Incidence Of Reperfusion Ventricular Fibrillation Research Articles

Comparison of amiodarone and esmolol for prevention of reperfusion ventricular fibrillation in individuals undergoing heart valve or aortic surgery: a study protocol for a randomized controlled clinical trial

BackgroundAmiodarone and esmolol can help to prevent and treat post-cardiac surgery reperfusion ventricular fibrillation. However, the relative efficacies of these two drugs remain unknown. The aim of the current trial is to compare the performances of amiodarone and esmolol for preventing reperfusion ventricular fibrillation following open heart surgery.Methods/designThis is a single-center, prospective, double-blind, controlled clinical trial. A total of 260 patients undergoing heart valve or aortic surgery will be assigned randomly to treatment with prophylactic esmolol (intervention group) or amiodarone (control group). The main outcome is the incidence of reperfusion ventricular fibrillation following aortic opening during extracorporeal circulation. The secondary outcomes are the rate of automatic cardiac resuscitation, energy and frequency of electrical defibrillation, number of electrical defibrillations, and pacemaker use in the two groups of patients. Information on the patients’ general condition and the durations of anesthesia, extracorporeal circulation, aortic occlusion, and operation time will be recorded. We will also compare the heart rate, mean arterial pressure, and central venous pressure between the two groups of patients at induction of anesthesia (T1), start of surgery (T2), start of extracorporeal circulation (T3), aortic block (T4), aortic opening (T5), after opening for 10 (T6), 20 (T7), and 30 min (T8), at cessation of extracorporeal circulation (T9), and at the end of surgery (T10) and compare blood gas analysis results at T1, T5, T9, and T10.DiscussionThis study will determine if prophylactic esmolol is more effective than amiodarone for reducing the incidence of reperfusion ventricular fibrillation in patients undergoing heart valve or aortic surgery.Trial registrationChina Clinical Trials Registry ChiCTR1900026429. Registered on 2019.10.9.

Limited Sanguineous Reperfusion Reduces Ventricular Fibrillation Following Intermittent Cold Crystalloid Cardioplegic Arrest.

SourceURL:file://localhost/Users/alex/Desktop/ICFJ%20VF%20submission/Abstract.doc<p><strong>Background</strong></p><p>Cold crystalloid cardioplegic arrest does not allow for a controlled hyperkalaemic sanguineous reperfusate, administered under constant flow and pressure conditions in order to limit reperfusion injury. We investigated the use of intermittent, antegrade cold crystalloid cardioplegia combined with a limited flow normokalaemic sanguineous reperfusion and measured the outcome in terms of the incidence of reperfusion ventricular fibrillation.</p><p> </p><p><strong>Methods</strong></p><p>Patients requiring coronary revascularization of at least two coronary arteries, including an internal thoracic artery (ITA) anastomosis, were studied in this prospective randomized trial. Myocardial protection was by intermittent, antegrade cold crystalloid cardioplegia. In the control group (n=100), after completion of the distal anastomoses, the heart was reperfused by releasing the aortic and ITA clamps concomitantly. In the study group (n=100) the ITA was allowed to perfuse the heart for 3 minutes before the aortic cross-clamp was removed. The presence of reperfusion ventricular fibrillation from the moment of reperfusion until weaning from cardiopulmonary bypass was recorded.</p><p> </p><p><strong>Results</strong></p><p>The incidence of ventricular fibrillation decreased with an increase in the number of grafts and was significantly lower in the study group (double grafts 2/9, 22.2% vs 19/25, 76.0% <em>p</em>=0.004; triple grafts 2/39, 4.9% vs 16/33, 48.5% <em>p</em><0.001; and quadruple grafts 2/45, 4.4% vs 13/35, 28.7% <em>p</em><0.001).</p><p> </p><p><strong>Conclusions</strong></p><p>This strategy of myocardial protection combines the advantages of conventional crystalloid cardioplegia with the added benefit of limited sanguineous reperfusion. The results suggest a beneficial effect with regard to reperfusion-induced injury, as evidenced by a significantly reduced incidence of reperfusion ventricular fibrillation.</p>

Continuous infusion of magnesium–lidocaine mixture for prevention of ventricular arrhythmias during on-pump coronary artery bypass grafting surgery

BackgroundDuring on-pump coronary artery bypass grafting (CABG) surgery, the incidence of reperfusion ventricular fibrillation (VF) is high and post-bypass ventricular arrhythmias are common. Both reperfusion VF and ventricular arrhythmias can cause additional myocardial injury to the already ischemic myocardium. This trial aimed to test the assumption that continuous combined magnesium and lidocaine infusion would be efficient and long lasting for the prevention of post-myocardial vascularization ventricular arrhythmias including VF.MethodsEighty ASA III patients, who were candidates for CABG surgery, were randomly assigned into two groups: Group I (control group, n = 40) and Group II (Group ML, n = 40). After endotracheal intubation, patients of control group were infused with plain normal saline in a volume equivalent to study drugs’ mixture volume. Patients of Group ML were infused with magnesium–lidocaine mixture to achieve a bolus of magnesium sulfate 2 g and lidocaine 100 mg followed by continuous infusion of Mg sulfate 500 mg/h and lidocaine 1 mg/min. The initial cardiac rhythm after aortic cross clamp (ACC) release and the occurrence of post-CPB significant ventricular arrhythmias were recorded.ResultsThe incidences of reperfusion VF and post-CPB ventricular arrhythmias in Group ML were significantly lower than that in control group (22.5% vs. 72.5%) (P < 0.001) and (7.5% vs. 25%) (P < 0.05), respectively. However, in Group ML, this beneficial effect was associated with higher incidence of sinus bradycardia (72.5% vs. 17.5%) and hence pacing needs (22.5% vs. 0.0%) when compared with control group.ConclusionOur study concluded that, during on-pump CABG surgery, the combined administration of magnesium and lidocaine as a bolus dose starting after intubation followed by continuous infusion reduced the incidence of reperfusion VF by 62% and post-CPB ventricular arrhythmias by 70% on expense of increased the incidence of sinus bradycardia and pacing.

Antiarrhythmic and arrhythmogenic effects of L-carnitine in ischemia and reperfusion

Isolated rat hearts were subjected to 30-min coronary artery occlusion followed by 120-min reperfusion. The hearts (n=8-12) were perfused with Krebs-Henseleit solution enriched with L-carnitine (0.5, 2.5 and 5 mM) for 10 min before and after ischemia or reperfusion and for the whole period of ischemia and reperfusion. Two-hour perfusion with L-carnitine during ischemia/reperfusion markedly (p<0.05) and dose-dependently decreased the incidence of ventricular tachycardia (VT, maximum 65%). The incidence of reperfusion ventricular fibrillation (VF) also decreased from 63% (control) to 17% in hearts perfused with 5 mM L-carnitine, as reflected by a significant (p<0.05) decline in VF duration from 218+/-99 sec in control to 19+/-19 sec. Perfusion of etomoxir (palmitoylcarnitinetransferase-1 inhibitor) along with L-carnitine reversed the antiarrhythmogenic action of L-carnitine. Interestingly, short time preischemic administration of L-carnitine produced a concentration-dependent arrhythmogenic effects on both ischemia and reperfusion-induced arrhythmias. These results show that L-carnitine produced a protective effect against reperfusion arrhythmias only when it was perfused for the whole period of the experiment. This protective action was reversed by concomitant use of etomoxir, suggesting that the efficacy of L-carnitine is due to its mitochondrial action but cannot be solely attributed to increased fatty acid oxidation.

Effects of L-carnitine and its derivatives on postischemic cardiac function, ventricular fibrillation and necrotic and apoptotic cardiomyocyte death in isolated rat hearts.

The study aimed to examine whether L-carnitine and its derivatives, acetyl-L-carnitine and propionyl-L-carnitine, were equally effective and able to improve postischemic cardiac function, reduce the incidence of reperfusion-induced ventricular fibrillation, infarct size, and apoptotic cell death in ischemic/reperfused isolated rat hearts. There are several studies indicating that L-carnitine, a naturally occurring amino acid and an essential cofactor, can improve mechanical function and substrate metabolism not only in hypertrophied or failing myocardium but also in ischemic/reperfused hearts. The effects of L-carnitine, acetyl-L-carnitine, and propionyl-L-carnitine, on the recovery of heart function, incidence of reperfusion-induced ventricular fibrillation (VF), infarct size, and apoptotic cell death after 30 min ischemia followed by 120 min reperfusion were studied in isolated working rat hearts. Hearts were perfused with various concentrations of L-carnitine (0.5 and 5 mM), acetyl-L-carnitine (0.5 and 5 mM), and propionyl-L-carnitine (0.05, 0.5, and 5 mM), respectively, for 10 min before the induction of ischemia. Postischemic recovery of CF, AF, and LVDP was significantly improved in all groups perfused with 5 mM of L-carnitine, acetyl-L-carnitine, and propionyl-L-carnitine. Significant postischemic ventricular recovery was noticed in the hearts perfused with 0.5 mM of propionyl-L-carnitine, but not with the same concentration of L-carnitine or L-acetyl carnitine. The incidence of reperfusion VF was reduced from its control value of 90 to 10% (p < 0.05) in hearts perfused with 5 mM of propionyl-L-carnitine only. Other doses of various carnitines failed to reduce the incidence of VF. The protection in CF, AF, LVDP, and VF reflected in a reduction in infarct size and apoptotic cell death in hearts treated with various concentrations of carnitine derivatives. The difference between effectiveness of various carnitines on the recovery of postischemic myocardium may be explained by different membrane permeability properties of carnitine and its derivatives.

Lidocaine for prevention of reperfusion ventricular fibrillation after release of aortic cross-clamping

Objective: To determine the efficacy of a bolus of lidocaine administered by way of the pump before releasing the aortic cross-clamp (ACC) in preventing the occurrence of reperfusion ventricular fibrillation. Design: Prospective, randomized study. Setting: University hospital. Participants: Patients undergoing coronary artery bypass graft surgery (n = 34). Interventions: Seventeen patients received 100 mg of lidocaine by way of the pump 2 minutes before releasing the ACC, and a control group of 17 patients received 5 mL of normal saline. Measurements and Main Results: In the control group, the incidence of reperfusion ventricular fibrillation was 70%, which was significantly decreased to 11% in the lidocaine group. A higher cardiac output after weaning from cardiopulmonary bypass was observed in the lidocaine group; this may be attributed to the lower incidence of reperfusion ventricular fibrillation and consequently the lower need for defibrillation by electric countershocks. Conclusions: The results suggest that a bolus of 100 mg of lidocaine administered 2 minutes before release of the ACC can safely decrease the incidence of reperfusion ventricular fibrillation and is associated with better hemodynamics after weaning from cardiopulmonary bypass. Copyright © 2000 by W.B. Saunders Company

Suppression of reperfusion arrhythmias by preconditioning is inhibited by an ATP-sensitive potassium channel blocker, 5-hydroxydecanoate, but not by protein kinase C blockers in the rat.

It has been suggested that preconditioning (PC) against infarction in the rat heart is mediated by opening of ATP-sensitive potassium (KATP) channels, which may be induced by receptor-triggered activation of protein kinase C (PKC). However, the mechanism of suppression of reperfusion arrhythmias by PC remains unclear. This study first examined whether suppression of reperfusion arrhythmias by PC requires the activation of KATP channels, PKC, and opioid receptors. In anesthetized rats, reperfusion arrhythmias were induced by occluding the left main coronary artery for 5 min and subsequent reperfusion. In untreated control rats, the incidence of reperfusion ventricular tachycardia (VT) was 100%, and 80% of the VT deteriorated to ventricular fibrillation (VF). PC with 2-min ischemia/5-min reperfusion reduced the incidences of VT and VF to 30% and 0, respectively. Although a KATP channel blocker, 5-hydroxydecanoate (5-HD), alone caused no significant effect on the incidence of reperfusion VT, this agent blocked the suppression of reperfusion VT by PC (VT incidence, 91%). The incidence of reperfusion VF in the 5-HD-treated rats tended to be lower than that in the untreated controls and was not different between preconditioned and nonpreconditioned groups (30 vs. 27%). PKC inhibitors staurosporine and calphostin C modified neither reperfusion arrhythmias nor the antiarrhythmic effect of PC on reperfusion VT and VF. Naloxone (6 mg/kg, i.v.) did not alter the incidence or duration of VT in the nonpreconditioned heart. However, suppression of reperfusion VT by PC was prevented by naloxone (VT incidence, 70%). The incidence of reperfusion VF was similarly low in the naloxone-treated rats in both nonpreconditioned and preconditioned groups (20% vs. 0). In the second series of experiments, the effect of 5-HD on repetitive PC was assessed. Repetitive PC was performed with three cycles of 2-min ischemia/5-min reperfusion, which totally abolished reperfusion VT and VF. This antiarrhythmic effect of repetitive PC was not inhibited by 5-HD. These results suggest that KATP channels and opioid receptors may be partly involved in suppression of reperfusion arrhythmias, although their roles may be compensated for by other antiarrhythmic mechanisms in repetitive PC. In contrast with PC against infarction, PKC is unlikely to play a major role in PC against reperfusion arrhythmias in the rat.

Incidence of Ventricular Fibrillation after Aortic Cross-Clamp Release using Lignocaine Cardioplegia

The occurrence of ventricular fibrillation after aortic de-clamping during cardiac surgery is common, and if prolonged may contribute to myocardial ischaemia. The use of lignocaine cardioplegia to minimize reperfusion ventricular fibrillation was studied in 141 patients undergoing first time coronary artery surgery in a double blind prospective randomized trial: 71 patients received lignocaine 100 mg/l in their cardioplegia, whereas a control group of 70 patients received cardioplegia without lignocaine. Lignocaine cardioplegia reduced significantly the incidence of reperfusion ventricular fibrillation from 63% to 42%. Of those patients developing reperfusion ventricular fibrillation, a higher proportion receiving lignocaine cardioplegia underwent spontaneous defibrillation (30% vs 11%) though this was not statistically significant. The incidence of atrio-ventricular (A-V) block necessitating ventricular pacing to separate from cardiopulmonary bypass was significantly higher in the lignocaine treated group (44%) than in the control group (20%): this may have been due to the additive effect of procaine in the cardioplegia solution. In the majority of cases this A-V block was transient and had resolved prior to the completion of surgery.

Antiarrhythmic properties of specific inhibitors of sarcoplasmic reticulum calcium ATPase in the isolated perfused rat heart after coronary artery ligation

Objective. T. hypothesis tested was that sequestration of calcium by the sarcoplasmic reticulum and internal calcium oscillations may play a rote in the genesis of ischemic and reperfusion ventricular arrhythmias.Background. Previous data suggest that inhibition of the release of intracellular calcium from the sarcoplasmic reticulum by ryamodine may prevent ventricular fibrillation.Methods. The isolated Langendorff perfused rat heart was treated with two specific inhibitors of the calcium ATPase pump of the sarcoplasmic reticulum (thapsigargin [10−6mol/liter] or cyclopiazomic acid[10−7mol/liter]) for 5 min before left anterior descending coronary artery ligation was performed, One group of hearts was subject to 30 min of coronary artery ligation, and ischemic arrhythimias were monitored. In a second group, the incidence of reperfusion arrhythmias was measured after 10,15, 20, 25 and 30 min of coronary artery ligation.Results. Thapsigargin treatment during ischemia and reperfusion decreased the incidence of reperfusion ventricular fibrillation after 10 min of coronary artery ligation from 67% (n = 6) to 0% (n = 6) (p < 0.05), after 15 mm from 81% (n = 16) to 25% (n = 20) (p < 0.002) and after 20 mm of ischemia from 90% (n = 10) to 46% (n = 13) (p < 0.05). Thapsigargin treatment also decreased the incidence of ischemic ventricular fibrillation from 83% (a = 12) to 0% (n = 12) (p < 0.002). Cyclopiazonic acid treatment during ischemia and reperfusion likewise decreased the incidence of ischemic and reperfusion arrhythmias.Conclusions. The highly specific inhibitors of the calcium uptake pump of the sarcoplasmic reticulum—thapsigargin and cyclopiazonic acid—have antifibrilltory properties in the isolated perfused rat heart. They appear to act by restriction of calcium oscillations between the sarcoplasmic reticulum and the cytosol.

Lidocaine cardioplegia for prevention of reperfusion ventricular fibrillation

Lidocaine addition to crystalloid cardioplegic solution for prevention of reperfusion ventricular fibrillation after the release of the aortic cross-clamp was studied in 50 patients undergoing coronary artery bypass grafting and in 30 patients undergoing mitral or aortic valve replacement. Twenty-six of the patients undergoing coronary artery bypass grafting received lidocaine, 100 mg/L of cardioplegia, whereas a control group of 24 patients received cardioplegia without lidocaine. In the group undergoing valve replacement, 14 patients received lidocaine cardioplegia and 16 patients served as control. In the coronary artery bypass grafting group, lidocaine cardioplegia reduced significantly the incidence of reperfusion ventricular fibrillation from 100% to 42%. In the valve group, lidocaine cardioplegia also reduced significantly the incidence of reperfusion ventricular fibrillation from 93% to 42%. In both groups, lidocaine cardioplegia decreased the number of direct-current countershocks required to defibrillate the heart, with no significant increase in the incidence of high-grade atrioventricular block.

Effects of the PAF antagonists BN50726 and BN50739 on arrhythmogenesis and extent of necrosis during myocardial ischaemia/reperfusion in rabbits.

1. The effects of two novel platelet activating factor (PAF) antagonists BN50726 and BN50739 on arrhythmias, haemodynamics and extent of necrosis during myocardial ischaemia and reperfusion were investigated in anaesthetized rabbits subjected to coronary artery ligation. 2. BN50739 reduced heart rate prior to coronary artery occlusion (P < 0.005) but had no other significant haemodynamic effects at this time. BN50739 and BN50726 did not significantly alter heart rate or blood pressure during 30 min of ischaemia or 30 min of reperfusion, compared to control hearts. 3. BN50739 and BN50726 had no effect on the incidence of arrhythmias during ischaemia. BN50726 significantly reduced the incidence of reperfusion ventricular fibrillation compared to controls (0% v 40%, P < 0.05), and improved survival (80% v 39%, P < 0.05). Similar trends were observed with BN50739. 4. BN50726 reduced the extent of necrosis compared to control hearts (18 +/- 2% v 30 +/- 3%, P < 0.01). A similar trend was observed with BN50739. 5. These results demonstrate that PAF antagonism with BN50726 attenuates reperfusion-induced arrhythmias and preserves myocardium in the early phase of ischaemia, independently of haemodynamic effects.

Ventricular fibrillation during partial reperfusion following severe myocardial ischemia in the canine model

The authors examined whether partial reperfusion protects against reperfusion ventricular fibrillation (VF) following severe acute myocardial ischemia. Fifty-seven dogs were divided into two groups. In group A (n = 21), the left anterior descending coronary artery was occluded for 10 minutes, followed by full reperfusion. In the remaining 36 dogs (group B), myocardial ischemia was induced by retrograde blood flow (RBF) for 10 minutes. Thereafter, these dogs were divided into three subgroups: in group B1 (n = 10), full reperfusion was made by a carotid-left anterior descending coronary artery bypass; in group B2 (n = 13), partial reperfusion was achieved by collateral flow into the ischemic zone due to stopping RBF; in group B3 (n = 13), RBF was continued for an additional 5 minutes. During 10 minute ischemia, the myocardial blood flow at the ischemic zone measured by the H2 gas-clearance method was 12.3 ± 2.0 ml/min/100 g in A, 3.4 ± 0.9 ml/min/100 g in B1, 4.7 ± 0.6 ml/min/100 g in B2, and 4.7 ± 0.6 ml/min/100 g in B3 (A vs B1, p < 0.02; A vs B2 and B3, p < 0.01). Maximal ST-segment elevation was 11.4 ± 1.8 mV in A, 28.2 ± 2.7 mV in B1, 25.1 ± 3.0 mV in B2, and 27.0 ± 1.9 mV in B3 (A vs B1, B2, and B3, p < 0.001). Maximal conduction delay was 48.6 ± 9.4 ms in A, 106.4 ± 5.2 ms in B1, 101.6 ± 9.9 ms in B2, and 91.2 ± 5.1 ms in B3 (A vs B1, B2, and B3, p < 0.001). The incidence of reperfusion VF was 14% ( 3 21 ) in A, 80% ( 8 10 ) in B1, and 69% ( 9 13 ) in B2 (A vs B1, p < 0.001; A vs B2, p < 0.005). In group B3, VF occurred in only 1 of 13 dogs for the additional 5 minutes. It is concluded that reperfusion VF occurred frequently when ischemia was severe even though the duration of ischemia was short (B1), and that reperfusion VF was not prevented by partial reperfusion when the ischemia was severe (B2).

Efficacy of diltiazem in two experimental feline models of sudden cardiac death

The potential role of calcium entry blockers in the prevention of life-threatening arrhythmias associated with acute myocardial ischemia and reperfusion is still controversial. In 98 anesthetized cats, the effect of diltiazem was examined in two experimental models. In protocol I, ventricular tachycardia or fibrillation was consistently induced by the interaction between a 2 minute coronary artery occlusion and a 30 second left stellate ganglion stimulation. After three trials under control conditions, if the same pattern of arrhythmia was induced, the drug under study was administered and three additional trials were performed. In 16 animals the administration of saline solution did not modify the pattern of arrhythmias. In contrast, diltiazem (0.1 mg/kg body weight plus 0.2 mg/kg per h) abolished both ventricular tachycardia and fibrillation that had occurred in 64 and 36%, respectively, of the cats in the control state. In protocol II, a 20 minute coronary artery occlusion was released in three groups; one served as the control group, one received diltiazem 15 minutes before occlusion and one received diltiazem 3 minutes before reperfusion. The incidence of reperfusion ventricular fibrillation was 62% (16 of 26) in the control group. It was significantly (p less than 0.05) reduced by diltiazem administered before the occlusion to 25% (4 of 16), whereas it was not affected when diltiazem was administered just before reperfusion (7 [47%] of 15). These results indicate that diltiazem exerts a striking protective effect against the malignant arrhythmias induced by the combination of acute myocardial ischemia and sympathetic hyperactivity. Diltiazem was also effective in reducing the incidence of life-threatening reperfusion arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of arrhythmic death during coronary artery reperfusion: Effect of perfusion bed size

To further our understanding of the factors determining the consequences of transient episodes of ischemia, we studied the influence of the size of the ischemic bed on the incidence of ventricular fibrillation (VF). The circumflex coronary artery (CFX) was occluded at various locations in 19 dogs. After 20 minutes of occlusion followed by 10 minutes of reperfusion the dogs were killed. The portion of the left ventricle (LV) at risk of infarcting ( R LV ) was defined as the region supplied by the occluded CFX and determined by simultaneous perfusion of the CFX with saline solution, just beyond the occlusion site, and of the aorta with Evan's blue. Bread loaf slices of the heart were photographed and projected, and the normal (blue) and risk regions (unstained) traced. The product of area and slice weight yielded mass of normal and risk regions. The R LV of dogs that died of reperfusion VF (n = 6) was 42.3 ± 5.0%, larger ( p < 0.001) than R LV in all surviving dogs (n = 13), 24.2 ± 9.4%. Twelve of the 13 survivors had R LV < 35% , whereas all dogs that died had R LV > 35% ( p = 0.0005). As is true for VF occurring during coronary artery occlusion, the incidence of reperfusion VF is related to the size of the ischemic insult.

Reperfusion ventricular tachyarrhythmias: Correlation with antecedent coronary artery occlusion tachyarrhythmias and duration of myocardial ischemia

The incidence and severity of reperfusion ventricular tachyarrhythmias were correlated with: (1) the duration of antecedent acute coronary artery occlusion and (2) the incidence, severity, and time course of ventricular tachyarrhythmias occurring during the antecedent period of coronary occlusion in 98 dogs studied postligation for 5 to 60 minutes. The incidence of reperfusion ventricular fibrillation (VF) increased significantly as coronary artery ligation periods were lengthened from 5 minutes to either 20 minutes (2 of 19 dogs vs 12 of 18 dogs, p < 0.001) or 30 minutes (16 of 24, p < 0.001), but notably decreased when reperfusion was delayed further from 30 minutes to 60 minutes after coronary artery ligation (4 of 18 dogs, p < 0.001). Seven dogs were resuscitated from VF during coronary ligation and all seven suffered VF on reperfusion, whereas 37 dogs were arrhythmia-free during ligation and only one (3%, p < 0.001) had VF on reperfusion, in addition, reperfusion ventricular tachyarrhythmias correlated with the occurrence of both immediate ventricular tachyarrhythmias (those peaking at 5 to 6 minutes postligation) and delayed ventricular tachyarrhythmias (those peaking at 18 minutes' postligation) of the antecedent acute ligation period. These observations provide a further basis for improved clinical understanding and management of potentially malignant tachyarrhythmias consequent to early myocardial reperfusion following acute myocardial ischemia and infarction.

Failure of antiarrhythmic drugs to prevent experimental reperfusion ventricular fibrillation.

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 1 -- 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 Mantel-Haenszel 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.