Amiodarone Treatment in the Early Phase of Acute Myocardial Infarction Protects Against Ventricular Fibrillation in a Porcine Model

Figures

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  Fig. 1. Experimental setup. A After premedication and implantation of the venous and arterial sheaths, the animal was left for stabilization. A mid-sternal thoracotomy was performed, the mid-left anterior descending artery (LAD) was dissected free and a silk snare was placed. Monophasic action potential (MAP) electrodes were placed and after a stabilization phase the snare was tightened around the LAD. Ten minutes after ligation, 3 mg/kg body weight amiodarone was given intravenously. After 120 min of occlusion, the snare was opened, reperfusion occurred, and the pig was monitored for another 60 min. B Coronary anatomy (left) and surgical procedure (right). Exposed heart after a mid-line sternotomy with a silk snare and counter bearing (asterisk) placed around the LAD. RA, right atrium, LA, left atrium, RV, right ventricle, LV, left ventricle, D1, diagonal branch 1, PC, pericardium

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  Fig. 2. Electrocardiogram (ECG) during acute myocardial infarction (AMI). A Mean ST segment elevation plotted over time across 2 h of coronary occlusion of the left anterior descending artery (LAD) and 1 h of reperfusion (¤¤¤P < 0.0001 for time and **P < 0.005 for treatment, two-way ANOVA). B Percentage of pigs with T wave alternans (TWA) was not markedly changed with amiodarone infusion. C Longer RR intervals during the occlusion period were observed in the amiodarone group (**P < 0.001 for treatment, two-way ANOVA). D QRS duration was affected by AMI (¤p < 0.05 for time, two-way ANOVA) to the same extent in both groups. E and F PQ interval and QT interval showed no differences. G At baseline, P wave (green), QRS complex (purple), ST segment (red), and T wave (orange) are indicated. AMI leads to an elevation of the ST segment (red arrow) and inverted and increased T waves. TWA (asterisk) is present between 5 and 20 min with a maximum after 10–15 min of coronary occlusion. Occ, occlusion, Rep, reperfusion

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  Fig. 3. Monophasic action potentials (MAP) and arrhythmias. A Duration of MAP at 90% of repolarization compared to baseline (ΔMAPD90) during occlusion in the infarcted (MI) and non-infarcted (non-MI) area of the left ventricle. While non-MI MAPD90 was stable, MI MAPD90 shortened within the first 10 min. B Variation of MAPD90 due to beat-to-beat alternans increased during myocardial infarction in the MI area. Amiodarone treatment reduced this dispersion. C Mean number of premature ventricular contractions (PVC) per minute during the first hour of AMI was lower after amiodarone infusion (*P = 0.013). D A single PVC during sinus rhythm (left) and accelerated idioventricular rhythm during reperfusion (right). Retrograde p waves can be seen in all PVCs. E Amiodarone was able to prevent ventricular fibrillation (VF) in all pigs when given 10 min after coronary occlusion (P < 0.01, Log-Rank test). F Sinus rhythm (SR) was present in all pigs before VF occurred. PVC during SR are marked red. Short coupled PVC can be identified as triggering event in all VF episodes (asterisk). Occ, occlusion, Rep, reperfusion

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  Fig. 4. Hemodynamic parameters. Mean arterial blood pressure (A) and cardiac output (B) were analyzed as safety parameters. Coronary occlusion caused a drop in all hemodynamic parameters, but none of the hemodynamic parameters was affected by amiodarone treatment (¤¤¤P < 0.0001 for time, two-way ANOVA). Occ, occlusion, Rep, reperfusion