Circulation, Vol 85, 1879-1887, Copyright © 1992 by American Heart Association
J Brugada, L Boersma, H Abdollah, C Kirchhof and M Allessie
BACKGROUND. Based on epicardial mapping, different mechanisms of
termination of reentrant ventricular tachycardia by various pharmacological
interventions are described. METHODS AND RESULTS. In 40
Langendorff-perfused rabbit hearts, rings of anisotropic left ventricular
epicardium were made by a cryoprocedure. Sustained monomorphic ventricular
tachycardia based on continuous circus movement of the impulse around the
ring was induced by programmed stimulation. Increasing doses of heptanol (n
= 10), potassium (n = 10), tetrodotoxin (n = 6), RP62719 (a new class III
drug) (n = 4), flecainide (n = 5), and propafenone (n = 5) were
administered to terminate ventricular tachycardia. Epicardial mapping (248
points) was used to study the mechanism of termination of ventricular
tachycardia. In 28 of 40 hearts, ventricular tachycardia terminated because
the drugs produced complete conduction block of the impulse in a segment of
the reentrant pathway. In the remaining 12 hearts (heptanol, n = 2;
potassium, n = 3; tetrodotoxin, n = 2; RP62719, n = 2; flecainide, n = 1;
and propafenone, n = 2), termination of ventricular tachycardia occurred by
collision of the circulating impulse with a spontaneous antidromic wave
front reflected within the circuit. This phenomenon occurred when the
circulating impulse encountered an arc of functional conduction block that
did not extend along the whole width of the ring. As a result, the impulse
dissociated into a continuing orthodromic circulating wave and a returning
antidromic echo-wave caused by microreentry within the ring. CONCLUSIONS.
Independent of their mechanisms of action, sodium channel blockers,
electrical uncouplers, and class III drugs terminate reentrant ventricular
tachycardia either by complete conduction block or by collision of the
impulse with an echo-wave.
ARTICLES
Echo-wave termination of ventricular tachycardia. A common mechanism of termination of reentrant arrhythmias by various pharmacological interventions
Department of Physiology, University of Limburg, Maastricht, The Netherlands.
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