Shinichi Niwano

Incidence and mechanism of interruption of reentrant ventricular tachycardia with rapid ventricular pacing.

BackgroundInformation concerning the electrophysiological characteristics of the reentrant circuit is still limited. To understand the incidence and mechanism of pacing-induced interruption of ventricular tachycardia (VT), rapid pacing was performed to entrain VT, and the local electrogram at the VT origin and the surface electrocardiogram were analyzed. Methods and ResultsAmong 25 patients, evidence of transient entrainment was confirmed in 20 patients, but the critical paced cycle length at which VT was interrupted was obtained in 13 patients when the paced cycle length was decreased in steps of 10 msec. During pacing at the critical cycle length (defined as block cycle length), changes in the local electrogram at VT origin were confirmed in all of the 13 patients; that is, 1) a change in morphology and 2) a change in the timing of activation: a sudden shortening in the stimulus to local electrogram time (third entrainment criterion by Waldo). The two changes mean that the exit is activated from a different direction (retrograde capture) because of an orthodromic block in the slow conduction zone. The QRS complex in the surface electrocardiogram showed a change in configuration from the fusion complex to the fully paced one at the same time when the exit was captured antidromically. ConclusionsBased on our observations in these patients, ventricular tachycardia interruption is very often associated with orthodromic block in the reentrant circuit at a critical cycle length of rapid pacing.

Electrophysiologic Evaluation of Asymptomatic Patients with the Wolff-Parkinson-White Pattern

In the past 4 years, 34 asymptomatic patients with the Wolff‐Parkinson‐White (WPW) pattern underwent electrophysiologic study. The effective refractory period (ERP) of antegrade conduction over the accessory pathway was 288 ± 29 msec. In three asymptomatic patients (9%), the antegrade ERP of the accessory pathway was shorter than 250 msec. The antegrade ERP of the accessory pathway became shorter than 250 msec in an additional 12 of 22 (55%) patients after isoproterenol administration. Nineteen (56%) of the asymptomatic patients showed the absence of retrograde conduction over the accessory pathway even after isoproterenol administration. The rate of induction of orthodromic reciprocating tachycardia in the asymptomatic WPW patients was 15% (5/34), which was significantly lower than that in the symptomatic patients. These data suggest that in the asymptomatic patients, the absence of retrograde conduction over the accessory pathway is the reason they remained asymptomatic, free of reciprocating tachycardia. However, even in the asymptomatic patients, some had the accessory pathway in which antegrade ERP was shorter than 250 msec. They may result in rapid ventricular conduction over the accessory pathway when atrial fibrillation develops.

Fragmented atrial activity in patients with transient atrial fibrillation.

Prediction of atrial fibrillation (AF) is very important in patients with Wolff-Parkinson-White syndrome or in the selection of pacemaker therapeutic modality. In 25 patients with transient AF, the response of the atrial activity width to extrastimuli was examined in comparison with 25 patients without AF to see if the results could be used as an index of subsequent occurrence of AF. Programmed electrical stimulation using eight basic stimuli followed by single or double extrastimuli (P1P2 or P1P2P3) were delivered to the high right atrium, and the atrial activities were examined. The prolongation of the atrial activity caused by extrastimuli was termed fragmentation (Frg), and it was defined as the prolongation of more than 150% of the basic stimuli. Frg zone was defined as the zone of coupling intervals of the extrastimuli (P1P2 or P2P3) that caused Frg, and delta max Frg was defined as the difference between the widest Frg and the atrial wave width during basic stimuli. Fragmentation was reproducibly induced by extrastimuli, and there was an inverse relationship between Frg duration and the coupling interval of the extrastimuli (P1P2 or P2P3). Frg zone and delta max Frg were wider and longer in patients with transient AF in comparison with the control group for both single and double extrastimuli (p less than 0.001). AF inducibility using double extrastimuli was significantly high in patients with AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation

The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid‐right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachmans bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120‐ms cycle length was performed five times at each pacing site to evaluate the in‐ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200‐ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.

Repetitive Ventricular Responses Induced by Radiofrequency Ablation for Idiopathic Ventricular Tachycardia Originating from the Outflow Tract of the Right Ventricle

In 23 consecutive patients, radiofrequency (RF) ablation was used as treatment for idiopathic ventricular tachycardia (VT) originating from the outflow tract of the right ventricle. In this study, we focused on the repetitive ventricular response (> 5 consecutive QRS beats during RF application). The incidence and clinical implications of the repetitive ventricular response were examined through the results of endocardial mapping and RF ablation. VT origin was mapped as the earliest activation site during VT, and it was determined within 0.5 × 0.5 cm (narrow site) in 13 patients and wider than 0.5 × 0.5 cm (wide origin) in the other 10 patients. The repetitive ventricular response was induced during application of RF current in 14 of 23 patients (61%), and it was more frequently observed in VT from a wide origin (100%) than in the VT from a narrow site (31%). The QRS morphology of the repetitive ventricular response was identical to that of clinical VT. As RF application was continued and/or repeated, the RR interval of the repetitive ventricular response was gradually prolonged, the number of consecutive QRS complexes was decreased, and clinical VT was finally eliminated. The overall success rate of RF ablation was 96% (22/23 patients), and no complications were observed. In conclusion, a repetitive ventricular response was frequently observed in idiopathic right VT. The changing pattern of repetitive ventricular response, slowing, and/or disappearing was consistent with successful RF ablation.

The use of the block cycle length as a safe and efficient means of interrupting sustained ventricular tachycardia and its pharmacological modification.

In nine patients who had inducible monomorphic sustained ventricular tachycardia (VT), rapid pacing was performed in 11 episodes of morphologically distinct VT at progressively shorter cycle lengths and VT was interrupted at a critical cycle length. The VT interrupting critical cycle length was defined as the block cycle length (BCL) and the effect of Class I antiarrhythmic drugs were examined. Both the VT cycle length (VTCL) and the BCL were prolonged after administration of either drug. The overall mean ratio of the BCL to the VTCL was unchanged after procainamide administration, but increased after the use of mexiletine. The ratio, however, varied in individual VTs and the BCL after treatment with Class I antiarrhythmic drugs could not be predicted from the ratio baseline value, although the ratio was always > 60% and the hazard of VT acceleration might be avoided if the BCL is used.

The Usefulness of Holter Monitoring in Selecting Pharmacologic Therapy for Patients With Sustained Monomorphic Ventricular Tachycardia

The usefulness of Holter monitoring (HM) in selecting pharmacologic therapy for patients with sustained monomorphic ventricular tachycardia (VT) was evaluated in patients in whom no effective pharmacologic therapy could be determined in an electrophysiologic study (EPS). The study population consisted of 49 consecutive patients with sustained VT who were receiving long-term pharmacologic therapy despite the fact that no pharmacologic therapy had been found to be effective in the EPS. The efficacy of the pharmacologic therapies was assessed by HM. A reduction in frequent (10/h) premature ventricular contractions (PVCs) was used as an index of treatment efficacy, with therapies achieving substantial PVC suppression (>70% of all PVCs) being considered to be effective (HM effective group). When no therapy was found to be effective when assessed by HM, a drug with any other beneficial effect, eg, reduction in VT rate, was chosen (HM ineffective group). VT recurrence and survival were compared between groups. During the follow-up period of 31+/-28 months, VT recurrence was observed in a total of 25/49 patients: 3/17 patients in the HM effective group, in 18/25 in the HM ineffective group, and in 4/7 in the HM undetermined group (p=0.0487). Sudden cardiac death occurred in a total 7/49 patients: 2/17 patients in the HM effective group, 4/25 patients in the HM ineffective group, and 1/7 patient in the HM undetermined group (p=0.2828). Among patients in whom no effective therapy could be determined by EPS, the VT recurrence rate was significantly lower in the group in whom treatment was effective as assessed by HM than among those in whom treatment was assessed by HM to be ineffective. Sudden cardiac death rate was also lowest in the HM effective group, although the difference was not statistically significant. HM assessment was considered useful in selection of pharmacologic therapy for patients in whom no effective therapy could be determined in the EPS.

Augmented fragmentation of atrial activity upon premature electrical stimuli by verapamil

The significance of fragmented activity obtained from the atrium during electrophysiologic study (EP study) was confirmed since it was al ways observed just at the onset of fi brillation. It was preceded by extra stimuli or atrial flutter, and the initial site of fragmentation varied from case to case. The premature-stimu lus-induced widening of the atrial wave was observed in some cases who had normal size of atrium and no heart failure. The widening was aug mented by administration of vera pamil but not by procainamide, suggesting that for such widening or fragmented activity, slow-fiber-medi ated conduction seems to be responsi ble. One case with intraatrial reen trant tachycardia developed fragmentation lasting for 1.0 second after verapamil. Therefore, some apparently nor mal atria may have a subclinical elec trophysiologic abnormality that can be disclosed by premature stimula tions or verapamil.

Iron Deposition in Myocardium Documented on Standard Computed Tomography in Cardiac Hemochromatosis

A 46-year-old woman with pure red-cell aplasia suffered blood transfusion of >200 units, ie, >20 g in iron weight, over 4 years because treatment with a series of immunosuppressants resulted in no effect. Tissue iron deposition caused by iron overload resulted in skin discoloration, hepatic injury, diabetes mellitus, and slight left ventricular dysfunction. Left ventricular end-diastolic and end-systolic dimensions were 45 …

Structure of the Reentrant Circuit of Idiopathic Left Ventricular Tachycardia: New Insights Into the Role of the Purkinje Network

In idiopathic left ventricular tachycardia (ILVT), the reentrant circuit is considered to involve the Purkinje system, and the Purkinje potential (P-potential) appears to be a marker for successful ablation. However, the characteristics of the reentrant circuit in ILVT have not yet been defined. In 2 cases of ILVT, we performed detailed mapping along the left ventricular septum during VT and sinus rhythm. ILVTs were successfully ablated at the posteroapical area of the left ventricular septum where the high frequency P-potential was recorded and this portion was considered to be the exit site of the reentrant circuit. A small P-potential was also recorded at the portion proximal to the exit site, and it preceded the P-potential at the exit site. However, the local ventricular electrogram at the exit site preceded that at the proximal site during VT. Moreover, the small P-potential was orthodromically entrained by ventricular pacing from the proximal site. These findings suggest that the reentry circuit of ILVT appeared to have considerable size.