PMID- 20676844
OWN - NLM
STAT- MEDLINE
DCOM- 20101122
LR  - 20211020
IS  - 1615-2573 (Electronic)
IS  - 0910-8327 (Linking)
VI  - 25
IP  - 4
DP  - 2010 Jul
TI  - Acute amiodarone promotes drift and early termination of spiral wave re-entry.
PG  - 338-47
LID - 10.1007/s00380-009-1184-8 [doi]
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 microM) 
      caused prolongation of action potential duration (APD) by 5.6%-9.1%, whereas 
      lidocaine (15 microM) 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.
FAU - Nakagawa, Harumichi
AU  - Nakagawa H
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan.
FAU - Honjo, Haruo
AU  - Honjo H
FAU - Ishiguro, Yuko S
AU  - Ishiguro YS
FAU - Yamazaki, Masatoshi
AU  - Yamazaki M
FAU - Okuno, Yusuke
AU  - Okuno Y
FAU - Harada, Masahide
AU  - Harada M
FAU - Takanari, Hiroki
AU  - Takanari H
FAU - Sakuma, Ichiro
AU  - Sakuma I
FAU - Kamiya, Kaichiro
AU  - Kamiya K
FAU - Kodama, Itsuo
AU  - Kodama I
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100731
PL  - Japan
TA  - Heart Vessels
JT  - Heart and vessels
JID - 8511258
RN  - 0 (Anti-Arrhythmia Agents)
RN  - 98PI200987 (Lidocaine)
RN  - N3RQ532IUT (Amiodarone)
SB  - IM
MH  - Action Potentials
MH  - Amiodarone/*pharmacology
MH  - Animals
MH  - Anti-Arrhythmia Agents/*pharmacology
MH  - Cardiac Pacing, Artificial
MH  - Disease Models, Animal
MH  - Electrophysiologic Techniques, Cardiac
MH  - Heart Conduction System/*drug effects/physiopathology
MH  - Heart Ventricles/drug effects/physiopathology
MH  - Kinetics
MH  - Lidocaine/*pharmacology
MH  - Perfusion
MH  - Rabbits
MH  - Tachycardia, Ventricular/*drug therapy/physiopathology
EDAT- 2010/08/03 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/08/03 06:00
PHST- 2009/02/20 00:00 [received]
PHST- 2009/07/09 00:00 [accepted]
PHST- 2010/08/03 06:00 [entrez]
PHST- 2010/08/03 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
AID - 10.1007/s00380-009-1184-8 [doi]
PST - ppublish
SO  - Heart Vessels. 2010 Jul;25(4):338-47. doi: 10.1007/s00380-009-1184-8. Epub 2010 
      Jul 31.