Circulation, Vol 72, 1092-1103, Copyright © 1985 by American Heart Association
JH Levine, JF Spear, T Guarnieri, ML Weisfeldt, CD de Langen, LC Becker and EN Moore
The identification of afterdepolarizations and their relationship to
arrhythmias in vivo is not available. Experiments were undertaken to
determine whether afterdepolarizations could be detected in monophasic
action potentials (MAPs) recorded in vivo and whether they were related to
arrhythmias in an intact canine preparation of the long QT syndrome.
Isolated cardiac tissues from six dogs were studied to validate the
technique. In simultaneous MAP and transmembrane recordings,
afterdepolarizations induced with barium (early) or acetylstrophanthidin
(delayed) were detected in MAPs when present in microelectrode recordings.
MAPs were then recorded in situ in eight dogs with cesium chloride-induced
long QT syndrome associated with ventricular arrhythmias.
Afterdepolarizations were identified in each of the dogs and were similar
to early afterdepolarizations identified in vitro; they occurred during
phase 3 and were attenuated during overdrive pacing. The
afterdepolarizations were closely related to arrhythmias: (1)
afterdepolarizations always preceded ventricular arrhythmias, (2) the
coupling intervals (CI) of the afterdepolarizations (AD) and the
ventricular premature beats (VPB) were nearly identical (VPB CI = 1.06 AD
CI -10.24; r2 = .87), (3) the take-off potentials of the ventricular
premature beats were nearly identical to the amplitude of the
afterdepolarizations (take-off potential = 0.98 afterdepolarization
amplitude +0.46, r2 = .87), and (4) afterdepolarizations and ventricular
arrhythmias resolved concurrently during overdrive pacing and with time.
Thus, a new catheter technique has been validated and has been used to
directly identify afterdepolarizations and triggered activity in vivo.
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Cesium chloride-induced long QT syndrome: demonstration of afterdepolarizations and triggered activity in vivo
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