PMID- 9180130
OWN - NLM
STAT- MEDLINE
DCOM- 19970619
LR  - 20190708
IS  - 0735-1097 (Print)
IS  - 0735-1097 (Linking)
VI  - 29
IP  - 7
DP  - 1997 Jun
TI  - Electrophysiologic effects of sodium channel blockade on anisotropic conduction 
      and conduction block in canine myocardium: preferential slowing of longitudinal 
      conduction by flecainide versus disopyramide or lidocaine.
PG  - 1639-44
AB  - OBJECTIVES: The purpose of this study was to determine the effects of sodium 
      channel blockade on anisotropic excitation propagation in the intact canine left 
      ventricle. BACKGROUND: Anisotropic ventricular conduction- electric conductivity 
      dependent on the myocardial fiber direction-is one of the important mechanisms of 
      ventricular arrhythmia. However, the effects of sodium channel blockade, 
      especially the differential effect of a subclass of this agent, on the 
      anisotropic properties remain unknown. METHODS: In 28 anesthetized, open chest 
      dogs, a small cannula was inserted into the left anterior descending coronary 
      artery. Saline (control), disopyramide, lidocaine or flecainide was infused 
      selectively into the cannula. An array of 64 epicardial electrodes was placed on 
      the anterior surface of the ventricle. Activation time (AT) was measured along 
      the longitudinal (L) and transverse (T) directions. RESULTS: High dose flecainide 
      (100 microg/kg body weight per min) delayed the AT along the L direction markedly 
      (mean [+/-SE] 227 +/- 38%, p < 0.02) and mildly (121 +/- 10%, p < 0.02) along the 
      T direction in regular beats (p < 0.007, L vs. T). Lidocaine and disopyramide did 
      not show direction-dependent prolongation of the AT on regular beats. When 
      examined on premature beats, AT was delayed, depending on the coupling interval 
      and the fiber direction when saline, flecainide or lidocaine was infused. The 
      conduction blocks along the L direction were observed in three of seven dogs on 
      regular beats after flecainide and ventricular fibrillation ensued in two of 
      these three dogs. CONCLUSIONS: A peculiar slowing of L conduction by flecainide 
      may relate to the character of proarrhythmia.
FAU - Kondo, T
AU  - Kondo T
AD  - First Department of Internal Medicine, Yamagata University School of Medicine, 
      Iida-Nishi, Japan.
FAU - Yamaki, M
AU  - Yamaki M
FAU - Kubota, I
AU  - Kubota I
FAU - Tachibana, H
AU  - Tachibana H
FAU - Tomoike, H
AU  - Tomoike H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Am Coll Cardiol
JT  - Journal of the American College of Cardiology
JID - 8301365
RN  - 0 (Anti-Arrhythmia Agents)
RN  - 0 (Sodium Channels)
RN  - 98PI200987 (Lidocaine)
RN  - GFO928U8MQ (Disopyramide)
RN  - K94FTS1806 (Flecainide)
SB  - IM
MH  - Animals
MH  - Anti-Arrhythmia Agents/*pharmacology
MH  - Cardiac Complexes, Premature/physiopathology
MH  - Disopyramide/*pharmacology
MH  - Dogs
MH  - Electric Conductivity
MH  - Electrophysiology
MH  - Flecainide/*pharmacology
MH  - Heart Conduction System/*drug effects
MH  - Heart Ventricles/*innervation
MH  - Lidocaine/*pharmacology
MH  - Sodium Channels/*drug effects
MH  - Ventricular Fibrillation/physiopathology
EDAT- 1997/06/01 00:00
MHDA- 1997/06/01 00:01
CRDT- 1997/06/01 00:00
PHST- 1997/06/01 00:00 [pubmed]
PHST- 1997/06/01 00:01 [medline]
PHST- 1997/06/01 00:00 [entrez]
AID - S0735109797825430 [pii]
AID - 10.1016/s0735-1097(97)82543-0 [doi]
PST - ppublish
SO  - J Am Coll Cardiol. 1997 Jun;29(7):1639-44. doi: 10.1016/s0735-1097(97)82543-0.