Effect of procainamide and lidocaine on ventricular automaticity and reentry during acute coronary occlusion

Han, Jaok; Goel, Brij G.; Yoon, Myung S.; Rogers, Rosalyn

doi:10.1016/0002-9149(74)90196-9

Cited by 24 publications

(4 citation statements)

References 10 publications

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“…These arrhythmias are readily suppressed by procaineamide24 as well as lidocaine25 as would be predicted for an automatic rhythm in contradistinction to a re-entrant arrhythmia. 26 Similarly, Wellens et al.,27 employing electrical stimulation of the heart to assess the mechanism of sustained ventricular tachycardia in man, studied 3 to 20 hours following the onset of acute myocardial infarction, concluded that this arrhythmia was due to increased automaticity rather than re-entry. During the first 24 hours following the acute infarction (excluding the first 120 minutes), these episodes of ventricular tachycardia remained stable and did not degenerate into ventricular fibrillation; they appeared to be nonparasystolic and could not be terminated by successive premature stimuli.…”

Section: Methodsmentioning

confidence: 99%

Subendocardial origin of ventricular arrhythmias in 24-hour-old experimental myocardial infarction.

Horowitz¹,

Spear²,

Moore³

1976

Circulation

122

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MethodsTwelve healthy mongrel dogs weighing 10-15 kg were employed in these experiments. They were anesttetized with intravenous sodium pentobarbital (30 mg/kg) and ventilated with room air through a pharyngotracheal tube by a Harvard pump. The chest was opened through a small left thoracotomy in the fourth interspace and the pericardium was opened. The left anterior descending coronary artery was occluded by the Harris 2-stage procedure5 3-7 mm from the border of the left atrial appendage. The chest was closed and the animal was allowed to recover. Preoperative and 4-6 hour postoperative electrocardiograms were obtained.Twenty-four hours following the initial procedure the animals were reanesthetized with morphine (2.5 mg/kg) and sodium pentobarbital (10 mg/kg) and ventilated with room air through a tracheostomy by a positive pressure ventilator at a minute volume determined from a body weight nomogram. Body temperature was maintained at 101-102°F by a thermal mattress. The chest was opened in the fifth left interspace and the heart was suspended in a pericardial sling. Standard electrocardiographic leads were monitored. A bipolar catheter electrode was inserted via the right femoral or internal jugular vein and placed in the right atrium to record the His bundle electrogram (HBE).Because of the constraints of the mapping procedure, it was necessary to establish a unifocal ventricular tachycardia (UVT) or stable pattern of unifocal ectopic ventricular depolarizations in the animals in this study. If stable UVT was not initially present a stable pattern of unifocal ectopic depolarizations was established by pacing the heart through an atrial electrode at the sinus rate and crushing the sinus node. A sequence of 3-10 supraventricular beats followed by a pause was established with a digitally pro-

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Section: Methodsmentioning

confidence: 99%

Subendocardial origin of ventricular arrhythmias in 24-hour-old experimental myocardial infarction.

Horowitz¹,

Spear²,

Moore³

1976

Circulation

122

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“…No serious cardiovascular side effects have been associated with bidisomide [3]. The efficacy of class I antiarrhythmic agents against ventricular ectopic beats occurring several hours after the onset of myocardial infarction has been established in animal experiments [4,5], but there is some controversy concerning the efficacy of these drugs for early-phase ventricular arrhythmias resulting from myocardial ischemia [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Effects of bidisomide (SC-40230), a new class I antiarrhythmic agent, on ventricular arrhythmias induced by coronary artery occlusion and reperfusion in anesthetized rats; comparison with mexiletine and disopyramide

Komori

Sano

et al. 1995

Heart Vessels

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We investigated the antiarrhythmic effects of bidisomide (SC-40230), a new class I antiarrhythmic drug, in early-phase ventricular arrhythmias induced by coronary artery occlusion and reperfusion in anesthetized rats. The effects of bidisomide were compared with those of mexiletine (MXT) and disopyramide (DSP), established class I antiarrhythmic drugs. Drugs were administered intravenously, 5 min before induction of coronary occlusion. Bidisomide (5 mg/kg) reduced the number of premature ventricular complexes and the incidence of ventricular tachycardia and ventricular fibrillation similarly to MXT and DSP in rats with ventricular arrhythmias induced by coronary artery occlusion. In rats with ventricular arrhythmias induced by coronary artery reperfusion following a 5-min coronary occlusion, the antiarrhythmic effects of 5 mg/kg of bidisomide were similar to those of the same doses of MXT and DSP. All three drugs significantly slowed the heart rate. Our results suggest that bidisomide may effectively reduce the severity of life-threatening ventricular arrhythmias that occur during acute coronary syndrome.

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“…[17][18][19][20] Other studies, using either coronary artery ligation or reperfusion models, have also suggested that a large and variable number of animals do not develop ventricular fibrillation, even without prior antiarrhythmic therapy (approximately 60% and 30%, respectively).2 29 Previous studies in this laboratory, however, indicate that the risk for developing ventricular fibrillation on reperfusion might be predicted for individual animals based on the incidence, time course and severity of arrhythmias occurring during the antecedent period of acute coronary artery ligation. 30' 31 This was predicated on the observation that different animals subjected to acute one-stage ligation of the proximal left anterior descending coronary artery developed either immediate (occurring 2-12 minutes after ligation), delayed (occurring 14-30 minutes after ligation), both types or no ventricular arrhythmias at all;32' 33 and that the risk for ventricular fibrillation during the subsequent period of coronary artery reperfusion correlated closely with the occurrence of these ligation arrhythmias.…”

mentioning

confidence: 99%

Failure of antiarrhythmic drugs to prevent experimental reperfusion ventricular fibrillation.

Naito¹,

Michelson²,

Kmetzo³

et al. 1981

Circulation

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SUMMARY Ninety-nine adult mongrel dogs underwent acute ligation of the proximal left anterior descending coronary artery. Thirty minutes later, the occlusion was released to evaluate the effectiveness of five antiarrhythmic protocols in eliminating reperfusion ventricular fibrillation. The five protocols included: protocol 1 -i.v. lidocaine, preligation and prerelease (n = 19); protocol 2 i.v. lidocaine, prereperfusion only (n = 22); protocol 3 chronic, oral, daily amiodarone for 2 weeks preligation (n = 19); protocol 4 -i.v. procainamide, preligation and prereperfusion (n = 21); and protocol 5 i.v. verapamil, prereperfusion (n = 18). Each regimen was evaluated with respect to the incidence of reperfusion ventricular fibrillation in dogs that survived to reperfusion, and the results were compared to 77 control dogs that underwent identical coronary artery occlusion and release procedures without drug therapy. The incidence of reperfusion ventricular fibrillation was as follows: protocol I -seven of 15 dogs (47%); protocol 2 -six of 18 (33%); protocol 3 11 of 16 dogs (69%); protocol 4-eight of 17 dogs (47%); and protocol 5-10 of 17 dogs (59%), compared with 36 of 60 (60%) in control dogs.Using chi-square analysis, protocol 2 was beneficial (p < 0.05). The dogs were then stratified into high-and low-risk subgroups based on the arrhythmic events of the antecedent coronary artery ligation periods, and predictive risk indexes for the occurrence of reperfusion ventricular fibrillation were developed. The MantelHaenszel method of statistical analysis revealed that none of these protocols resulted in a statistically significant reduction in the incidence of reperfusion ventricular fibrillation. Thus, use of these predictive indexes plus appropriate statistical methods has revealed, unexpectedly, limitations in the efficacy of a spectrum of antiarrhythmic agents in preventing reperfusion ventricular fibrillation.CANINE coronary artery occlusion and reperfusion models have been studied extensively as a means for understanding the life-threatening ventricular arrhythmias that occur after myocardial ischemia and infarction. However, as useful as these canine models have been in revealing electrophysiologic mechanisms, their use as models for evaluating anti-

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Effect of procainamide and lidocaine on ventricular automaticity and reentry during acute coronary occlusion

Cited by 24 publications

References 10 publications

Subendocardial origin of ventricular arrhythmias in 24-hour-old experimental myocardial infarction.

Subendocardial origin of ventricular arrhythmias in 24-hour-old experimental myocardial infarction.

Effects of bidisomide (SC-40230), a new class I antiarrhythmic agent, on ventricular arrhythmias induced by coronary artery occlusion and reperfusion in anesthetized rats; comparison with mexiletine and disopyramide

Failure of antiarrhythmic drugs to prevent experimental reperfusion ventricular fibrillation.

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