CLINICAL RESEARCH: HEART RHYTHM DISORDER
Preferential Conduction Across the Ventricular Outflow Septum in Ventricular Arrhythmias Originating From the Aortic Sinus Cusp
Takumi Yamada, MD*,*,
Yoshimasa Murakami, MD ,
Naoki Yoshida, MD,
Taro Okada, MD,
Takeshi Shimizu, MD,
Junji Toyama, MD,
Yukihiko Yoshida, MD ,
Naoya Tsuboi, MD,
Masahiro Muto, MD ,
Yasuya Inden, MD,
Makoto Hirai, MD,
Toyoaki Murohara, MD,
Hugh T. McElderry, MD*,
Andrew E. Epstein, MD*,
Vance J. Plumb, MD* and
G. Neal Kay, MD*
* Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama
Division of Cardiology, Aichi Prefectural Cardiovascular and Respiratory Center, Ichinomiya, Japan
Division of Cardiology, Nagoya Dai-ni Red Cross Hospital, Cardiovascular Center, Nagoya, Japan
Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Manuscript received January 31, 2007;
revised manuscript received April 16, 2007,
accepted May 5, 2007.
* Reprint requests and correspondence: Dr. Takumi Yamada, Division of Cardiovascular Diseases, Cardiac Rhythm Management Laboratory, University of Alabama at Birmingham, VH B147, 1670 University Boulevard, 1530 3rd Avenue South, Birmingham, Alabama 35294-0019. (Email: takumi-y{at}fb4.so-net.ne.jp).
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Abstract
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Objectives: The purpose of this study was to examine the relationship between the origin and breakout site of idiopathic ventricular tachycardia (VT) or premature ventricular contractions (PVCs) originating from the myocardium around the ventricular outflow tract.
Background: The myocardial network around the ventricular outflow tract is not well known.
Methods: We studied 70 patients with idiopathic VT (n = 23) or PVCs (n = 47) with a left bundle branch block and inferior QRS axis morphology. Electroanatomical mapping was performed in both the right ventricular outflow tract (RVOT) and aortic sinus cusp (ASC) during VT or PVCs.
Results: The earliest ventricular activation (EVA) was recorded in the RVOT in 55 patients (group R) and in the ASC in 15 (group A). In all group R patients, the closest pace map and successful ablation were achieved at the EVA site. Although a successful ablation was achieved at the EVA site in all group A patients, the closest pace map was obtained at the EVA site in 8 and RVOT in 7 (with an excellent pace map in 4). The stimulus to QRS interval was 0 ms during pacing from the RVOT and 36 ± 8 ms from the ASC. The distance between the EVA and perfect pace map sites in those 4 patients was 11.9 ± 3.0 mm.
Conclusions: Ventricular arrhythmias originating from the ASC often show preferential conduction to the RVOT, which may render pace mapping or some algorithms using the electrocardiographic characteristics less reliable. In some of those cases, an insulated myocardial fiber across the ventricular outflow septum may exist.
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Abbreviations and Acronyms
| | ASC = aortic sinus cusp | | EVA = earliest ventricular activation | | PVC = premature ventricular contraction | | RF = radiofrequency | | RVOT = right ventricular outflow tract | | St-QRS = the interval from the pacing stimulus to the onset of the QRS | | VT = ventricular tachycardia |
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Ventricular tachycardia (VT) or premature ventricular contractions (PVCs) originating from the myocardium around the ventricular outflow tract are known as idiopathic ventricular arrhythmias not associated with structural heart disease (1–6). It has been shown that radiofrequency (RF) catheter ablation is a safe and reliable technique for curing those ventricular arrhythmias (2–8). However, it is often difficult to differentiate whether those ventricular arrhythmias originate from the right or left outflow tract, probably because the ventricular septum lies between both outflow tracts (6–9). The myocardial network around the ventricular outflow tract septum is not well known. The purpose of this study was to elucidate that by investigating the relationship between the origin and breakout site of those ventricular arrhythmias.
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Methods
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Patient characteristics.
The study population consisted of 70 consecutive patients (33 men, 54 ± 15 years, range 16 to 80 years) with symptomatic idiopathic VT (n = 23) or PVCs (n = 47) with a left bundle branch block and inferior QRS axis morphology. The patients with VT or PVCs with S waves in leads V5 and V6 and a QRS morphology, which were supposed to predict an infra-aortic valvular origin or left ventricular epicardial origin in the electrocardiographic algorithms previously proposed (6–9), were excluded. There was no echocardiographic evidence of structural heart disease in any of the patients. Each patient gave their informed consent, and all antiarrhythmic drugs were discontinued for at least 5 half-lives before the study.
Electrophysiological study.
A 6-F quadripolar catheter was introduced from the right femoral vein and placed in the right ventricular apex for pacing. Mapping and pacing were performed using a 7-F, 4-mm-tip ablation catheter (Navi-Star, Biosense Webster, Diamond Bar, California) introduced through a long sheath via the right femoral vein (for the right ventricular outflow tract [RVOT]) or right femoral artery (for the aortic sinus cusp [ASC]). When few PVCs were observed at the beginning of the electrophysiological study, induction of the VT or PVCs was attempted by burst pacing from the RVOT or right ventricular apex and/or an isoproterenol infusion. The surface 12-lead electrocardiogram and intracardiac electrograms were displayed on a computer monitor using a Bard Electrophysiology system (CR Bard Inc., Billerica, Massachusetts).
Mapping and catheter ablation.
First, electroanatomical mapping was performed in the RVOT during VT or PVCs and an activation map was constructed in all cases as previously reported (10,11). When VT or PVCs were infrequent, first, electroanatomical mapping of the RVOT was performed during sinus rhythm to create a geometry of the RVOT. After that, activation mapping of the VT or PVCs was performed in a limited area of interest on the remap, which was made by extracting the anatomical frame out of the baseline map during sinus rhythm (Fig. 1). Pace mapping was performed at a pacing cycle length of 500 ms at an output just greater than the diastolic threshold at the earliest ventricular activation (EVA) site that was identified by the activation map. The score for the pace mapping was determined from the R/S ratio and notch of the R-wave in the 12-lead electrocardiogram as previously reported (perfect pace mapping meant 24 points) (4). If a pace map score  20 and local ventricular activation preceding the onset of the QRS (V–QRS 0 ms) were obtained, an RF application with a target temperature of 60°C and maximum power output of 50 W was delivered at the EVA site in the RVOT. Otherwise, or if successful ablation was not achieved at the EVA site, electroanatomical mapping was added in the ASC. During the procedure in the ASC, intravenous heparin was administered to maintain an activated clotting time >250 s. Pace mapping was also performed at the EVA site in the ASC in the same maneuver as in the RVOT. If the EVA in the ASC was earlier than that in the RVOT, an RF application with a target temperature of 60°C and maximum power output of 50 W was delivered at the EVA site in the ASC. If the ablation site was close to the ostium of the coronary artery, the RF ablation was performed with an angiographic catheter deployed in the ostium of the coronary artery with frequent manual contrast injections. An RF application was never delivered to an area within 5 mm from the angiographic catheter. During the RF catheter ablation, when the VT or PVCs were not affected within 10 s, the RF discharge was terminated and the catheter was repositioned for a repeat attempt. When an acceleration or reduction in the VT or PVCs was observed dramatically during the first 10 s of the application, the RF delivery was continued for 30 to 60 s. The end point of the catheter ablation was the elimination and noninducibility of the VT or PVCs during an isoproterenol infusion (2 to 4 µg/min) and burst right ventricular pacing (to a cycle length as short as 300 ms). An acute success was defined as complete elimination of the target VT or PVCs during continuous electrocardiogram monitoring in-hospital for at least 3 days after the ablation procedure.
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Figure 1 Activation Map of the RVOT and the Cardiac Tracings During PVCs (Case 8)
Activation mapping of the premature ventricular contractions (PVCs) was performed in a limited area of interest on the remap, which was made by extracting the anatomical frame out of the baseline map during sinus rhythm. The earliest ventricular activation (EVA) indicated by the red area was observed in a fairly wide area on the posterior septum of the right ventricular outflow tract (RVOT) during the PVCs. The EVA relative to the onset of the QRS was 0 ms, and the unipolar electrogram at the EVA site showed a small initial r wave on the shoulder. A few radiofrequency applications targeting the EVA site in the RVOT could not eliminate the PVCs. ABLd/p = the distal/proximal electrode pair of the ablation catheter in the RVOT; ABLuni = the distal unipolar electrode of the ablation catheter in the RVOT; PA = posteroanterior.
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Follow-up.
Follow-up was performed at 2 weeks, 1 month, and every month thereafter, using 24-h Holter monitoring and cardiac recordings. All patients who reported symptoms were given an event monitor to document the cause of the symptoms.
Statistical analysis.
Continuous variables are expressed as the group mean ± 1 SD. Comparisons of the continuous variables between the groups were analyzed with the use of the Student t test or analysis of variance, as appropriate. Categorical variables expressed as numbers and percentages in the different groups were compared with a chi-square test. Statistical significance was selected at a value of p < 0.05.
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Results
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Mapping and RF catheter ablation in the RVOT.
Pace mapping at the EVA site in the RVOT revealed a score of <20 in 16 of the 70 patients. The EVA in the RVOT was earlier than the onset of the QRS in 9 (–25 ± 7 ms) and simultaneous with the onset of the QRS in 7 of those patients. In those 16 patients, mapping in the ASC was added without any RF ablation in the RVOT. In the residual 54 patients with a pace map score 20 (23 ± 2) and the EVA preceding the onset of the QRS (–23 ± 7 ms) in the RVOT, RF catheter ablation was performed at the EVA site in the RVOT. In 49 of those 54 patients, the targeted VT or PVCs could be eliminated by a mean of 8 ± 4 RF applications. In 5 patients whose targeted VT or PVCs could not be eliminated by the RF ablation in the RVOT, mapping in the ASC was added (Figs. 1 and 2).
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Figure 2 Pace Mapping (Case 8)
The PVCs with a left coronary sinus cusp (LCC) origin showed a left bundle branch block and inferior QRS axis morphology with a QRS transition between V4 and V5. An excellent pace map was obtained at the EVA site in the RVOT (pace map [PM] score = 22/24). However, a poor PM was obtained at the EVA site in the LCC (PM score = 5/24). The pacing stimulus to QRS interval was 0 ms and 50 ms during pace mapping from the RVOT and LCC, respectively. Abbreviations as in Figure 1.
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Mapping and RF catheter ablation in the ASC.
In 6 of the 21 patients who underwent mapping in the ASC, the EVA in the ASC was later than the EVA in the RVOT and the pace mapping score in the ASC was worse than that in the RVOT. In those patients, RF catheter ablation was finally performed at the EVA site in the RVOT and all of the targeted VT or PVCs could be successfully eliminated.
In all of the remaining 15 patients (9 men, 51 ± 13 years, range 29 to 74 years), the EVA in the ASC (12 in the left ASC and 3 at the junction between the left and right ASCs) was earlier (–29 ± 8 ms) than the EVA in the RVOT (Table 1, Fig. 3). In all 15 of those patients, the closest pace map on the left side was obtained at the EVA site. In 8 of those 15 patients (group 1), the pace map score in the ASC was >20, whereas that in the RVOT was  13. However, in 4 of those 15 patients (group 2), the pace map score in the RVOT was 20, whereas that in the ASC was 15 (Table 1, Fig. 2). In 3 of those 15 patients (group 3), the pace map score was poor (12) in the ASC as well as in the RVOT. In those 15 patients, the interval from the pacing stimulus to the onset of the QRS (St-QRS) was 0 ms during pacing from the RVOT and 36 ± 8 ms during pacing from the ASC (the St-QRS equaled 0 ms in none of those cases). In those 15 patients, RF catheter ablation was finally performed at the EVA site in the ASC and all targeted VT or PVCs could be successfully eliminated by a mean of 2 ± 1 RF applications (Fig. 4).
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Figure 3 Activation Map of the RVOT and LCC During PVCs (Case 8)
The EVA was observed in the LCC (white arrows), and a single RF application there could successfully eliminate the PVCs. The distance between the EVA in the RVOT and successful ablation site in the LCC was 9.7 mm. RL = right lateral; other abbreviations as in Figure 1.
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Figure 4 The Successful Ablation Site in the LCC (Case 8)
The local ventricular activation preceded the onset of the QRS by 24 ms, and the unipolar electrogram showed a QS pattern at the successful ablation site. The pink line indicates the coronary angiographic catheter deployed in the left coronary artery (LCA). ABL = the ablation catheter in the left coronary sinus cusp; LAO = left anterior oblique; RAO = right anterior oblique; RVA = right ventricular apex; RVOTd/p = the distal/proximal electrode pairs of the right ventricular outflow tract catheter; other abbreviations as in Figures 1 and 2.
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Electrophysiological characteristics of the VT or PVCs originating from the ASC.
There were no significant differences in the age (52 ± 13 years vs. 56 ± 12 years vs. 48 ± 14 years), male gender, type of ventricular arrhythmia, St-QRS (38 ± 9 ms vs. 30 ± 5 ms vs. 37 ± 3 ms), local activation time at the successful ablation site (–29 ± 8 ms vs. –32 ± 7 ms vs. –27 ± 11 ms), distance between the EVA site in the RVOT and successful ablation site (16.4 ± 8.0 mm vs. 11.9 ± 3.0 mm vs. 18.9 ± 1.8 mm), or location of the ventricular arrhythmia origin between groups 1 to 3 (Table 1). The QRS duration in group 3 was significantly shorter than that in groups 1 and 2 (158 ± 17 ms vs. 182 ± 11 ms and 176 ± 5 ms; p < 0.01 and p < 0.05). The transition zone of the QRS morphology tended to be observed earlier (V1 to V3) in the group 1 patients and later (V3 to V5) in the group 2 patients (Table 1). In 4 patients with a pace map score of 20 in the RVOT, the difference of the EVA between the RVOT and ASC was 25 ± 14 ms.
Follow-up.
The RF catheter ablation was successful in 52 patients with RVOT origins (95%) and 15 patients with ASC origins (100%) by the time of discharge from the hospital. None of those patients in whom the ablation was judged as successful at the time of the hospital discharge had any late recurrences of VT or PVCs during the follow-up (19 ± 7 months). Three patients with presumed RVOT origins had an early recurrence of PVCs with the same QRS morphology as before the ablation. Those patients continue to be followed up because both the frequency and duration of the PVC attacks have decreased and consequently the symptoms have remarkably improved. No complications occurred.
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Discussion
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This study showed that in about 25% of patients with ventricular arrhythmias of an ASC origin, pace mapping from the RVOT yielded a closer match of the QRS morphology than pacing from within the ASC. In addition, pacing from within the ASC was associated with a significantly longer St-QRS interval than pacing from the RVOT. The site of a successful ablation was more accurately guided by recording the EVA, suggesting that the arrhythmia origin was in the ASC, whereas pace mapping identified a preferential breakout site. Therefore, this study suggested that in about 25% of the ventricular arrhythmias with an ASC origin, there was a preferential localized breakout site in the RVOT (Fig. 5A). Storey et al. (12) reported that in a patient with the VT originating from the right ASC, noncontact mapping in the RVOT showed 2 distinct sites of early activation in the RVOT and right ventricular septum that preceded the QRS onset during the VT. However, in their case, a localized breakout site was observed in the right ASC. To the best of our knowledge, this is the first report that has suggested that some ventricular arrhythmias originating from the ASC show a preferential conduction to the RVOT. An anatomical study has shown that the larger part of the right coronary and a portion of the left coronary aortic leaflets are related to the ventricular septum and the free wall of the left ventricle, respectively (5). Therefore, in these areas, the semilunar leaflets are hinged superior to the aortic wall but inferior to the muscle, enclosing the ventricular muscle at the cusps of the sinuses (5). However, to the best of our knowledge, there have been no anatomical reports to explain the reason why some ventricular arrhythmias with an ASC origin show a preferential conduction to the RVOT. We speculate that anisotropic conduction between the ASC origin and breakout site in the RVOT may be associated with that.
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Figure 5 Schema of the Ventricular Arrhythmia Origin, Breakout Site, and Preferential Conduction From the LCC Origin to the RVOT or Left Ventricular Septum
(A) A schema corresponding to the group 2 cases. (B) A schema corresponding to the group 1 cases. (C) A schema corresponding to the group 3 cases. LAD = left anterior descending coronary artery; LCX = left circumflex coronary artery; NCC = noncoronary sinus cusp; RCC = right coronary sinus cusp; other abbreviations as in Figures 1 and 2.
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This study also might suggest the existence of myocardial fibers extending from the ASC to the ventricles because pace mapping from the ASC always showed some interval from the pacing stimulus to the onset of the QRS. Even if the breakout site in the RVOT was apart from the ASC origin, a selective capture of the ASC origin or myocardial fiber to the RVOT could have reproduced an excellent pace map. In that situation, an excellent pace map should be obtained in either the ASC or the RVOT and a longer St-QRS should be observed during pacing from the ASC origin than during pacing from the breakout site in the RVOT. Those findings could be strong evidence for a preferential conduction via the myocardial fibers from the ASC origin to the breakout site in the RVOT. However, there were actually no cases that showed such findings in this study. There might have been some combined mechanisms that would explain the reason why the origin could not be selectively captured by the pacing. First, there should also be myocardial fibers traveling from the ASC origin to the left ventricular septum (Fig. 5A). Second, the pacing might capture the myocardial fibers from the ASC origin that not only extended to the RVOT but also to the left ventricular septum and thus diminish the preferential conduction from the ASC origin to the RVOT (Fig. 5A).
In about 50% of the patients in this study with ventricular arrhythmias with an ASC origin, an excellent pace map in the ASC and a very poor pace map in the RVOT were obtained. In those cases, there should have been no myocardial fibers from the ASC origin to the RVOT because those myocardial fibers could not have reproduced an excellent pace map in the ASC for the same reasons as in the cases with a preferential conduction from the ASC origin to the RVOT (Fig. 5B). In those cases, no excellent pace maps with a shorter St-QRS than in the ASC were obtained from any other endocardial site in the left ventricle. Therefore, in those cases the breakout site might have been located in the epicardium.
In 20% of the patients in this study with ventricular arrhythmias with an ASC origin, a very poor pace map was obtained in both the RVOT and the ASC. There might have been some combined mechanisms that would have explained those findings. First, a preferential conduction from the ASC origin and not to the RVOT, but to the left ventricular septum should exist in those cases (Fig. 5C). Second, the pacing might have captured the myocardial fibers from the ASC origin that extended not only to the left ventricular septum but also to the RVOT and would have diminished the preferential conduction from the ASC origin to the left ventricular septum (Fig. 5C). In those cases, the QRS duration was significantly shorter as compared with that in the other cases. Therefore, in those cases the preferential breakout site might have been in a more septal area (Fig. 5C). Those findings might suggest a variety of myocardial fibers traveling from the ASC origin to the RVOT or left ventricular septum.
Some algorithms using the electrocardiographic characteristics, especially the QRS transition in the precordial leads, are useful for differentiating whether ventricular arrhythmias originate from the RVOT or ASC (6,13,14). However, those algorithms cannot always predict the ASC origins with a very high sensitivity (approximately 90%) (8). In this study, 20% of the ventricular arrhythmias with an ASC origin showed a late QRS transition after V3. Therefore, a preferential conduction from the ASC origin to the RVOT may reduce the sensitivity in predicting the ASC origin using the electrocardiographic characteristics.
In some ventricular arrhythmias with an ASC origin, a preferential conduction to the RVOT may render pace mapping less reliable. Therefore, when despite a good pace map the local ventricular activation does not precede the QRS onset of the VT or PVCs adequately or RF ablation is not effective in the RVOT, mapping of the ASC should be added. On the other hand, in 27% of the patients in this study with ventricular arrhythmias with an ASC origin, the local ventricular activation in the RVOT preceded the QRS onset of the VT or PVCs adequately, as Storey et al. (12) also reported. Therefore, when despite the local ventricular activation preceding the QRS onset of the VT or PVCs adequately, a good pace map is not obtained, or RF ablation is not effective in the RVOT, mapping of the ASC should be added.
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Conclusions
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Ventricular arrhythmias originating from the ASC often show preferential conduction to the RVOT, which may render pace mapping or some algorithms using the electrocardiographic characteristics less reliable. In some of those cases, an insulated myocardial fiber across the ventricular outflow septum may exist.
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References
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Abstract
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