Acute amiodarone promotes drift and early termination of spiral wave re-entry

Harumichi Nakagawa, Haruo Honjo, Yuko S. Ishiguro, Masatoshi Yamazaki, Yusuke Okuno, Masahide Harada, Hiroki Takanari, Ichiro Sakuma, Kaichiro Kamiya, Itsuo Kodama

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Intravenous application of amiodarone is commonly used in the treatment of life-threatening arrhythmias, but the underlying mechanism is not fully understood. The purpose of the present study is to investigate the acute effects of amiodarone on spiral wave (SW) re-entry, the primary organization machinery of ventricular tachycardia/fibrillation (VT/VF), in comparison with lidocaine. A two-dimensional ventricular myocardial layer was obtained from 24 Langendorff-perfused rabbit hearts, and epicardial excitations were analyzed by high-resolution optical mapping. During basic stimulation, amiodarone (5 μM) caused prolongation of action potential duration (APD) by 5.6%-9.1%, whereas lidocaine (15 μM) caused APD shortening by 5.0%-6.4%. Amiodarone and lidocaine reduced conduction velocity similarly. Ventricular tachycardias induced by DC stimulation in the presence of amiodarone were of shorter duration (sustained-VTs >30 s/total VTs: 2/58, amiodarone vs 13/52, control), whereas those with lidocaine were of longer duration (22/73, lidocaine vs 14/58, control). Amiodarone caused prolongation of VT cycle length and destabilization of SW re-entry, which is characterized by marked prolongation of functional block lines, frequent wavefront-tail interactions near the rotation center, and considerable drift, leading to its early annihilation via collision with anatomical boundaries. Spiral wave re-entry in the presence of lidocaine was more stabilized than in control. In the anisotropic ventricular myocardium, amiodarone destabilizes SW re-entry facilitating its early termination. Lidocaine, in contrast, stabilizes SW re-entry resulting in its persistence.

Original languageEnglish
Pages (from-to)338-347
Number of pages10
JournalHeart and Vessels
Volume25
Issue number4
DOIs
Publication statusPublished - 01-07-2010

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Amiodarone
Lidocaine
Ventricular Tachycardia
Action Potentials
Ventricular Fibrillation
Tail
Cardiac Arrhythmias
Myocardium
Rabbits

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Nakagawa, H., Honjo, H., Ishiguro, Y. S., Yamazaki, M., Okuno, Y., Harada, M., ... Kodama, I. (2010). Acute amiodarone promotes drift and early termination of spiral wave re-entry. Heart and Vessels, 25(4), 338-347. https://doi.org/10.1007/s00380-009-1184-8
Nakagawa, Harumichi ; Honjo, Haruo ; Ishiguro, Yuko S. ; Yamazaki, Masatoshi ; Okuno, Yusuke ; Harada, Masahide ; Takanari, Hiroki ; Sakuma, Ichiro ; Kamiya, Kaichiro ; Kodama, Itsuo. / Acute amiodarone promotes drift and early termination of spiral wave re-entry. In: Heart and Vessels. 2010 ; Vol. 25, No. 4. pp. 338-347.
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Nakagawa, H, Honjo, H, Ishiguro, YS, Yamazaki, M, Okuno, Y, Harada, M, Takanari, H, Sakuma, I, Kamiya, K & Kodama, I 2010, 'Acute amiodarone promotes drift and early termination of spiral wave re-entry', Heart and Vessels, vol. 25, no. 4, pp. 338-347. https://doi.org/10.1007/s00380-009-1184-8

Acute amiodarone promotes drift and early termination of spiral wave re-entry. / Nakagawa, Harumichi; Honjo, Haruo; Ishiguro, Yuko S.; Yamazaki, Masatoshi; Okuno, Yusuke; Harada, Masahide; Takanari, Hiroki; Sakuma, Ichiro; Kamiya, Kaichiro; Kodama, Itsuo.

In: Heart and Vessels, Vol. 25, No. 4, 01.07.2010, p. 338-347.

Research output: Contribution to journalArticle

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T1 - Acute amiodarone promotes drift and early termination of spiral wave re-entry

AU - Nakagawa, Harumichi

AU - Honjo, Haruo

AU - Ishiguro, Yuko S.

AU - Yamazaki, Masatoshi

AU - Okuno, Yusuke

AU - Harada, Masahide

AU - Takanari, Hiroki

AU - Sakuma, Ichiro

AU - Kamiya, Kaichiro

AU - Kodama, Itsuo

PY - 2010/7/1

Y1 - 2010/7/1

N2 - Intravenous application of amiodarone is commonly used in the treatment of life-threatening arrhythmias, but the underlying mechanism is not fully understood. The purpose of the present study is to investigate the acute effects of amiodarone on spiral wave (SW) re-entry, the primary organization machinery of ventricular tachycardia/fibrillation (VT/VF), in comparison with lidocaine. A two-dimensional ventricular myocardial layer was obtained from 24 Langendorff-perfused rabbit hearts, and epicardial excitations were analyzed by high-resolution optical mapping. During basic stimulation, amiodarone (5 μM) caused prolongation of action potential duration (APD) by 5.6%-9.1%, whereas lidocaine (15 μM) caused APD shortening by 5.0%-6.4%. Amiodarone and lidocaine reduced conduction velocity similarly. Ventricular tachycardias induced by DC stimulation in the presence of amiodarone were of shorter duration (sustained-VTs >30 s/total VTs: 2/58, amiodarone vs 13/52, control), whereas those with lidocaine were of longer duration (22/73, lidocaine vs 14/58, control). Amiodarone caused prolongation of VT cycle length and destabilization of SW re-entry, which is characterized by marked prolongation of functional block lines, frequent wavefront-tail interactions near the rotation center, and considerable drift, leading to its early annihilation via collision with anatomical boundaries. Spiral wave re-entry in the presence of lidocaine was more stabilized than in control. In the anisotropic ventricular myocardium, amiodarone destabilizes SW re-entry facilitating its early termination. Lidocaine, in contrast, stabilizes SW re-entry resulting in its persistence.

AB - Intravenous application of amiodarone is commonly used in the treatment of life-threatening arrhythmias, but the underlying mechanism is not fully understood. The purpose of the present study is to investigate the acute effects of amiodarone on spiral wave (SW) re-entry, the primary organization machinery of ventricular tachycardia/fibrillation (VT/VF), in comparison with lidocaine. A two-dimensional ventricular myocardial layer was obtained from 24 Langendorff-perfused rabbit hearts, and epicardial excitations were analyzed by high-resolution optical mapping. During basic stimulation, amiodarone (5 μM) caused prolongation of action potential duration (APD) by 5.6%-9.1%, whereas lidocaine (15 μM) caused APD shortening by 5.0%-6.4%. Amiodarone and lidocaine reduced conduction velocity similarly. Ventricular tachycardias induced by DC stimulation in the presence of amiodarone were of shorter duration (sustained-VTs >30 s/total VTs: 2/58, amiodarone vs 13/52, control), whereas those with lidocaine were of longer duration (22/73, lidocaine vs 14/58, control). Amiodarone caused prolongation of VT cycle length and destabilization of SW re-entry, which is characterized by marked prolongation of functional block lines, frequent wavefront-tail interactions near the rotation center, and considerable drift, leading to its early annihilation via collision with anatomical boundaries. Spiral wave re-entry in the presence of lidocaine was more stabilized than in control. In the anisotropic ventricular myocardium, amiodarone destabilizes SW re-entry facilitating its early termination. Lidocaine, in contrast, stabilizes SW re-entry resulting in its persistence.

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