Most idiopathic ventricular arrhythmias (VAs) including ventricular tachycardia (VT) and premature ventricular contractions (PVCs), originate from the right ventricular (RV) outflow tract (RVOT) [1,2]. A few studies have demonstrated idiopathic VAs arising from the para-Hisian region [3–9]. In terms of their electrocardiographic and electrophysiological features, VAs originating from the para-Hisian area are similar to those originating from the RVOT, the coronary cusp adjacent to the membranous septum, or the left ventricular (LV) septum below the aortic valve [4,5,10]. In addition, VAs arising from the posterior wall of the RVOT have a left bundle branch block (LBBB) QRS morphology, with an inferior axis, late precordial transition, and an R wave in lead I—features similar to those of RV para-Hisian VAs. Although the efficacy of radiofrequency catheter ablation (RFCA) in this area is improving, the potential risk of atrioventricular conduction disturbances related to the ablation procedure still exists. Several previous studies have reported the use of cryo energy as an alternative energy source in close proximity to the conduction system [11,12]. The purpose of this study was to investigate the prevalence, electrocardiographic and electrophysiological characteristics, and the results of RFCA of VAs originating from the para-Hisian area, in comparison with VAs arising from the posterior wall of RVOT.
Material and methods Patient populationThe study population included 250 consecutive patients (132 women, 118 men; mean age, 45±14 years) who underwent RFCA for symptomatic idiopathic VAs at our institute between January 2006 and December 2011. The VAs included sustained monomorphic VT (defined as ≥3 consecutive PVCs with a duration ≥30 s) in 64 patients, non-sustained VT (defined as ≥3 consecutive PVCs with a duration <30 s) in 29 patients, and PVCs in 157 patients. Of the 250 patients, 8 (5 women, 3 men; mean age, 50±17 years) had VAs originating near the His bundle region. None of the patients had structural heart disease according to echocardiography or coronary angiography.
The control group included 27 consecutive patients (16 women, 11 men; mean age, 40±14 years) with idiopathic VAs originating from the posterior wall of the RVOT. We recorded a complete medical history, a 12-lead surface ECG, and 24-h Holter monitoring for each patient. The 12-lead ECGs with arrhythmias were analyzed for QRS morphology, QRS width, axis, precordial transition, the QRS configuration in leads I, aVL and V1, the R wave amplitude in lead I, the mean amplitude of the R wave in leads II, III, and aVF, and the amplitude ratio of the R waves in leads II/III.
Electrophysiological study and radiofrequency catheter ablationAfter written informed consent was obtained, all patients underwent an electrophysiological study and RFCA. Prior to the procedure, all antiarrhythmic drugs were discontinued for more than at least 5 half-lives. An electrophysiological study was performed using a duodecapolar Halo catheter (St. Jude Medical, St. Paul, MN, USA) in the coronary sinus, and 2 quadripolar catheters in the His bundle region and RV apex via the right or left femoral vein. For retrograde aortic approaches, a decapolar catheter was advanced into the LV for recording left-sided His potentials. If clinical VAs did not occur spontaneously, isoproterenol (2–5 μg/min) was administered intravenously. Induction of the VT or PVCs was attempted using programmed electrical stimulation from the RV apex, with burst pacing or triple extrastimuli pacing. During the procedures in the LV, intravenous heparin was administered to maintain an activated clotting time of >250 s.
Mapping and ablation were performed with a quadripolar deflectable 7-French 4-mm tip non-irrigated ablation catheter (EP Technology, San Jose, CA, USA) in all but 1 patient, in whom an open irrigated tip ablation catheter was substituted during the ablation procedure.
Activation mapping was performed in all cases to identify the earliest site of VA origin. In cases of infrequent PVCs, pace mapping was used to identify the site of origin. Pace maps were classified as full matching (≥11/12 leads) or not matching (≤10/12 leads).
An RF application with a target temperature of 60 °C and maximum power of 50 W was delivered at the presumed ablation site. If the earliest ventricular activation and best pace mapping were observed close to the para-Hisian area, RF energy was delivered starting with an initial power of 20 W. RF energy was gradually increased to the target output if a reduction in the para-Hisian VAs was observed without any effect on the atrioventricular conduction. When an acceleration or reduction in the incidence of VT or PVCs was observed during the first 30 s of application, the RF current was delivered for an additional 60–90 s. Otherwise, RF delivery was terminated, and the catheter was repositioned. The success of the procedure was defined as the complete elimination and non-inducibility of clinical VT or PVCs during burst ventricular pacing with or without isoproterenol infusion (2–5 μg/min).
Definition of His bundle regions and para-Hisian areaTo identify the specific electrophysiological feature of para-Hisian VAs, the His bundle region was defined as the site recording the largest His bundle potential, and the para-Hisian region was considered as the area of RV or LV septum near the His bundle and within 10 mm of the largest His bundle potential recording site.
Follow-upAfter the ablation, continuous telemetric monitoring was performed for 24 h in all patients. In the case of acutely successful ablation, all antiarrhythmic drugs were discontinued after the ablation procedure. Patients were seen in the outpatient clinic every 3 months after the procedure for assessment of VA recurrence. All patients underwent a post-procedural surface ECG and 24-h Holter monitoring during follow-up.
Statistical analysisContinuous variables were expressed as mean±standard deviation. Comparisons were performed using Student's t-test. Categorical variables were presented as number and percentages. Discrete variables were compared using Fisher's exact test or a chi-square analysis, as appropriate. A value of P <0.05 was considered statistically significant.
Results Patient characteristicsOf the total of 250 patients, 8 (3.2%) had a VA originating in the para-Hisian region in either the RV (n=6) or the LV (n=2). These 8 patients included 5 women aged between 33 and 73 years (mean age, 52±15 years). Their clinical, electrocardiographic, and electrophysiological characteristics are summarized in Table 1. The duration of symptoms prior to the ablation procedure had a wide range (1 month to 25 years). Of the 8 patients, 3 (37.5%) experienced pre-syncope or syncope. Seven patients were non-responsive to at least 1 antiarrhythmic medication before RFCA. One VT patient had not taken any antiarrhythmic drugs. Echocardiography demonstrated a mean LV ejection fraction of 55±10% (range 50–77%), and neither structural abnormalities nor wall-motion abnormalities were found in any patient. The clinically presenting VA was a sustained VT in 1 patient, non-sustained VT in 1 patient and frequent PVCs (PVC burden, >10%/day) in the other 6.
Clinical, electrocardiographic, and electrophysiological characteristics of para-Hisian ventricular arrhythmias.RV para-Hisian (n=6) | LV para-Hisian (n=2) | |||||||
Case 1 | Case 2 | Case 3 | Case 4 | Case 5 | Case 6 | Case 7 | Case 8 | |
Age, years | 35 | 50 | 46 | 73 | 72 | 63 | 33 | 40 |
Sex | Male | Female | Female | Male | Female | Female | Female | Male |
Duration of symptoms | 24 month | 36 month | 25 year | 4 month | 6 month | 24 month | 24 month | 1 month |
Failed AADs | PPF | FLE | PPF | Sotalol | BB | PPF | None | PPF |
LVEF, % | 51 | 63 | 50 | 50 | 51 | 53 | 50 | 77 |
ECG | ||||||||
Presenting arrhythmia | PVCs | PVCs | PVCs | NSVT | PVCs | PVCs | VT | PVCs |
QRS morphology | LBBB | LBBB | LBBB | LBBB | LBBB | LBBB | LBBB | RBBB |
Axis | Inf | Inf | Lt. sup | Inf | Lt. sup | Inf | Lt.sup | Lt. sup |
QRS duration, ms | 130 | 122 | 120 | 108 | 112 | 92 | 130 | 88 |
Lead I | R | R | R | R | R | R | R | R |
aVL | rR | rs | rR | R | R | R | R | rS |
V1 | rS | QS | QS | QS | QS | QS | QS | Rs |
R amplitude in lead I, mV | 1.1 | 0.5 | 1.0 | 1.2 | 1.3 | 1.5 | 1.5 | 0.5 |
Mean R amplitude in inf. leads, mV | 0.93 | 0.67 | 0.4 | 0.9 | 0.4 | 0.77 | 0.37 | 1.03 |
R ratio in leads II/III | 2.6 | 1.3 | 4.0 | 6.0 | 5.0 | 6.5 | 7.0 | 1.1 |
Transition zone | V4–5 | V4 | V4–5 | V2 | V4 | V3 | V2 | <V1 |
EPS and ablation | ||||||||
Induction of arrhythmia | Spont | Spont | Spont | Spont | Spont | Spont | PES | Spont |
Induction with PES | No | No | No | No | No | No | Yes | No |
Provocation with ISP | No | Yes | No | Yes | No | No | No | Yes |
Ablation site | RV | RV | RV | RV | RV | RV | LV | LV |
V-QRS, ms | 68 | 18 | 28 | 24 | 21 | 35 | 50 | 34 |
Pace map | 12/12 | 12/10 | 12/12 | 12/11 | 12/12 | 10/12 | 12/10 | 12/10 |
His potential at ablation catheter | Yes | Yes | Yes | No | No | Yes | Yes | Yes |
Different VAs morphology, n | 1 | 2 | 2 | 3 | 2 | 1 | 2 | 3 |
Acute success | Yes | No | Yes | Yes | Yes | Yes | Yes | Yes |
Follow-up | ||||||||
Duration, months | 41 | 41 | 13 | 8 | 6 | 5 | 53 | 17 |
Recurrence | No | Yes | No | No | No | No | No | Yes |
AADs, antiarrhythmic drugs; BB, beta blocker; ECG, electrocardiogram; EPS, electrophysiological study; Inf, inferior; ISP, isoproterenol; LBBB, left bundle branch block; Lt. sup, left superior; LV, left ventricle; LVEF, left ventricular ejection fraction; PES, programmed electrical stimulation; PPF, propafenone; PVCs, premature ventricular complex; RBBB, right bundle branch block; RV, right ventricle; Spont, spontaneous; Sup, superior; V-QRS, local ventricular activation time relative to the QRS onset; VAs, ventricular arrhythmias; VT, ventricular tachycardia.
Electrocardiographic findingsPara-Hisian VT or PVCs showed left bundle branch block (LBBB) with inferior axis QRS morphology in 4 patients, LBBB with superior axis QRS morphology in 3, and right bundle branch block (RBBB) with superior axis QRS morphology in 1. The mean QRS duration during VT or PVCs was 112±17 ms. The monophasic R wave in lead I was observed in all patients and R or rR in lead aVL in 6 patients (75%). The R wave amplitude in lead I was 1.11±0.40 mV. The qS or QS pattern in lead V1 was observed in 6 patients (75%). The mean R wave amplitude was 0.68±0.27 mV in the inferior leads and the R wave amplitude ratio in leads II/III was 4.2±2.3. The precordial transition zone was in leads V1−V3 in 4 patients and in leads V4−V6 in 4 patients.
Electrophysiological findings and result of catheter ablationThe baseline ECG during the procedure showed PVC in 7 patients and sustained VT in 1 patient. At baseline, the AH and HV intervals were normal. Of the 7 patients with PVCs or nonsustained VT, all had spontaneous PVCs in the electrophysiological study; in addition, 3 of the 8 patients showed provocation of PVCs and non-sustained VT after isoproterenol infusion. In 1 patient with sustained VT as the clinical arrhythmia (Case 7), VT was induced after programmed ventricular stimulation during the electrophysiological study.
RFCA was performed at the site of the earliest ventricular activation with or without full matched pace mapping (Fig. 1). The site of origin of the VAs was the RV in 6 patients and the LV in the remaining 2 patients. In all 4 patients whose para-Hisian VAs had a left superior axis, the successful ablation site was below the His bundle area in the RV or LV. In 6 patients, at the earliest site of ventricular activation during the PVCs or VT, His potentials were observed in the proximal bipole of the ablation catheter during sinus rhythm. The local ventricular electrogram preceded the onset of the surface QRS complex by 18–68 ms (mean 35±16 ms). At the successful ablation site, low amplitude fragmented potentials in the distal bipolar electrogram were observed in 3 patients. However, in the remaining 5, a narrow component R wave with a steep upstroke was observed in the distal bipolar electrogram. In 6 patients with RV para-Hisian VAs, a long sheath with an SR0 or SR1 curve (St. Jude Medical, St. Paul, MN, USA) was used to stabilize the ablation catheter. After the initial ablation, the QRS morphology changed slightly in 6 patients, into 2 or 3 different patterns: a wider QRS duration in the precordial leads in 4 patients (Cases 3–5, and 7); an increase in R wave amplitude in the inferior leads in 3 patients (Cases 2–4); a counter–clockwise rotation of the transition zone in 3 patients (Cases 3–5); and the appearance of an S wave in an inferior lead in 1 patient (Case 8). Additional ablation targeting a relatively distal area around the para-Hisian lesion was required to completely eliminate VAs.
Fig. 1. Activation mapping, pace mapping and fluoroscopic images of the successful ablation site of premature ventricular complexes (PVCs) originating from the para-Hisian area in the right ventricle (A, Case 3), and of ventricular tachycardia (VT) in the left ventricle (B, Case 7). (A) Local ventricular electrogram (left panel) recorded from the distal bi-pole of the ablation catheter, preceding the onset of the QRS by 28ms. His potentials at the proximal ablation catheter were observed during sinus rhythm (SR). Pace mapping (middle panel) from the site of earliest activation during PVC showing fully matched 12-lead ECG. Right and left anterior oblique fluoroscopic images (right panel) showing the successful ablation site. The ablation catheter is positioned in the right para-Hisian area. (B) Local ventricular electrogram (left panel) recorded from the distal bipole of the ablation catheter, preceding the onset of the QRS by 50ms. His potentials at proximal ablation catheter were observed during sinus rhythm. Pace mapping (middle panel) from the site of earliest activation during VT showing unmatched 12-lead ECG. Right and left anterior oblique fluoroscopic images (right panel) showing the ablation site. The ablation catheter was positioned in the left para-Hisian area. ABL, ablation catheter; HB, His bundle; RV, right ventricle.
In all but 1 patient, successful ablation was achieved using a conventional non-irrigated RF ablation catheter. No acceleration of the VT or PVCs occurred during RF applications in any patient. In 3 patients, a transient junctional rhythm was observed during ablation. RFCA was unsuccessful in 1 patient because of proximity to the His bundle and concern about atrioventricular nodal injury. In 1 patient with VA recurrence, redo RFCA was performed using the conventional method. No atrioventricular conduction disturbances related to the procedure were observed. The mean follow-up periods was 23±18 months. During follow-up examination after the last procedure, 6 patients were found free of the VAs, and 2 had PVC recurrence. However, their symptoms significantly improved with a significant reduction in the incidence of PVCs (PVC burden, <2% per day in 1 patient and <1% in 1 patient) without antiarrhythmic drugs.
Comparison between RV para-Hisian VAs and posterior RVOT VAsTable 2 compares the characteristics of VAs originating from para-Hisian VAs in the RV with those of idiopathic posterior RVOT VAs. The groups were not significantly different in age, gender, duration of symptoms, or baseline LVEF. Representative 12-lead ECGs of RV para-Hisian VAs and posterior RVOT VAs are shown in Fig. 2.
Comparison between characteristics of patients with right ventricular para-Hisian ventricular arrhythmias and those with arrhythmias originating in the posterior right ventricular outflow tract.RV para-Hisian (n=6) | Posterior RVOT (n=27) | P value | |
ECG | |||
Axis, superior/inferior | 2/4 | 0/27 | 0.001* |
QRS width during arrhythmia | 114±12 | 139±12 | 0.003* |
Precordial transition (≤V3/≥V4) | 2/4 | 6/21 | 0.57 |
R wave in lead aVL, n (%) | 5 (83.3) | 0 | <0.001* |
QS wave in lead V1, n (%) | 5 (83.3) | 6 (22.2) | 0.004* |
R wave amplitude in lead I, mV | 1.15±0.34 | 0.34±0.18 | 0.001* |
Mean R wave amplitude in inferior lead, mV | 0.68±0.23 | 1.58±0.55 | <0.001* |
R wave ratio in leads II/III | 4.2±2.0 | 1.1±0.2 | 0.01* |
EPS and ablation | |||
Induction with PES, n (%) | 0 (0) | 2 (7.4) | 0.49 |
Provocation with ISP, n (%) | 2 (33.3) | 10 (37.0) | 0.86 |
Activation time at ablation site, ms | 32±17 | 34±9 | 0.79 |
His potential at ablation site, n (%) | 4(66.7) | 0 | <0.001* |
Different VAs morphology, n (%) | 4 (66.7) | 4 (14.8) | 0.007* |
RF delivered, min | 10±6 | 7±5 | 0.75 |
Procedure time, min | 105±41 | 83±45 | 0.69 |
PES, programmed electrical stimulation; ISP, isoproterenol; VAs, ventricular arrhythmias; RF, radiofrequency; RVOT, right ventricular outflow tract.
Statistically significant differences between the para-Hisian and RVOT groups.
Fig. 2. Representative 12-lead ECG of ventricular arrhythmias (VAs) originating from the right ventricular (RV) para-Hisian area (A) and posterior RV outflow tract (RVOT) (B). The R wave amplitude in lead I was greater for RV para-Hisian VAs than for posterior RVOT VAs. A QS wave in lead V1 was frequently identified in RV para-Hisian VAs.
The para-Hisian VAs had a narrower QRS complex compared to the RVOT VAs (114±12 ms vs. 139±12 ms, P=0.003). Two para-Hisian VAs showed a left superior axis compared with none in posterior RVOT VAs (P=0.001). Five patients in the para-Hisian group, but none in the RVOT group, had an R wave in lead aVL (P<0.001). A QS wave in lead V1 was more frequently observed in RV para-Hisian VAs than in posterior RVOT VAs (83.3% vs. 22.2%, P=0.004). The R wave amplitude in lead I of para-Hisian VAs was significantly higher than that of posterior RVOT VAs (1.15±0.34 mV vs. 0.34±0.18 mV, P=0.001), whereas the mean R wave amplitude in the inferior leads of para-Hisian VAs was significantly smaller than that of posterior RVOT VAs (0.68±0.23 mV vs.1.58±0.55 mV, P<0.001). The R wave amplitude ratio in leads II/III was significantly greater in para-Hisian VAs than in posterior RVOT VAs (4.2±2.0 vs. 1.1±0.2, P=0.01) (Fig. 3).
Fig. 3. Comparison of the R wave amplitude in lead I (A), mean R wave amplitude in the inferior leads (B), and R wave amplitude ratio in leads II/III (C), between the right ventricular (RV) para-Hisian group and the posterior RV outflow tract (RVOT) group.
His potentials were identified in the proximal bipole of the ablation catheter at the successful ablation sites in 4 patients with para-Hisian VAs, but none in the posterior RVOT group (P<0.001). Two or 3 different QRS morphologies after ablation were more frequently observed in para-Hisian VAs than in RVOT VAs (4/6, 66.7% vs. 4/27, 14.8%, P=0.007).
The groups were not significantly different as regards the local activation time to the onset of the QRS (32±17 ms vs. 34±9 ms, P=0.79). Arrhythmias originating from the para-Hisian area required a longer RF application and procedure times than RVOT VAs; however, the differences between the 2 groups were not significant (10±6 min vs. 7±5 min, P=0.75; 105±41 min vs. 83±45 min, P=0.69, respectively). The relatively longer ablation time may have been related to catheter instability during ablation and to the higher incidence of incomplete elimination of VT or PVC immediately after ablation. One patient with RV para-Hisian VAs had recurrent PVCs after an initial ablation. However, the patient remained off antiarrhythmic medications because of a significant improvement in symptoms. In the RVOT group, 4 patients had recurrent VAs after ablation and a redo RFCA procedure was performed in these patients. Over the follow-up period, no significant difference was seen in the recurrence rate of VAs between the 2 groups (16.7% vs. 14.8%, P=0.91).
Discussion Main findingsVAs arising from the para-Hisian area in the RV or LV were characterized by a narrower QRS width, the presence of an R wave in lead I and aVL, and a QS wave in lead V1. In 4 patients with a superior axis, para-Hisian VAs originating from the site below the His bundle area in the RV or LV were identified. In addition, a higher R wave amplitude in lead I, a lower R wave amplitude in the inferior leads, and a higher R wave amplitude ratio in leads II/III were major ECG characteristics. Despite the proximity of atrioventricular node, para-Hisian VAs could be uneventfully eliminated by RF application at the distal bipole of the ablation catheter, while a His potential was recorded at the proximal bipole.
Electrocardiographic and electrophysiological considerationsThis study demonstrated the electrocardiographic characteristics of para-Hisian VAs that may help differentiate them from VAs arising from other sites of the RV or LV.
The electrocardiographic features of VAs originating from para-Hisian VAs are similar to those of RVOT VAs [4]. RVOT VAs usually had LBBB with an inferior axis. No patients with RVOT VAs had an R wave pattern in lead aVL, whereas an R or rR pattern QRS morphology in lead aVL was observed in most para-Hisian VAs. All para-Hisian VAs had an R wave in lead I. Therefore, this distinct ECG pattern in the lateral lead was characteristic of para-Hisian VAs. However, posterior RVOT VAs also had the monophasic r or R wave in lead I.
In the present study, the R wave amplitude in lead I could be used to differentiate between RV para-Hisian VAs and posterior RVOT VAs. In addition, these arrhythmias could be seen as having either RBBB or LBBB morphology. However, in patients with VAs originating from the para-Hisian area, the origin of the left- or right-sided VAs was determined by the precordial transition rather than by the bundle branch block morphology. In cases of LV para-Hisian VAs, an early (V1−V2) precordial transition was identified, whereas in VAs of RV origin the transition was in V3 or later in all cases except 1. The QRS complex of VT or PVC in the para-Hisian group was narrower than that of RVOT VAs because ventricular activation is caused by rapid transseptal activation in nearby His bundles of the conduction system.
Recently, Komatsu et al. [9] classified para-Hisian VAs into 2 subgroups according to their origin either above or below the His bundle region. In their study, some patients in the latter group had a superior axis. In our study, 4 para-Hisian VAs had a left superior axis, which indicated a site below the His bundle region. Another previously published study has demonstrated that idiopathic right VAs not arising from the outflow tract were associated with distinct electrocardiographic features of the free wall or apical area in the RV, such as an S wave in leads V2 and V3 or precordial transition, respectively [13]. Therefore, the origin of the VA should be considered to be the para-Hisian region if the other ECG criteria are fulfilled, even if the VA had an LBBB QRS morphology with a superior axis.
In 7 of 8 cases, PVCs were provoked by intravenous isoproterenol, but were not inducible with programmed ventricular stimulation. This finding suggested that a triggered or abnormal automaticity was the major mechanism, rather than reentry.
Previous studies demonstrated QRS alteration following RFCA at the outflow tract, and additional RF energy application in different or separate regions was required for the complete elimination of outflow tract VAs [14,15]. It remains to be determined whether this was caused by exit block from the arrhythmia focus, or whether the VA had shifted to another exit or a different focus.
In this study, 6 patients with para-Hisian VAs presented with 2 or 3 different QRS morphologies after ablation. Yamada et al. suggested that a single VA origin with preferential conduction to multiple exit sites may result in different QRS morphologies after ablation [16]. In addition, the close proximity of the ablation site suggested that subtle differences in morphologies most likely originated from a single focus.
Recently, Komatsu et al. demonstrated a distinctive local electrogram at the successful ablation site of para-Hisian VAs. They found high-frequency fragmented potentials of the R wave with a longer duration in the distal bipolar electrogram. This might be the result of the wavefront from the arrhythmogenic foci moving away with a disturbed, slow propagation through the myocardial tissue of the para-Hisian ventricular septum [7]. However, we only found low-amplitude fragmented potentials in the ablation site in the para-Hisian area in 3 patients, in whom RFCA was successful without VA recurrence.
This study has several important clinical implications. The ECG features of RV para-Hisian VAs could be useful in differentiating them from posterior RVOT VAs prior to ablation. The mapping should be performed from both the right and left side, taking account of the precordial transition, early in the LV and late in the RV. The use of a long sheath to keep the ablation catheter stable during the ablation procedure was important to prevent inadvertent atrioventricular conduction disturbances. A better understanding of the pathophysiological mechanisms and precise localization of the critical sites of para-Hisian VAs was crucial in order to achieve successful ablation without untoward effects.
LimitationsThe diagnosis of para-Hisian VAs was mainly demonstrated at the anatomical sites of successful ablation in the RV or LV. However, the aortic cusp, such as a right coronary cusp or non-coronary cusp, could be considered as the origin site of the VAs because the para-Hisian area might be the preferential exit site [5]. In cases of idiopathic VAs with the earliest activation in the His bundle region and suggestive ECG characteristics, an additional aortic sinus cusp mapping is recommended with a view to finding a safer and more efficient ablation site.
This was a retrospective study with a small number of patients; therefore, a further prospective study with a large number of patients is warranted to confirm the results.
ConclusionsIn comparioson with posterior RVOT VAs, VAs arising from the para-Hisian area were characterized by a narrower QRS width, the presence of an R wave in leads I and aVL and a QS wave in lead V1, and a higher R wave amplitude ratio in leads II/III. RF application at the distal bipole of the ablation catheter, which showed His potentials at the proximal bipole, successfully eliminated para-Hisian VAs without causing atrioventricular conduction disturbances.
Conflict of interestNone of the authors has any conflict of interest with regard to this study.
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Abstract
Background
We investigated the prevalence and the electrocardiographic and electrophysiological characteristics of ventricular arrhythmias (VAs) originating from the para-Hisian area.
Methods
Among 250 patients with idiopathic VAs, 8 (3.2%) had an ablation site in the para-Hisian region. For comparison with right ventricular (RV) para-Hisian VAs (n=6), 27 patients with VAs originating from the posterior RV outflow tract (RVOT) were studied.
Results
Para-Hisian VAs had an R wave in leads I and aVL. The VAs originating from the site below the His bundle region were determined to have a superior axis (n=4, 50%). A His potential was recorded at the proximal bipole of the successful ablation site in 6 patients. RV para-Hisian VAs had a narrower QRS width (114±12 ms vs. 139±12 ms, P=0.003), as well as a higher incidence of R waves in lead aVL (83.3% vs. 0%, P<0.001) and QS waves in lead V1 (83.3% vs. 22.2%, P=0.004) compared to posterior RVOT VAs. A greater R wave amplitude in lead I (1.15±0.34 mV vs. 0.34±0.18 mV, P=0.001) and a smaller R wave amplitude in the inferior leads (0.68±0.23 mV vs. 1.58±0.55 mV, P<0.001), with a higher R wave amplitude ratio in leads II/III (4.2±2.0 vs. 1.1±0.2, P=0.01) were the major ECG characteristics.
Conclusions
Para-Hisian VAs have distinctive electrocardiographic features and can be successfully eliminated without disturbance of atrioventricular conduction.
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Details
1 Division of Cardiology, Department of Internal Medicine, Korea University Medical Center, Seoul, Republic of Korea