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Canine Model of Brugada Syndrome Using Regional Epicardial Cooling of the Right Ventricular Outflow Tract
Author(s) -
NISHIDA KUNIHIRO,
FUJIKI AKIRA,
MIZUMAKI KOICHI,
SAKABE MASAO,
SUGAO MASATAKA,
TSUNEDA TAKAYUKI,
INOUE HIROSHI
Publication year - 2004
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1046/j.1540-8167.2004.04041.x
Subject(s) - medicine , cardiology , endocardium , brugada syndrome , ventricular outflow tract , qt interval , repolarization , electrophysiology
Myocardial cooling can induce J point elevation (Osborn wave) as seen on ECG of the Brugada syndrome by activating transient outward current (I to ) and causing a spike‐and‐dome configuration of the monophasic action potential (MAP) in the ventricular epicardium in isolated canine ventricular wedge preparations. We determined the effect of regional epicardial cooling of the right ventricular outflow tract (RVOT) on surface ECG and ventricular vulnerability 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°C ± 2.2°C) elevated the J point from 0.05 ± 0.06 mV to 0.12 ± 0.11 mV and induced T wave inversion (from 0.02 ± 0.12 mV to −0.27 ± 0.20 mV) in lead V 1 in association with “spike‐and‐dome” configuration of the epicardial MAP. Cooling prolonged MAP duration in the RVOT epicardium from 172 ± 27 ms to 213 ± 30 ms (P < 0.01) but not in the RV endocardium and increased transmural dispersion of MAP duration from 9 ± 8 ms to 44 ± 21 ms (P < 0.01). Cooling also prolonged the QT interval in lead V 1 from 191 ± 19 ms to 212 ± 23 ms (P < 0.05), but not in lead V 5 , and increased spatial dispersion of QT interval from 7 ± 5 ms to 20 ± 10 ms (P < 0.01). QT interval in lead V 1 correlated positively with MAP duration in the RVOT epicardium (r = 0.75). T wave amplitude in lead V 1 correlated inversely with transmural dispersion of MAP duration in the RVOT (r =−0.74). Vagal nerve stimulation accentuated the cooling‐induced changes. During cooling, ventricular fibrillation was induced by a single extrastimulus in 2 of 4 dogs, and additional vagal nerve stimulation during isoproterenol administration induced spontaneous ventricular fibrillation in one dog. Conclusion: Localized epicardial cooling of the RVOT could be an in vivo experimental model of Brugada syndrome. (J Cardiovasc Electrophysiol, Vol. 15, pp. 936‐941, August 2004)