Objective : To further identify the occurrence and mechanism of spontaneous ventricular tachycardia caused by thrombotic coronary occlusion- Methods : Regionalischemia was induced by thrombotic occlusion using a wire ...
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Objective : To further identify the occurrence and mechanism of spontaneous ventricular tachycardia caused by thrombotic coronary occlusion- Methods : Regionalischemia was induced by thrombotic occlusion using a wire electrode to deliver a 200 ～300 μA anodic currentto the intima of the proximalleft circumflex artery (LCX) in 10 open chest dogs- Results : Total occlusion occurred 47 ±18 minutes after delivery ofthe current as indicated by a Doppler flowmeter- Current required to totalk occlusion of LCXwas 200 ～300 ( mean 255)μA- In nine dogs ,nonsustained VT(NSVT) originated from numerous ,differentfocalsites wasinitiated and maintained- Sustained VT(susVT) occurred in six dogs and was alsoinitiated by focal mechanisms located nearthe ischemic borderin four dogs and within the ischemic region in the other two- In three dogs ,the susVT was maintained primarily through a focal mechanism , which arose in the ischemic border region- In the other three dogs ,susVT was maintained by macroreentry extended from the subendocardium of the ischemic regionanteriorly through the septum as the fast pathway , towards the epicardium of the posterior area of LV and then intramurally back to the subendocardium as the slow pathway- VTchanged into VF within 10 ～41 seconds in four of these six dogs- The transition from VTto VF was due exclusively to intramural reentry with multiple wavefronts involving the nonischemic region in three dogs ,the ischemic border region in one ,and the ischemic region in one- Conclusion : Thrombotic occlusion of coronary artery by delivering anodic current to intima of the vessel is a useful model to study the pathophysiological mechanism of acute ischemia-
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