Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation
Background Amiodarone is administered during resuscitation, but its antiarrhythmic effects during targeted temperature management are unknown. The purpose of this study was to determine the effect of both therapeutic hypothermia and amiodarone on arrhythmia substrates during resuscitation from cardi...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2021-05-01
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| Series: | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
| Subjects: | |
| Online Access: | https://www.ahajournals.org/doi/10.1161/JAHA.120.016676 |
| _version_ | 1797301646315749376 |
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| author | Joseph S. Piktel Yi Suen Shalen Kouk Danielle Maleski Gary Pawlowski Kenneth R. Laurita Lance D. Wilson |
| author_facet | Joseph S. Piktel Yi Suen Shalen Kouk Danielle Maleski Gary Pawlowski Kenneth R. Laurita Lance D. Wilson |
| author_sort | Joseph S. Piktel |
| collection | DOAJ |
| description | Background Amiodarone is administered during resuscitation, but its antiarrhythmic effects during targeted temperature management are unknown. The purpose of this study was to determine the effect of both therapeutic hypothermia and amiodarone on arrhythmia substrates during resuscitation from cardiac arrest. Methods and Results We utilized 2 complementary models: (1) In vitro no‐flow global ischemia canine left ventricular transmural wedge preparation. Wedges at different temperatures (36°C or 32°C) were given 5 µmol/L amiodarone (36‐Amio or 32‐Amio, each n=8) and subsequently underwent ischemia and reperfusion. Results were compared with previous controls. Optical mapping was used to measure action potential duration, dispersion of repolarization (DOR), and conduction velocity (CV). (2) In vivo pig model of resuscitation. Pigs (control or targeted temperature management, 32–34°C) underwent ischemic cardiac arrest and were administered amiodarone (or not) after 8 minutes of ventricular fibrillation. In vitro: therapeutic hypothermia but not amiodarone prolonged action potential duration. During ischemia, DOR increased in the 32‐Amio group versus 32‐Alone (84±7 ms versus 40±7 ms, P<0.05) while CV slowed in the 32‐Amio group. Amiodarone did not affect CV, DOR, or action potential duration during ischemia at 36°C. Conduction block was only observed at 36°C (5/8 36‐Amio versus 6/7 36‐Alone, 0/8 32‐Amio, versus 0/7 32‐Alone). In vivo: QTc decreased upon reperfusion from ischemia that was ameliorated by targeted temperature management. Amiodarone did not worsen DOR or CV. Amiodarone suppressed rearrest caused by ventricular fibrillation (7/8 without amiodarone, 2/7 with amiodarone, P=0.041), but not pulseless electrical activity (2/8 without amiodarone, 5/7 with amiodarone, P=0.13). Conclusions Although amiodarone abolishes a beneficial effect of therapeutic hypothermia on ischemia‐induced DOR and CV, it did not worsen susceptibility to ventricular tachycardia/ventricular fibrillation during resuscitation. |
| first_indexed | 2024-03-07T23:25:31Z |
| format | Article |
| id | doaj.art-399b861d8cdc4095a0641dbbb3a929db |
| institution | Directory Open Access Journal |
| issn | 2047-9980 |
| language | English |
| last_indexed | 2024-03-07T23:25:31Z |
| publishDate | 2021-05-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
| spelling | doaj.art-399b861d8cdc4095a0641dbbb3a929db2024-02-21T04:33:36ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802021-05-01101010.1161/JAHA.120.016676Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During ResuscitationJoseph S. Piktel0Yi Suen1Shalen Kouk2Danielle Maleski3Gary Pawlowski4Kenneth R. Laurita5Lance D. Wilson6Department of Emergency Medicine and The Heart and Vascular Research Center MetroHealth Campus Case Western Reserve University Cleveland OHDepartment of Emergency Medicine and The Heart and Vascular Research Center MetroHealth Campus Case Western Reserve University Cleveland OHDepartment of Emergency Medicine and The Heart and Vascular Research Center MetroHealth Campus Case Western Reserve University Cleveland OHDepartment of Emergency Medicine and The Heart and Vascular Research Center MetroHealth Campus Case Western Reserve University Cleveland OHDepartment of Emergency Medicine and The Heart and Vascular Research Center MetroHealth Campus Case Western Reserve University Cleveland OHDepartment of Emergency Medicine and The Heart and Vascular Research Center MetroHealth Campus Case Western Reserve University Cleveland OHDepartment of Emergency Medicine and The Heart and Vascular Research Center MetroHealth Campus Case Western Reserve University Cleveland OHBackground Amiodarone is administered during resuscitation, but its antiarrhythmic effects during targeted temperature management are unknown. The purpose of this study was to determine the effect of both therapeutic hypothermia and amiodarone on arrhythmia substrates during resuscitation from cardiac arrest. Methods and Results We utilized 2 complementary models: (1) In vitro no‐flow global ischemia canine left ventricular transmural wedge preparation. Wedges at different temperatures (36°C or 32°C) were given 5 µmol/L amiodarone (36‐Amio or 32‐Amio, each n=8) and subsequently underwent ischemia and reperfusion. Results were compared with previous controls. Optical mapping was used to measure action potential duration, dispersion of repolarization (DOR), and conduction velocity (CV). (2) In vivo pig model of resuscitation. Pigs (control or targeted temperature management, 32–34°C) underwent ischemic cardiac arrest and were administered amiodarone (or not) after 8 minutes of ventricular fibrillation. In vitro: therapeutic hypothermia but not amiodarone prolonged action potential duration. During ischemia, DOR increased in the 32‐Amio group versus 32‐Alone (84±7 ms versus 40±7 ms, P<0.05) while CV slowed in the 32‐Amio group. Amiodarone did not affect CV, DOR, or action potential duration during ischemia at 36°C. Conduction block was only observed at 36°C (5/8 36‐Amio versus 6/7 36‐Alone, 0/8 32‐Amio, versus 0/7 32‐Alone). In vivo: QTc decreased upon reperfusion from ischemia that was ameliorated by targeted temperature management. Amiodarone did not worsen DOR or CV. Amiodarone suppressed rearrest caused by ventricular fibrillation (7/8 without amiodarone, 2/7 with amiodarone, P=0.041), but not pulseless electrical activity (2/8 without amiodarone, 5/7 with amiodarone, P=0.13). Conclusions Although amiodarone abolishes a beneficial effect of therapeutic hypothermia on ischemia‐induced DOR and CV, it did not worsen susceptibility to ventricular tachycardia/ventricular fibrillation during resuscitation.https://www.ahajournals.org/doi/10.1161/JAHA.120.016676amiodaronehypothermiaischemia‐reperfusionoptical mappingresuscitationventricular fibrillation |
| spellingShingle | Joseph S. Piktel Yi Suen Shalen Kouk Danielle Maleski Gary Pawlowski Kenneth R. Laurita Lance D. Wilson Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease amiodarone hypothermia ischemia‐reperfusion optical mapping resuscitation ventricular fibrillation |
| title | Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation |
| title_full | Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation |
| title_fullStr | Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation |
| title_full_unstemmed | Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation |
| title_short | Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation |
| title_sort | effect of amiodarone and hypothermia on arrhythmia substrates during resuscitation |
| topic | amiodarone hypothermia ischemia‐reperfusion optical mapping resuscitation ventricular fibrillation |
| url | https://www.ahajournals.org/doi/10.1161/JAHA.120.016676 |
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