+11.8 to 32.0±10.1 mV (p<0.01), MAP duration at 50% repolarization shortened from 160±29 to 148+±34 msec (p<0.01), and MAP duration at 90% repolarization shortened from 198+±38 to 189± 46 msec (p<0.01). MAPs recorded from the posterior wall (the reference site) were unchanged. Delayed afterdepolarizations were recorded at the site of ouabain infusion, but not at the reference site, when the heart was paced at cycle lengths of 200-600 msec. Additional infusion of ouabain induced sustained monomorphic ventricular tachycardia (VT) (mean cycle length, 369±12 msec) in all 15 dogs studied. The mean concentration of ouabain required to induce VT was 20.9±+10.0 jig/kg. Paced QRS complexes when stimulated at the site of ouabain infusion had the same morphology as those of spontaneous VT. Local perfusion of verapamil, 0.015-0.034 mg/kg, through the MAP recording catheter onto the site of ouabain infusion completely eliminated VT and premature ventricular contractions. After perfusion of verapamil, delayed afterdepolarizations could no longer be induced by pacing. These observations indicate that induced VT originated from the site of ouabain infusion, and the presence of delayed afterdepolarizations before development of VT strongly suggests that the induced VT was due to triggered activity. Using this model, we examined the responses to rapid ventricular pacing of "focal" triggered VT. The first beat of the reinitiated tachycardia displayed the same morphology as the spontaneous VT. The recovery interval of the first postpacing impulse decreased as the pacing cycle length shortened and demonstrated overdrive acceleration at a relatively short pacing cycle length (less than 65% of the original VT). The recovery interval of the first postpacing impulse was shorter when the pacing site was closer to the focus of the triggered arrhythmia. The coupling interval of the second postpacing impulse was slightly shorter than the recovery interval of the first postpacing impulse. It gradually lengthened after the second postpacing impulse and returned to the original VT cycle length at 7±1 impulses after cessation of pacing. Constant fusion only occurred at a pacing cycle length identical to that of the original VT, and thus, by definition, the arrhythmia could not have possibly been entrained. We conclude that the responses to overdrive pacing of focal triggered ventricular arrhythmias may be helpful in distinguishing this type of arrhythmia from arrhythmias due to reentry or due to global influences that may generate triggered activity. (Circulation 1990;82:549-559) From the Departments of Medicine (Cardiology) and Pharma-Florida Affiliate (R.J.M.). cology,
doi:10.1161/01.cir.82.2.549 pmid:2372901 fatcat:pe3lynv5r5cnheggdozg7fem2q