心室性不整脈の発生機序に関する電気生理学的研究—（II）心室頻拍症の発生，停止様式

Electrophysiological study on the genesis of ventricular arrhythrnias in acute ischemia.:(II) Modes of initiation and termination of ventricular tachycardia

　急性心筋梗塞症でみられる心室頻拍症は重篤な血行力学的障害を伴うのみならず，心室細動へと移行し患者を死に至らしめる危険がきわめて高い。従ってその発生および停止機序の解明は，その発生を予知し，適切な抗不整脈剤を選択する上で重要である。

　古くからHarrisの実験的心筋梗塞モデル^1,2）で生ずる不整脈がヒトのそれと類似していることが知られ，広くこの分野の研究に用いられてきた。第1報において，虚血心筋内で著しく遅延した興奮が虚血部心内膜下プルキンエ線維網を介して正常心筋へとリエントリーし，心室性不整脈が発生することを示したが^3），ここでは，如何なる機序でリエントリーが持続して頻拍症となり，また，それが停止するかについて検討を試みた。

Thirty-nine episodes of ventricular tachycardia (VT) observed in 11 dogs with acute coronary ischemia were analyzed for the patterns of initiation and termination. Maximal ischemic zone epicardial (IZepi) delay during the first 10 minutes following coronary ligation was significantly longer in 11 dogs with VT (194±24.0 msec) than in those wi-thout ventricular arrhythmias (91±16.8) and with ventricular premature complexes (160±18.6) (P<0.05). In each experiment with VT, the degree of IZepi delay immediately preceding the initiation of VT, or the coupling interval of a first VT beat was not significantly different between a transientVT and persistent VT. Rather, continuation of reentry appeared to be critically related to a beat-to-beat variation of IZepi delay and cycle length during VT.

Two patterns of termination of VT were identi-fied; one associated with a sudden disappearance of IZepi delay (19/39). In these cases, disappearance of IZepi delay was in most instances (13/19) asso-ciated with a lengthening of a preceding R-R in-terval, thus suggesting a bradycardia-related impro-vement of IZepi conduction. In other 6 episodes, a shortening of a preceding R-R interval could result in deteriolation of IZepi conduction and a shortened IZepi fragmentation. In contrast, VT terminated in the presence of a marked IZepi fra-gmentation (20/39). A possible mechanism in these cases appeared to be a conduction block in the effe-rent reentry pathways secondary to a change in refractoriness or activation sequences within the reentry pathways.