Idiopathic Ventricular Fibrillation Induced With Vagal Activity in Patients Without Obvious Heart Disease

BACKGROUND: Recently, idiopathic ventricular fibrillation (VF) has gained much attention. Although several subgroups have been described, its pathogenesis, mechanism, treatment, and prognosis remain unknown. METHODS AND RESULTS: We studied six cases of idiopathic VF with transient late r' waves and ST elevation (late r'/ST elevation) in leads V1 through V3. Late r'/ST elevation was augmented before and after VF episodes. Signal-averaged ECGs showed late potentials even when no late r'/ST elevation occurred. During late r', a conduction delay was observed by use of body-surface maps at the anterior wall and outflow tract of the right ventricle without inhomogeneity of the repolarization phase. There was a decrease or total disappearance of late r'/ST elevation with isoproterenol, atropine, and exercise stress testing and induction or exacerbation with propranolol, edrophonium, and hyperventilation. VF was induced by programmed electrical stimulation in all cases but two, in which it was induced only after edrophonium injection. In two cases, VF was exacerbated by propranolol, and in all cases, it was uninducible with isoproterenol. Heart rate spectral analysis just before VF episodes showed a sudden rise in vagal activity in two cases. As the VF mechanism, a conduction delay exists at the anterior wall and outflow tract of the right ventricle that is possibly exacerbated by an abrupt rise in vagal activity, inducing random reentry that results in VF. Class I antiarrhythmic agents and beta-blockers were ineffective for this VF. All subjects required implantable cardioverter-defibrillators. CONCLUSIONS: We propose this VF associated with late r'/ST elevation in the precordial leads and influenced by vagal activity as a new possible mechanism of idiopathic VF.