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Title:A CANINE MODEL OF BRUGADA SYNDROME USING REGIONAL EPICARDIAL COOLING OF THE RIGHT VENTRICULAR OUTFLOW
DOI No:10.1142/9789812702234_0032
Source:ADVANCES IN ELECTROCARDIOLOGY 2004 (pp 119-123)
Author(s):KUNIHIRO NISHIDA
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan

AKIRA FUJIKI
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan

KOICHI MIZUMAKI
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan

MASAO SAKABE
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan

MASATAKA SUGAO
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan

TAKAYUKI TSUNEDA
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan

HIROSHI INOUE
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan

Abstract:Introduction: Myocardial cooling could induce J-point elevation (Osborn wave) as seen in electrocardiogram (ECG) of Brugada 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 endocardia1 MAP were recorded. Regional cooling (29.7±2.2°C) induced J-point elevation, T-wave inversion and QT prolongation in lead V1 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 V1 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.
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