The efficacy of lidocaine and verapamil alone and in combination on spontaneously occurring automatic ventricular tachycardia in conscious dogs one day after right coronary artery occlusion

Abstract

Occlusion of the right coronary artery (RCA) in the dog is associated with spontaneous sustained ventricular tachycardia (VT) during the 18 to 26 hours post occlusion period. Electrophysiologic studies suggest that these tachycardias are caused mainly by an automatic mechanism. In the present study we evaluated in 16 conscious dogs with VT 1 day after RCA occlusion the efficacy of (1) lidocaine (L), which depresses primarily the mechanism of enhanced normal automaticity; (2) verapamil (V), which depresses the mechanism of abnormal and triggered automaticity; and (3) combination of both L and V on these VTs. The RCA was occluded in 16 anesthetized closed-chest dogs by intracoronary balloon inflation. All 16 dogs had spontaneous VT while in the conscious state during the 18 to 26 hours post occlusion study period. L (5 mg/kg intravenously) bolus restored within 1 minute normal sinus rhythm (NSR), with a mean rate of 118 ± 14 bpm, in dogs (n = 7) which had their VTs overdrive suppressed and had a mean rate of 145 ± 14 bpm (range 110 to 150 bpm). L was ineffective in dogs (n = 9) which did not have their VTs overdrive suppressed and had a mean VT rate of 192 ± 24 bpm (range 175 to 250 bpm). In contrast, however, V (0.15 mg/kg intravenously) was ineffective in all seven dogs with the slower VT rates, but was effective in restoring NSR with a mean rate of 140 ± 14 bpm in six out of nine dogs with the faster VT rates. The addition of L, up to 5 mg/kg intravenously to V's regimen did not improve V's efficacy against these V-resistant VTs. We conclude that (1) spontaneous VTs 1 day after RCA occlusion appear to be caused by an automatic mechanism; (2) VTs with rates slower than 150 bpm are suppressed by L but not by V, consistent with enhanced “normal” automatic mechanism as a cause of these VTs; and (3) VTs with faster rates are refractory to L but are often suppressed by V, consistent with abnormal or triggered automaticity as a cause of these VTs. These findings might be helpful in the rational management of VTs in patients with acute myocardial infarction with predominant right ventricular involvement.