Spontaneous, electrically, and cesium chloride induced arrhythmia and afterdepolarizations in the rapidly paced dog heart

Citation
Dl. Jones et al., Spontaneous, electrically, and cesium chloride induced arrhythmia and afterdepolarizations in the rapidly paced dog heart, PACE, 24(4), 2001, pp. 474-485
Citations number
47
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
ISSN journal
01478389 → ACNP
Volume
24
Issue
4
Year of publication
2001
Part
1
Pages
474 - 485
Database
ISI
SICI code
0147-8389(200104)24:4<474:SEACCI>2.0.ZU;2-V
Abstract
Despite frequent arrhythmia and sudden death in heart failure, attempts to study arrhythmia mechanisms in patients are difficult. The dog heart, paced for several weeks at a fast rate to induce heart failure is prone to arrhy thmia. The aim of this study was to determine the activation patterns of sp ontaneous and electrically induced arrhythmia and the susceptibility of the failing dog heart to arrhythmia and early afterdepolarization (EAD) induce d triggered activity elicited by exogenous administration of cesium chlorid e (CsCl). The hearts of 56 mongrel dogs were paced at 240 beats/min for 3-5 weeks (heart failure group). Twenty-one similarly operated, but not paced dogs served as the control group. At baseline, all dogs were healthy as ass essed electrophysiologically and hemodynamically. Spontaneous (bradycardia, tachycardia, and arrhythmic deaths) and electrically induced arrhythmia wa s frequent in dogs with heart failure. Also, the minimal dose of CsCl that produced ventricular tachycardia was significantly lower in the heart failu re than the control dogs (1.02 +/- 0.02 vs rhythmia in the heart failure do gs showed initiation patterns with focal origin, often from multiple sites. This pattern was consistent with the patterns observed with CsCl induced v entricular tachycardia. In in vitro microelectrode studies, CsCl superfusio n (2.5-5 mMol/L) induced triggered activity due to EADs within 30 minutes, in seven of the eight Purkinje fibers from four heart failure dogs. EADs we re also found in ventricular myocytes of papillary muscle from two heart fa ilure dogs. In contrast, 5 mMol/L CsCl induced EADs in only one of eight Pu rkinje fibers from the hearts of four control dogs and no papillary myocyte s even with continuous superfusion for up to 60 minutes (P < 0.01). These r esults demonstrate that pacing induced heart failure in the dog has an incr eased tendency to develop ventricular tachycardia and triggered activity un masked by CsCl.