Author + information
- Received July 14, 2015
- Revision received September 23, 2015
- Accepted September 24, 2015
- Published online December 15, 2015.
- Zili Liao, MD∗,
- Xianzhang Zhan, MD∗,
- Shulin Wu, MD∗∗ (, )
- Yumei Xue, MD∗,
- Xianhong Fang, MD∗,
- Hongtao Liao, MD∗,
- Hai Deng, MD∗,
- Yuanhong Liang, MD∗,
- Wei Wei, MD∗,
- Yang Liu, MD∗ and
- Feifan Ouyang, MD†
- ∗Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangdong, China
- †Department of Cardiology, Asklepios Klinik St. Georg, Hamburg, Germany
- ↵∗Reprint requests and correspondence:
Dr. Shulin Wu, Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong General Hospital, Zhongshan Road #106, Yuexiu District, Guangzhou 510080, Guangdong, China.
Background Idiopathic ventricular arrhythmias (VAs) originating from the pulmonary sinus cusp (PSC) have not been sufficiently clarified.
Objectives The goal of this study was to investigate the prevalence, electrocardiographic characteristics, mapping, and ablation of idiopathic VAs arising from the PSC.
Methods Data were analyzed from 218 patients undergoing successful endocardial ablation of idiopathic VAs with a left bundle branch block morphology and inferior axis deviation.
Results Twenty-four patients had VAs originating from the PSC. In the first 7 patients, initial ablation performed in the right ventricular outflow tract failed to abolish the clinical VAs but produced a small change in the QRS morphology in 3 patients. In all 24 patients, the earliest activation was eventually identified in the PSC, at which a sharp potential was observed preceding the QRS complex onset by 28.2 ± 2.9 ms. The successful ablation site was in the right cusp (RC) in 10 patients (42%), the left cusp (LC) in 8 (33%), and the anterior cusp (AC) in 6 (25%). Electrocardiographic analysis showed that RC-VAs had significantly larger R-wave amplitude in lead I and a smaller aVL/aVR ratio of Q-wave amplitude compared with AC-VAs and LC-VAs, respectively. The R-wave amplitude in inferior leads was smaller in VAs localized in the RC than in the LC but did not differ between VAs from the AC and LC.
Conclusions VAs arising from the PSC are not uncommon, and RC-VAs have unique electrocardiographic characteristics. These VAs can be successfully ablated within the PSC.
The right ventricular outflow tract (RVOT) and left ventricular outflow tract are the most common sites of origin for idiopathic ventricular tachycardia (VT) or premature ventricular contractions (PVCs) absent overt structural heart disease (1–6). Less commonly, idiopathic ventricular arrhythmias (VAs) can originate from the pulmonary artery (PA) (7–10). Histopathological studies have shown that ventricular myocardium may extend into the aorta and PA beyond the semilunar valves (11–13). Thus, by extending into the great vessels with abnormal automaticity or triggered activity, the ventricular myocardium may be the underlying mechanism of these VAs (8). VAs originating from the aortic root may be ablated within the aortic sinus cusp (ASC) or from the right/left coronary cusp commissure (2,14,15). However, most PA-VAs are located >10 mm above the pulmonary valve (PV) and could be successfully ablated in the PA (9,10). Given that little is known about the characteristics of VAs originating from the pulmonary sinus cusp (PSC) (9,16), the goal of the present study was to evaluate the prevalence, electrocardiographic characteristics, mapping, and ablation of idiopathic VAs arising from the PSC.
Between August 2012 and August 2014, a total of 244 patients (148 men; age 56.1 ± 14.5 years) underwent endocardial radiofrequency catheter ablation (RFCA) at Guangdong General Hospital for idiopathic VAs with a left bundle branch block (LBBB) morphology and inferior axis deviation. In 26 patients, the arrhythmia could not be eliminated because of latent serious radiofrequency (RF)-related complications, indeterminate site of earliest ventricular activation, or inability to stabilize the ablation catheter during the procedure. In the remaining 218 patients, the successful ablation site was located on the endocardial RVOT (n = 148), in the ASC (n = 46), or within the PSC (n = 24). The present study consisted of the latter 24 patients. When the QRS morphology of clinical VAs was tested with an electrocardiogram (ECG) algorithm to determine VA origin, all idiopathic VAs were identified as arising from the RVOT (2–10,17). In addition, no patients had any overt structural heart disease on echocardiography. The study was approved by the institutional review board of Guangdong General Hospital.
ECG and electrophysiological analyses
Detailed analysis of clinical PVC/VAs was performed offline by using an electrophysiological data acquisition system with a recording speed of 50 to 100 mm/s or 12-lead ECG with a recording speed of 25 to 50 mm/s. During clinical VAs, QRS morphology on leads I, II, III, aVR, and aVL was assessed, as well as: 1) R-wave amplitude in leads I, II, III, aVF, V1, and V2 and the III/II R ratio; 2) duration of R-wave complex in leads II, III, and aVF; 3) Q-wave amplitude in leads aVR and aVL and the QS aVR/aVL ratio; and 4) the precordial R/S transitional zone. In addition, the precordial R-wave transitional zone was analyzed during sinus rhythm (SR). All measurements were independently performed by 3 physicians.
After providing written informed consent, and after withdrawal of antiarrhythmic drugs for a duration of >5 half-lives, all patients underwent an electrophysiological evaluation. Catheters were placed into the heart under fluoroscopy through the femoral vessels. If clinical arrhythmias failed to occur spontaneously, programmed stimulation was performed. The protocol consisted of ventricular stimulation at 2 basic drive cycle lengths with <2 extra stimuli to a minimum coupling interval of 230 ms. If VA was not inducible at baseline, intravenous isoproterenol infusion (2 to 5 μg/min) was administered to provoke clinical arrhythmias.
Mapping and RFCA
In patients with frequent PVCs or short-run VT, 3-dimensional electroanatomical mapping was used, as reported previously (18). In brief, mapping was performed using a steerable 7.5-F, D-curve catheter with a 3.5-mm irrigated-tip electrode (NaviStar ThermoCool, Biosense Webster, Diamond Bar, California). If necessary, the mapping catheter was advanced via an SR0 long sheath introduced through the right femoral vein to the right ventricle. Point-by-point mapping was performed to create anatomic maps, and activation mapping was used to identify the origin during PVCs or VT in the study. Pace mapping was also performed, with the lowest pacing output (2 to 20 mA) and pulse width (0.5 to 10 ms), to capture the ventricular myocardium at the site of earliest activation. A suitable target for ablation was selected based on the earliest activation times during the arrhythmia.
In the initial 7 patients, mapping began in the RVOT. If suitable ablation sites were not found, the PA and left ventricular outflow tract were mapped. In the subsequent 17 patients, 3-dimensional mapping was initially performed in the RVOT and subsequently in the PA before ablation. Right ventriculography and/or pulmonary arteriography were also performed to locate the position of the PV (Figure 1) and to mark the pulmonary annulus on 3-dimensional mapping (Figures 2, 3, and 4). Detailed mapping in the PSC was achieved by using a reversed U curve of the ablation catheter, which can facilitate the stability of a mapping catheter within the PSC. Importantly, an 8.5-F long sheath was always used and advanced into the right ventricle to allow for a reversed U curve in the PA. The long sheath can stabilize the mapping catheter and help rotate it clockwise or counterclockwise to access 3 individual PSCs. Left ventricular access was achieved via a retrograde aortic and/or transseptal approach. For left-sided procedures, unfractionated heparin was administered to maintain activated clotting times between 250 and 300 s.
Irrigated RF current was delivered in power-controlled mode, with a maximum power of 40 W, a temperature limit of 43°C, and a flow rate of 20 ml/min. During RF delivery, if a decreased frequency/elimination of VAs occurred within the initial 15 s, the application was maintained and carefully titrated for 60 s. Ventriculography, PA angiography, or coronary angiography was performed to determine the precise location of the ablation catheter positioned at the successful application site. After successful ablation, intravenous administration of isoproterenol and programmed stimulation were performed to reinitiate clinical VAs.
Acute success was defined as either absence of spontaneous or provoked clinical VAs at the end of the procedure or absence of the latter on 24-h ECG monitoring post-ablation off antiarrhythmic drugs. Antiarrhythmic drugs were not reinitiated if ablation was acutely successful. Each patient returned for evaluation in the hospital’s outpatient arrhythmia center at 2 weeks, 1 month, and every 3 months thereafter. Transthoracic echocardiography and 24-h Holter monitoring were performed the day after the procedure and at the 3-month follow-up visit.
Continuous variables are expressed as mean ± SD, and categorical variables as numbers and percentages. The Student t test and Fisher exact test were used for comparisons of the continuous variables and categorical variables between the 2 groups, respectively. A p value <0.05 was considered significant.
Patient and clinical data are shown in Table 1. Previous ablation had been performed in 7 of the 24 patients (1 ablation attempt in 5 patients and 2 attempts in 2 patients). Two of the 7 patients had failed ablation procedures; RFCA resulted in acute success in the remaining 5 patients. However, VAs with the same morphologies recurred during follow-up in these patients. Neither ventriculography nor intracardiac echocardiography was used to evaluate catheter position. VA burden on 24-h Holter ECG is shown in Table 1.
ECG and electrophysiological characteristics
The surface ECG during either VT or PVCs exhibited a typical LBBB morphology with an inferior axis in all patients (Figure 5, Online Figure 1). Before ablation, a small difference in QRS morphology existed in 2 of 24 patients; 1 was frequently observed, the other less frequently. The subtle differences in QRS morphology were mainly in the R-wave in inferior leads. The remaining 22 (92%) had single QRS morphologies.
Frequent PVCs or short runs of VT occurred spontaneously in 20 patients. Isoproterenol infusion was administered to provoke the frequent VAs in the other 4 patients. Clinical VAs were not inducible by programmed ventricular stimulation in any patients.
In the RVOT, the earliest activation was at the posteroseptal region in 3, the mid-septal in 3, the anteroseptal in 3, the middle free wall in 3, the anterolateral in 6, and the posterolateral region in 6 (Figure 2). The local ventricular activation preceded the onset of the QRS complex by 19.9 ± 3.3 ms, and a good pace map (10 of 12 leads matched in QRS morphology in 3 patients and 11 of 12 leads matched in 5 patients) was obtained at the site of earliest ventricular activation in 8 patients (33%). No presystolic or late diastolic potentials were recorded. The mean distance from the site of earliest ventricular activation in the RVOT to the closest PSC portion was 4.1 ± 2.6 mm.
In the initial 7 patients with RVOT ablation, RFCA resulted in transient suppression of VAs in 4 patients. However, additional RF energy deliveries in the RVOT could not abolish the VAs in any patient. After initial ablation in the RVOT, a small change in the QRS morphology developed in 3 patients; there was no evidence of subtle changes in QRS morphology before ablation in these 3 patients (Figure 6).
When mapping in the pulmonary root, a 2-component (near-field and far-field) activation was observed at the site of earliest ventricular activation during SR in all 24 patients (Figures 2, 3, and 4). During VAs, the reversal relationship of the near-field ventricular signal and the far-field signal was noted, and no isolated presystolic potentials were observed at that site in any patient. On bipolar recording, the earliest ventricular activation was identified in the PSC. The ventricular activation on unipolar recording demonstrated QS morphology with almost simultaneous activation and the earliest discrete potential on bipolar recording (Figures 2 and 4). Pace mapping was obtained in all 24 patients (mean lowest pacing output 7.5 ± 2.4 mA), but a good pace map was achieved in 20 patients only (83%). Of these 20 patients, paced ECG morphology matched the clinical VA in 12 of 12 leads in 1 patient (Figure 2), in 11 of 12 leads in 9 patients, and in 10 of 12 leads in 10 patients (Figure 3). The major differences between the spontaneous and paced QRS were in leads V1 and V2 (31%), similar to pacing in RVOT.
The final successful ablation site was in the right cusp (RC) in 10 patients (42%), the left cusp (LC) in 8 (33%), and the anterior cusp (AC) in the remaining 6 (25%). Of these 24 successful RF sites, 22 were at the bottom of the PSC; the remaining 2 (both LC-VAs) were located 4 mm and 4.5 mm beyond the PSC bottom, respectively. The targeted potential at the final ablation site preceded QRS complex onset of clinical VAs by 28.2 ± 2.9 ms, significantly greater than the earliest activation time recorded in the RVOT (p < 0.05). The number of RF lesions ranged from 5 to 15 (mean 8.3 ± 3.6) in the series of 24 patients (13.3 ± 1.8 in the initial 7 patients vs. 6.2 ± 1.4 in the last 17 patients; p < 0.05). Procedural time and fluoroscopic time were 124.9 ± 18.1 min and 5.3 ± 1.8 min, respectively. After successful ablation in the PSC, a discrete potential at the late phase of the QRS complex during SR was still recorded in all 24 patients.
Comparing ECG and electrophysiological parameters for PSC VAs
The results of the ECG parameters of these VAs with their determined origins are given in Table 2. There were no significant differences in the clinical characteristics. In comparing lead I polarity, QRS morphology exhibited a large R-wave in 10 RC-VAs, 1 AC-VA, and 2 LC-VAs (Table 2, Figure 5, Online Figure 1). The R-wave amplitude in lead I was significantly higher in the RC-VAs than in the AC-VAs and LC-VAs but did not differ between VAs from the AC and LC.
There was a notch on the R-wave in the inferior leads in 11 patients; the origin was located at the RC in 7 patients, at the AC in 2 patients, and at the LC in 2 patients. The R-wave amplitude in the inferior leads (the ratio of the R-wave amplitude in lead III/II) was significantly smaller in the RC-VAs than in the AC-VAs and LC-VAs. The QRS duration was longer in the RC-VAs than in both the AC-VAs and LC-VAs. A QS-wave was presented in aVR in all 24 patients and in aVL in 23 patients except 1 patient with RC-VAs. The transitional zone was often observed at V4, occurring from V3 in 2 of 10 RC-VAs, 2 of 6 AC-VAs, and 1 of 8 LC-VAs.
There were no differences between local ventricular activation time relative to the QRS onset, RF duration, and number of RF applications among the origin sites within the 3 PSCs. A sharp potential was recorded in all patients. Low-amplitude and broad atrial potentials were observed only in VAs with left atrial origin (4 of 8). A relatively low-output pacing was achieved in all patients.
No procedure-related complications occurred in any of the 24 patients, and no PV damage was found according to echocardiographic results. All patients were free of arrhythmias, without antiarrhythmic drugs, during a follow-up period of 9 ± 3 months. Post-ablation VA burden on 24-h Holter ECG is shown in Table 1.
The pulmonary root is the distal part of the RVOT that supports the 3 semilunar leaflets of the PV. There are 3 distinct junctions or rings that can be appreciated in the region (11–13). The semilunar valvular leaflets have distal attachment at the sinotubular junction, which separates the PSCs from the tubular component of the pulmonary trunk. The PSC wall is supported throughout its circumference by the muscular right ventricular (RV) infundibulum, where the 2 join across the anatomic ventriculoarterial junction. At the base, the semilunar attachments of the leaflets cross the anatomic ventriculoarterial junction, creating a third ring (i.e., the hemodynamic ventriculoarterial junction). The interdigitation of the semilunar attachments with the 3 rings presents a crown-like configuration. However, the 3 PSCs are not at the same level: the LC is situated at the lowest level, with the AC and RC situated relatively superior (Figure 1).
The RV musculature could extend at the base of the pulmonary root and, in a sleeve-like manner, more distally into the PA between the cusps and into the valve tissue itself. Hasdemir et al. (12) reported that in 17% of autopsied hearts, myocardium extending beyond the ventriculoarterial junction was present. Another autopsy study showed that the prevalence of such myocardium extensions was even higher, up to 74% (13). Nevertheless, these results were obtained from subjects in whom the majority had no clinical VAs. Recently, by using voltage mapping and intracardiac echocardiography, Liu et al. (19) speculated that the myocardial extension beyond the PV existed in 92% of control patients and 88% of patients with RVOT arrhythmia. The presence of fibrosis and fatty tissue among these muscular sleeves may create a possible VA substrate for PSC-VAs (12).
Prevalence of PSC-VAs
Several studies have reported the prevalence of VAs arising from PA, and among the RVOT arrhythmia foci, 21% to 46% were localized beyond the PV (9,19). Most of these VAs were located 8 mm above the PV. Only some cases had the successful ablation site located closely above the PV (8,16). However, the distance between the successful ablation site and bottom of the cusp of the PV has not been described in detail. In the present study, by using pulmonary arteriography and/or ventriculography, VAs with a PSC location were noted in 24 (11%) of 218 idiopathic outflow tract–like VAs treated by using RFCA (Central Illustration). The low incidence of PSC-VAs reported in previous studies may be due mainly to unawareness of ablation in the PSC without angiography or intracardiac echocardiography, especially for LC-VAs. Less commonly, standard ventriculography may not accurately reflect the relationship of the catheter position to the valve. In addition, small sample sizes could account for the low prevalence of PSC-VAs in previous reports. Conversely, the high incidence of PSA-VAs in our study may be an overestimation in real practice because most of these subjects were admitted to our center for complex arrhythmia ablation or for previously failed ablation elsewhere. Furthermore, the VAs were not induced by programmed stimulation in any patient, strongly suggesting a mechanism most likely due to automaticity from the myocardium with the PSC.
Mapping and RFCA within PSC
It has been reported that VAs can be successfully ablated in the PA (8–10,19). Similar to interruption conduction in an atrioventricular accessory pathway, PA-VAs could theoretically be successfully abolished by targeting the origin in the PA, the preferential conduction pathway, or the insertion into the RVOT. However, the proximal portion of the myocardial extension and its attachment with RV myocardium may be wide and bifurcated, resembling the breakthrough from the myocardial sleeves with the pulmonary veins (10,20). During arrhythmia, activation originating from the PSC would have conducted to the RVOT through the myocardial extensions and could lead to a change in QRS morphology due to the conduction block over the myocardial extension’s breakthrough and conduction property. In addition, this special anatomic structure may be responsible for detouring the activation impulse during RF delivery in the RVOT, as observed in 3 patients. Consequently, most of the successful ablation sites were at the distal and narrow portions of the myocardial extension or at the PA-VAs origin.
Discrete potentials noted within the great artery, representing myocardial extensions into the PA, were useful in guiding ablation of PA-VAs (8,10,16). In the present study, all VAs were successfully ablated in the PSC. The ablation target was only identified by the earliest ventricular activation, which preceded the QRS onset by 28.2 ± 2.9 ms with simultaneous activation in bipolar and unipolar recordings. The local electrograms at the successful site in the PSC-VAs in these 24 patients differ from those in VAs from ASC, which present with the earliest activation as isolated presystolic potentials and a mismatched timing in bipolar and unipolar recordings in most patients with VA from the left coronary sinus cusp (2,4–6). In all 24 patients, 2 components at the earliest activation site during VAs were demonstrated, and the first potential during VAs was recorded after the ventricular electrograms during SR before and after ablation. Pace mapping could be performed at the earliest activation site in all patients without high output; a good pace map was obtained at that site in 20 patients. However, no discrete potential was recorded in any patient at the earliest activation site in the RVOT, and initial ablation there failed to abolish the clinical VAs in the first 7 patients but resulted in small QRS morphological changes. Furthermore, mapping at the PSC can be facilitated with a reversed U curve, which was always supported with a long sheath in the right ventricle.
However, the high number of irrigated RF applications and the relatively short activation time of local electrogram-to-QRS onset of 28.2 ± 2.9 ms in our series was different from mapping and ablation results of VA from the ASC. This phenomenon may be explained by several factors: 1) it has a clear learning curve, and it remains challenging to position D-curve catheter tips with a reversed U curve in the PSC; 2) precise catheter tip movement in individual PSCs was sometimes difficult by clockwise/counterclockwise-rotated manipulation of the mapping catheter, which may lead to some tiny areas inaccessible in the PSC; and 3) while mapping and ablation found that the VAs were located at the PSC nadir in most of our patients, the origin from RVOT close to the PSC cannot be totally excluded in some patients (although irrigated RF energy at RVOT failed to abolish VAs in our initial 7 patients). Based on these results, we speculate that the arrhythmogenic foci in the present study may be within or near the PSC (13). During VAs, conduction propagates through preferential conduction pathways and exits from the distal RVOT.
Catheter ablation within the PSC carries the potential risk of PA stenosis and damage to the left main coronary artery (21,22). However, these complications were not reported in previous studies or in our study. This outcome may be due mostly to the larger vessel and more connective tissue compared with the pulmonary veins (11). In addition, better contact with effective energy delivery within the PSC by curving the ablation catheter to form a reversed U curve may be another potential factor. Accordingly, careful attention should be paid to power and impedance characteristics to avoid steam pop during RF delivery.
Several studies have attempted to describe ECG criteria to identify the successful ablation site in the PA. Sekiguchi et al. (9) reported that the R-wave amplitude in the inferior ECG leads, the aVL/aVR ratio of the Q-wave amplitude, and the R/S ratio in lead V2 were statistically larger in PA-VAs than in RVOT-VAs. Other previous reports demonstrated no such specific ECG findings for PA-VAs (8,10). The discrepancy might be explained because, in the study by Sekiguchi et al., 92% of PA-VAs were located in the LC, which is located most superiorly in the right ventricle and more leftward and more anteriorly, eventually resulting in higher inferior lead R-wave amplitudes, a larger aVL/aVR ratio of Q-wave amplitude, and a larger R/S ratio in lead V2. In our study, all patients with LC-VAs had high inferior lead R-wave amplitudes, which is consistent with the findings of Sekiguchi et al. For the VAs with RC origin, the R-wave amplitudes were significantly smaller than those with LC-VAs but did not differ from the AC-VAs, except for lead II. The QRS duration was longer in the RC-VAs than in the AC-VAs and LC-VAs. In addition, QRS features (e.g., a small III/II ratio, the higher incidence of notch in the inferior leads) were similar to that in VAs below the pulmonary cusp (23). In addition, a recent study reported that VAs arising from the PV region had a relatively smaller R-wave (0.14 ± 0.16 mV) in lead I (24). The detailed location of peripulmonic valve VAs was not mentioned in their report. In the present study, a large R-wave in lead I was frequently observed in the RC-VAs; the R-wave amplitude (0.37 ± 0.17 mV) was significantly larger than in AC-VAs (–0.30 ± 0.31 mV) and LC-VAs (–0.03 ± 0.29 mV). These findings can be explained by the phased excitation from the RVOT free wall to the left ventricle in RC-VAs, during which the total QRS duration could be prolonged and the absolute R-wave magnitude decreased (25).
Because of product unavailability in China, intracardiac echocardiography was not used to identify catheter location. Instead, pulmonary arteriography and/or ventriculography was performed to determine the PV position and the relationship of the successful ablation site in the PA and the PV cusp. In addition, the distance measurement according to 3-dimensional mapping provided the best estimation in this study. Second, there was no evidence of structural abnormality on echocardiography and abnormal voltage and activation on 3-dimensional mapping during SR in these 24 patients. Diagnosis of RV cardiomyopathy is unlikely, although occult fibrosis may not be totally excluded without cardiac magnetic resonance imaging. Finally, comparison of ECG characteristics between the RVOT-VA and PSC-VA was not performed; further investigation is needed to determine whether some ECG characteristics can differentiate both VAs.
In patients with VA demonstrating LBBB morphology and inferior axis deviation, mapping in the RVOT may not identify the site of earliest activation and/or mismatched QRS morphology by pace mapping. In such patients with failed ablation, mapping at the PSC should be performed, as VAs arising from the PSC are not uncommon, and RC-VAs have unique ECG characteristics. These VAs can be successfully ablated with a reversed U curve within the PSC.
COMPETENCY IN PATIENT CARE AND PROCEDURAL SKILLS: In patients with VA that exhibit LBBB and inferior axis morphology, pace mapping in the RVOT may not identify the site of earliest activation or generate mismatched QRS morphology. In such patients, particularly when ablation has failed, mapping at the PSC should be performed to identify VAs that can be successfully ablated.
TRANSLATIONAL OUTLOOK: Larger studies are needed to determine the prevalence of VA arising from the PSC and establish the long-term efficacy of ablation at this site.
The authors thank Dr. Michael Shehata for his assistance.
For a supplemental figure, please see the online version of this article.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Z. Liao and Zhan contributed equally to this work.
- Abbreviations and Acronyms
- anterior cusp
- aortic sinus cusp
- left bundle branch block
- left cusp
- pulmonary artery
- pulmonary sinus cusp
- pulmonary valve
- premature ventricular contraction
- right cusp
- radiofrequency catheter ablation
- right ventricle
- right ventricular outflow tract
- sinus rhythm
- ventricular arrhythmia
- ventricular tachycardia
- Received July 14, 2015.
- Revision received September 23, 2015.
- Accepted September 24, 2015.
- 2015 American College of Cardiology Foundation
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