Spontaneous ventricular tachycardia associated with isolated right ventricular infarction, one day after right coronary artery occlusion in the dog: studies on the site of origin and mechanism.

The electrophysiologic and arrhythmic properties of isolated infarcted right ventricle (RV) were studied in 17 dogs during the first 24 hours after complete occlusion of the right coronary artery (RCA). During the 16-to-20-hour post occlusion period, spontaneously occurring sustained monomorphic ventricular tachycardia (VT) was present in all 17 dogs. Overdrive ventricular pacing (cycle lengths 200 to 250 msec) caused significant suppression of the VT when the rate of the VT was slower than 150 bpm (range 120 to 145 bpm) (n = 9), but had negligible effect when VT rate was higher than 150 bpm (range 160 to 245 bpm (n = 8). Overdrive pacing could not terminate either the slow or the fast type of VT. Bipolar intramural electrograms have showed electrical activity in the infarcted RV zone to precede Q wave of the VT by 15.4 +/- 5.8 msec regardless of VT rate. Microelectrode studies on isolated RV endocardial infarcted tissues 24 hours after RCA occlusions have shown the presence of spontaneous repetitive activity at a rate of 87 +/- 47 bpm, which was overdrive suppressed in dogs with slow VT, and spontaneous activity at a rate of 115.2 +/- 36 bpm (p less than 0.05) which was not overdrive suppressed in dogs with fast VT. Maximum diastolic potential, action potential amplitude, and Vmax of surviving subendocardial Purkinje fibers (SEPF) in the infarct zone were slightly but significantly depressed (p less than 0.05), and they manifested enhanced phase 4 depolarization, giving rise to automatic impulse initiation. Although action potential duration of these fibers was somewhat prolonged (p less than 0.05), no conduction delay occurred. Histopathologic examinations have shown necrosis of the basal two thirds of the RV, with no left ventricular involvement. Electron microscopy revealed lipid accumulation in the surviving SEPF as the sole abnormality. We conclude (1) that occlusion of the RCA in the dog is associated with high survival rate despite extensive necrosis involving exclusively the RV and (2) that VT seen during the 20 to 24 hours after occlusion arise in the infarcted zone of the RV, by an enhanced automatic mechanism in the surviving SEPF, possibly caused by cytoplasmic lipid accumulation. This model, by virtue of its high survival rate and frequency of late VTs, should be useful in providing clues to determine factors involved in the genesis of early VT/VF and for the evaluation of new pharmacologic agents during the 20- to 24-hour VT period.