Electrophysiology underlying ventricular arrhythmias due to coronary ligation

Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.

“…Indeed, it was their inability to record these conditions which prompted them to discount reentry as the mechanism for the early occlusive arrhythmias. However, subsequently several different groups of investigators have studied the effects of acute ischemia on local electrophysiology with the use of bipolar electrodes (11)(12)(13)(14)(15)(16)(17)33). (36).…”

“…The inability to demonstrate enhanced automaticity (14), the finding of delayed conduction (11)(12)(13)(14)(15)(16)(17)33), and the recording ~of continuous electrical activity between normal and premature beats (12,13,37) support reentry as the most plausible mechanism responsible for early ischemic arrhythmias. However, since a reentry pathway has never been mapped in its entirety in the intact heart, this mechanism remains an unproven theory and has not gone unchallenged.…”

“…Although there has been an extensive investigation of the mechanisms underlying the arrhythmias of acute myocardial ischemia (11)(12)(13)(14)(15)(16)(17)(18)(19)(20), until recently there has been relatively little attempt to understand the mechanism for reperfusion arrhythmias. This may be related to the specialized conditions necessary to produce reperfusion arrhythmiasnamelv temporary myocardial ischemia.…”

Neuro-cardiac interaction in malignant ventricular arrhythmia and sudden cardiac death

“…The first report that vagus nerve stimulation (VNS) reduced the susceptibility of the ventricle to experimental arrhythmia was presented by Einbrodt in 1859 (Einbrodt 1859), who demonstrated that VF was harder to induce in the dog during stimulation of the vagus. The anti-arrhythmic action of VNS was later reproduced by Scherlag's group (Scherlag et al 1970) who showed that VNS interrupted the spontaneous occurrence of VT during coronary artery occlusion . Other studies in the 1970's (Goldstein et al 1973;Myers et al 1974;Kent et al 1973) confirmed the anti-arrhythmic action of VNS in the ventricle during ischaemia.…”

“…There is evidence from in vivo studies under anaesthesia in experimentally induced VF, that VNS is protective under these conditions (Scherlag et al 1970;Goldstein et al 1973). Conversely, bilateral vagotomy or atropine perfusion increases arrhythmic mortality in anaesthetised cats during (Corr & Gillis 1974) and following coronary artery occlusion (Zuanetti et al 1987) suggesting that intrinsic vagal activity was protective.…”