| Co-Investigator(Kenkyū-buntansha) |
IWAMI Yasuyo UOEH,School of Medicine, Regident, 医学部, 医員
HANADA Hideyuki UOEH,School of Medicine, Regident, 医学部, 医員
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| Research Abstract |
To test the hypotheses that slow conduction across an isthmus at rapid rate crilically depends on anisotropy, we studied conduction both parallel and perpendicular to cardiac fibers cross an isthmus. Using surgical techniques, we create lesions perpendicular and parallel to the longitudinal orientation of the sulcus terminalis in 8 dogs. Two types of lesions were created : Lesion#1 : the length of the isthmus was constant at 5 mm ; the width of the isthmus was 15 mm, and later narrowed to 10 mm ; pacing wave fronts were conducted perpendicular to cardiAc fibers (n=4). Lesion #2 : the width of the isthmus was constant at 10 mm ; the length of the isthmus was 5 mm, and then lenthen to 10 mm ; pacing wave fronts were conducted parallel to cardiac fibers (n=4). During rapid atrial pacing (from 200 msec to until either refractoriness at the pacing site or conduction block in the isthmus occurred), conduction was mapped over and around the isthmus using a very high dense electrode array with
… More
190 electrodes. Prior to
creating an isthmus, conduction velocity when the impulse was conducted parallel to the cardiac fibers did not change significantly at all pacing rates. However, conduction velocity when the pacing impulse was conducted perpendicular to the cardiac fibers decreased significantly. No fractionated signals were recorded. After creation of lesion #conduction velocity when the impulse was conducted perpendicular to fiber orientation decreased significantly when the isthmus was narrower (no lesion vs. 15 mm : P=ns, vs. 10 mm : P<0.05). Fractionated signals were recorded in the isthmus during pacing rate>= 440 bpm and conduction block occurred in the center of the isthmus at a rate>=550 bpm. After creation of lesion #conduction velocity when the impulse was conducted parallel tio the fiber orientation did not decrease significantly even when the isthmus was longer (no lesion ns. 5 mm or 10 mm length of isthmus : P=ns). Neither fractionated signals nor conduction block were recorded at any pacing rate. Anisotropic conduction alone did not produce critical slowing of conduction at any pacing rate. However, anisotropic conduction plus a critical width of an isthmus produced marked slowing of conduction and also conduction block in the isthmus. Our data suggests that an isthmus may play an important role for producing the area(s) of slow conduction of reentrant circuits. Less
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