A CANINE MODEL OF BRUGADA SYNDROME USINGREGIONAL EPICARDIAL COOLING OF THE RIGHTVENTRICULAR OUTFLOW

摘要

Introduction: Myocardial cooling could induce J-point elevation (Osborn wave) as seen in electrocardiogram (ECG) of Bragada syndrome by activating transient outward current (Ito) and causing spike-and-dome configuration of monophasic action potential (MAP) in the ventricular epicardium. We evaluated effect of regional, epicardial cooling of the right ventricular outflow tract (RVOT) on surface ECG in the dog. Methods and Results: In 12 dogs, a cooling device (20 mm diameter) was attached to the RVOT epicardium, and surface ECG, epicardial MAP and endocardial MAP were recorded. Regional cooling (29.7+-2.2(deg)C) induced J-point elevation, T-wave inversion and QT prolongation in lead VI in association with "spike-and-dome" configuration of the epicardial MAP. Cooling prolonged MAP duration in the RVOT epicardium but not in the RV endocardium, and increased transmural dispersion of MAP duration. QT interval in VI correlated positively with MAP duration in the RVOT epicardium. T-wave amplitude in V1 correlated inversely with transmural dispersion of MAP duration in the RVOT. An enhanced ventricular vulnerability was also observed during cooling. Conclusions: Localized epicardial cooling of the RVOT could be an in vivo experimental model of Brugada syndrome.