Yasunaga Hiyoshi

Double ventricular responses to a single atrial depolarization in a patient with dual AV nodal pathways

Electrophysiological study was performed in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). Double ventricular responses through dual AV nodal pathways were observed by atrial extrastimulus technique followed by initiation of AVNRT. The drfference in conduction time between the slow and fast AV nodal pathways was longer than 320 msec. A ventricular extrastimulus delivered during sinus rhythm, which was not followed by ventriculoatrial conduction, also induced AVNRT. These findings indicated the presence of an antegrade critical delay and retrograde block in the slow AV nodal pathway, criteria necessary for the occurrence of a double ventricular response.

Association of humps on monophasic action potentials and ST-T alternans in a patient with Romano-Ward syndrome.

A case of Romano‐Ward syndrome had episodes of torsade de pointes preceded by ST‐T alternans. ST‐T alternans was induced by isoproterenol and abolished by verapamil, lidocaine, mexiletine and MgSO4. A monophasic action potential (MAP) showed humps in MAPs at the right ventricular outflow tract but not at the right ventricular apex in alternate beats. Differences in the MAP duration were noted between the two areas and were associated with ST‐T alternans. Atrial pacing abolished both humps and ST‐T alternans. These results suggest that humps are a possible re/lection of early afterdepolarizations and their appearance is limited to localized regions of the ventricles, which produces regional disparity of repolarization and ST‐T alternans.

Supernormal conduction in a case of mobitz type II atrioventricular block

A 52-year-old woman exhibited Mobitz type II atrioventricular block with right bundle branch block and 1:1 atrioventricular conduction at or slower than 80 beats/min. Electrophysiologic study revealed transient HV interval block followed by recovery from the block at shorter coupling intervals without prolongation of the H1H2 and H2V2 intervals, suggesting true supernormal conduction. Isoproterenol enhanced the supernormal conduction, with shortening of blocked intervals and recovery of atrioventricular conduction, while atropine caused their less marked enhancement. Linking (ie, retrograde concealment of the impulse to the distal His bundle region through the blocked right bundle branch) is considered a possible mechanism of supernormal conduction in this case.

Factors for transient entrainment of ventricular tachycardias by rapid atrial pacing

Thirteen patients with sustained ventricular tachycardia (VT) were studied to elucidate predisposing factors for the development of constant and progressive fusion by rapid atrial pacing. All patients demonstrated transient entrainment by rapid ventricular pacing during VT. Constant and progressive fusion were observed in 7 patients (positive group) during rapid atrial pacing, but not in 6 (negative group). In the positive group, VT was induced by atrial pacing in 2 patients. The demonstration of constant and progressive fusion by atrial pacing was not dependent on QRS morphology or ventriculoatrial conduction during VT. VT cycle length in the positive group (363 +/- 59 ms) was longer than in the negative group (297 +/- 31 ms; p = 0.033). The maximal atrial pacing rate producing 1:1 atrioventricular (AV) conduction in the positive group was 171 +/- 18 beats/min compared with 125 +/- 22 beats/min in the negative group (p = 0.002). There were distinct differences between the positive and negative groups in the ratio of VT cycle length to minimal atrial cycle length causing 1:1 AV conduction (1.02 +/- 0.12 vs 0.61 +/- 0.12; p = 0.0001). It is concluded that AV conduction, VT cycle length and especially their ratio are important factors for the development of transient entrainment by rapid atrial pacing during VT. Therefore, atrial pacing can be used as an easy and useful method to examine transient entrainment during VT.