Spontaneous, electrically, and cesium chloride induced arrhythmia and afterdepolarizations in the rapidly paced dog heart.
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 arrhythmia. The aim of this study was to determine the activation patterns of spontaneous and electrically induced arrhythmia and the susceptibility of the failing dog heart to arrhythmia and early afterdepolarization (EAD) induced triggered activity elicited by exogenous administration of cesium chloride (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 assessed electrophysiologically and hemodynamically. Spontaneous (bradycardia, tachycardia, and arrhythmic deaths) and electrically induced arrhythmia was frequent in dogs with heart failure. Also, the minimal dose of CsCl that produced ventricular tachycardia was significantly lower in the heart failure than the control dogs (1.02 +/- 0.02 vs 1.21 +/- 0.07 mMol/kg, P < 0.05). Epicardial mapping during spontaneous and electrically induced arrhythmia in the heart failure dogs showed initiation patterns with focal origin, often from multiple sites. This pattern was consistent with the patterns observed with CsCl induced ventricular tachycardia. In in vitro microelectrode studies, CsCl superfusion (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 were also found in ventricular myocytes of papillary muscle from two heart failure dogs. In contrast, 5 mMol/L CsCl induced EADs in only one of eight Purkinje fibers from the hearts of four control dogs and no papillary myocytes even with continuous superfusion for up to 60 minutes (P < 0.01). These results demonstrate that pacing induced heart failure in the dog has an increased tendency to develop ventricular tachycardia and triggered activity unmasked by CsCl.
Jones
D L
DL
Departments of Physiology and Medicine, University of Western Ontario, London, Ontario, Canada, N6A 5C1. DLJones@Physiology.UWO.Ca
Petrie
J P
JP
Li
H G
HG
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D002586:Cesium / Q000633:toxicity*; D002712:Chlorides / Q000633:toxicity*; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography / Q000187:drug effects; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D006333:Heart Failure / Q000139:chemically induced / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D013610:Tachycardia / Q000139:chemically induced / Q000503:physiopathology*
D002712:Chlorides; D002586:Cesium; C028019:cesium chloride