Author + information
- Received April 9, 2018
- Revision received August 13, 2018
- Accepted August 14, 2018
- Published online September 26, 2018.
- Jackson J. Liang, DO,
- Simon A. Castro, MD,
- Daniele Muser, MD,
- David F. Briceno, MD,
- Yasuhiro Shirai, MD,
- Andres Enriquez, MD,
- Ramanan Kumareswaran, MD,
- Pasquale Santangeli, MD, PhD,
- Erica S. Zado, PA-C,
- Jeffrey S. Arkles, MD,
- Robert D. Schaller, DO,
- Gregory E. Supple, MD,
- David S. Frankel, MD,
- Saman Nazarian, MD, PhD,
- Michael P. Riley, MD, PhD,
- Fermin C. Garcia, MD,
- David Lin, MD,
- Sanjay Dixit, MD,
- David J. Callans, MD and
- Francis E. Marchlinski, MD∗ ()
- Electrophysiology Section, Cardiovascular Division, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
- ↵∗Address for correspondence:
Dr. Francis E. Marchlinski, Electrophysiology Section, Cardiovascular Division, Hospital of the University of Pennsylvania, 9 Founders Pavilion, 3400 Spruce Street, Philadelphia, Pennsylvania 19104.
Objectives This study sought to investigate the substrate, procedural strategies, safety, and outcomes of catheter ablation (CA) for ventricular tachycardia (VT) in patients with aortic valve replacement (AVR).
Background VT ablation in patients with AVR is challenging, particularly when mapping and ablation in the periaortic region are necessary.
Methods We identified consecutive patients with mechanical, bioprosthetic, and transcatheter AVR who underwent CA for VT refractory to antiarrhythmic drugs and analyzed VT substrate, approach to LV access, complications, and long-term outcomes.
Results Overall, 29 patients (87% men, mean age 67.9 ± 9.8 years, left ventricular ejection fraction 39 ± 10%) with prior AVR (13 mechanical, 15 bioprosthetic, 1 transcatheter AVR) underwent 40 ablations from 2004 to 2016. Left-sided mapping/CA was performed in 27 patients (36 procedures). Access was retrograde aortic in 11 procedures (all bioprosthetic), transseptal in 24 (13 mechanical; 10 bioprosthetic; 1 transcatheter AVR), or transventricular septal in 1. Periaortic bipolar or unipolar scar was detected in all 24 patients in whom detailed periaortic mapping was performed. Clinical VT circuit(s) involved the periaortic region in 10 patients (34%), 2 (7%) had bundle branch re-entry VT, and 17 (59%) had substrate unrelated to AVR. There were 2 major complications (both related to vascular access). Only 2 patients (9.1%) had VT recurrence. Over median follow-up of 12.8 months, 11 patients died (none as a result of recurrent VT).
Conclusions Whereas most patients undergoing CA for VT after AVR had VT from substrate unrelated to AVR, periaortic scar is universally present and bundle branch re-entry can be the VT mechanism. CA can be safely performed with excellent long-term VT elimination.
Sustained monomorphic ventricular tachycardia (VT) occurs most commonly in patients with structurally abnormal hearts in the presence of scar due to prior myocardial infarction or nonischemic cardiomyopathy. Catheter ablation (CA) is an effective treatment option to eliminate VT and prevent implantable cardioverter-defibrillator (ICD) shocks. When VT occurs after valve surgery, the mechanism of VT (i.e., underlying ischemic cardiomyopathy and prior infarction or nonischemic cardiomyopathy) may be unrelated to aortic valve replacement (AVR). Additionally, VT can also originate from perivalvular substrate related to the prior AVR or due to bundle branch re-entry (BBR) VT. AVR-related VT has been reported to present in a bimodal manner—either immediately post-operatively or years later (1). Ablation in patients with prior AVR is feasible, but it may be technically complicated when access to the left ventricle (LV) is necessary, particularly when the VT substrate involves the periaortic region. Small series have reported on the safety and outcomes after VT ablation in patients, but data remain limited.
We report our institution’s experience with VT ablation in patients with prior AVR. Specifically, we describe patient characteristics, electrophysiologic findings including VT mechanism and underlying VT substrate, ablation techniques, and approach to LV access, safety, and long-term outcomes.
We screened our institution’s VT ablation database to identify all patients with prior AVR who were treated with VT ablation. Of the 3,367 VT and premature ventricular complex ablation procedures performed at the University of Pennsylvania between January 1, 2004 and December 31, 2015, we identified a total of 40 VT ablation procedures performed in 29 unique patients who had undergone prior AVR. Per institutional guidelines of the University of Pennsylvania Health System, all patients provided written informed consent both for CA and for their anonymized medical information to be included in research studies.
Electrophysiologic study, mapping, and ablation
For patients with mechanical AVR or those who were on warfarin for other reasons, warfarin was held and therapeutic unfractionated heparin infusion was initiated when the international normalized ratio became subtherapeutic, targeting a goal-activated partial thromboplastin time of 56 to 80 s. After providing informed consent, patients underwent electrophysiologic study and ablation in the post-absorptive state. When feasible, beta-blocker, calcium channel blocker, and antiarrhythmic medications were discontinued for at least 5 half-lives before the study, and intravenous antiarrhythmic drugs (AAD) were stopped 12 h before the procedure. Conscious sedation was utilized preferentially; general anesthesia was induced prior to obtaining epicardial access or when necessary for patient comfort or stability. In each case an 8-F AcuNav (Siemens Medical Solutions, Mountain View, California) or 10-F SoundStar (Biosense Webster, Diamond Bar, California) intracardiac echocardiography (ICE) probe was advanced into the right atrium and right ventricle to define anatomy, facilitate mapping, and assess contact during ablation. Electroanatomical mapping (Carto, Biosense Webster) was performed during sinus or paced rhythm to define areas of low voltage and abnormal electrograms consistent with scar (with bipolar and unipolar voltage cutoffs of <1.5 mV and <8.3 mV, respectively) (2,3). When assessing confluent bipolar and unipolar voltage regions based on amplitude (including for assessment of “periaortic” scar), we excluded areas <1.0 cm of the aortic and mitral valve annuli (as defined on ICE) from the measurement. The periaortic region was defined as being involved with VT in cases where abnormal electrograms and critical sites responsible for VT were identified in the periaortic region within 2 cm of the aortic valve annulus—either with activation or entrainment mapping when possible, or with substrate characterization including abnormal electrograms and concordant pace maps for unstable VT. Intravenous heparin was administered to maintain an activated clotting time above 300 s prior to LV access. In patients with a mechanical aortic valve, the valve was not crossed in a retrograde fashion to gain access to the LV endocardium for mapping. Otherwise, LV access was obtained either via transseptal, retrograde aortic, or transventricular septal approach, per the operator’s discretion. Long sheaths were occasionally used per the operator’s discretion in patients in whom a retrograde aortic approach was chosen, mainly to improve support to permit catheter manipulation and achieve stability during ablation within the LV.
Mapping and ablation of VT was performed as we have previously described (2–4). Briefly, when sustained VT was not present spontaneously or with catheter manipulation, programmed electrical stimulation or burst pacing from multiple sites and isoproterenol infusion (2 to 20 μg/min) were performed in an attempt to provoke ventricular arrhythmias. The mechanism of VT (re-entrant vs. automatic/triggered) was determined via pacing maneuvers during sustained VT. In the case of automatic/triggered VT, detailed activation mapping and pace-mapping were performed to approximate the site of origin. In patients with re-entrant VT, entrainment mapping and ablation was performed in our standard fashion as we have previously described targeting a goal of complete noninducibility of VT (4). Ablation in the LV was delivered using an open-irrigated 3.5-mm tip catheter (Navistar Thermocool; Biosense Webster) with power 30 to 45 W and temperature limit 42°C to achieve impedance drops of 10 to 15 Ω. During ablation in the periaortic region, power was generally set at 20 W to begin and titrated up to 40 to 45 W, targeting impedance drops of 10 to 15 Ω or 10% to 12%. Ablation of automatic/triggered VT was deemed successful with immediate suppression and in the absence of spontaneous/inducible premature ventricular complexes/VT after repeating the induction protocol with isoproterenol and/or ventricular pacing. A minimum of 60-min waiting period was observed after successful elimination of the ventricular arrhythmia. Ablation for re-entrant VT was considered successful when clinical VT was rendered noninducible after ablation. At the end of the case, arterial hemostasis was achieved using Perclose ProGlide closure device (Abbott Vascular, Santa Clara, California) or manual compression, and venous hemostasis was achieved with manual compression.
Following the procedure, patients were monitored on telemetry for recurrent VT. Heparin infusion was reinitiated with no bolus 4 h after hemostasis was achieved, and warfarin was typically restarted the day after the procedure. For patients in whom clinical VT was unable to be induced at the end of the ablation procedure and did not occur spontaneously post-ablation, noninvasive programmed stimulation (NIPS) was typically performed within several days of ablation (5). For patients in whom clinical or nonclinical VT was inducible at NIPS, repeat ablation, AAD adjustment, or ICD reprogramming was performed per physician’s discretion based on inducible VT information. The decision to continue, decrease, or discontinue AAD including amiodarone after ablation was left to the discretion of the physician and was based on the presumed likelihood of ablation success, as indexed by inducibility of clinical and nonclinical VT at the end of the procedure and at NIPS (4).
For patients who chose to follow-up at the Penn Arrhythmia Center, our routine practice is to arrange an outpatient follow-up appointment 6 weeks following ablation and then at 3- to 6-month intervals thereafter. For patients who chose to continue their clinical follow-up elsewhere, we attempted to contact either the patient or referring cardiologists at 6- to 12-month intervals and reviewed ICD interrogations to determine arrhythmia recurrence. For patients who were lost to follow-up from our institution before 2014, vital status was also assessed by querying the Social Security Death Index for mortality data available up to February 1, 2014.
Continuous variables were expressed as mean ± SD if normally distributed or median (interquartile range [IQR]: 25th, 75th percentile) if not normally distributed. All continuous variables were tested for normal distribution using the 1-sample Kolmogorov–Smirnov test. Categorical data were expressed as counts and percentages. Survival curves were generated by the Kaplan–Meier method. All the analyses were performed using IBM SPSS software (version 23.0; Armonk, New York).
Between 2004 and 2016, 29 patients (87% men, mean age 67.9 ± 9.8 years) with prior AVR underwent 40 VT ablation procedures. Baseline characteristics at time of VT ablation for all patients can be found in Table 1. A total of 10 patients (34%) had at least 1 prior failed VT ablation attempt before being referred to our center (range 1 to 4 prior failed attempts elsewhere). Over the entire study period, 7 patients (24%) underwent ≥2 ablation procedures at our institution (range 2 to 4 ablations: 2 procedures in 4 patients, 3 procedures in 2 patients, and 4 procedures in 1 patient). The type of AVR was mechanical AVR in 13, bioprosthetic AVR in 15, and transcatheter aortic valve replacement (TAVR) in 1. Mean LVEF was 40 ± 10% and 12 patients (41%) had LV ejection fraction ≤35%. Overall, there were 13 patients (45%) with only ischemic cardiomyopathy and a history of myocardial infarction, 10 patients (34%) with only nonischemic cardiomyopathy (1 with cardiac sarcoidosis diagnosed with cardiac magnetic resonance imaging and positron emission tomography, and 9 with idiopathic dilated or valvular cardiomyopathy), and 6 patients (21%) with mixed ischemic/nonischemic cardiomyopathy (with scar on imaging or voltage abnormalities on electroanatomical mapping in regions not related to prior known myocardial infarction). A total of 12 patients (41%) had prior coronary artery bypass graft surgery. An ICD and biventricular ICD were present in 24 patients (83%) and 10 (35%), respectively, at time of VT ablation. Twenty-seven patients (93%) had failed ≥1 AAD, 25 (86%) of whom had failed amiodarone. At the time of VT ablation, 25 (86%) were taking ≥1 AAD and 21 (72.4%) were taking amiodarone.
The first episode of sustained VT in 3 patients preceded the AVR surgery and these patients continued to have persistent VT after AVR for which VT ablation was performed. Meanwhile, in the remaining 26 patients, VT began after AVR surgery (median 65.5 months after AVR; IQR 11.5, 132.2 months). Median time interval between the last AVR surgery and first VT ablation procedure was 9.0 months (IQR: 2.7, 23.4 months). In 4 patients, VT ablation was performed within 7 days of the AVR surgery due to refractory VT in the post-operative setting.
Procedural characteristics can be found in Table 2. Conscious sedation only was used in 24 procedures (60%), whereas general anesthesia was used in 16 (40%). Left-sided mapping and/or ablation was performed in 27 patients (36 total procedures). Of these, access was obtained via a retrograde aortic approach in 11 procedures (31%) (all in patients with bioprosthetic AVR), transseptal in 24 (67%) (13 mechanical AVR; 10 bioprosthetic AVR; 1 TAVR), or transventricular septal in 1 (3%) in a patient with dual mechanical aortic and mitral valves (Figure 1). There was only 1 patient (with septal substrate) who had different LV access approaches at different ablation procedures. A transseptal approach was used at the first ablation, and a retrograde aortic approach was instead used at the second ablation procedure to facilitate simultaneous unipolar ablation from both sides of the septum. There were no cases in this series in whom simultaneous transseptal and retrograde accesses were obtained. There was 1 patient with a bioprosthetic AVR in whom the catheter could not be advanced through the aortic valve via a retrograde aortic approach, thus a transseptal approach was used instead. Patients had a mean 2.7 ± 2.0 spontaneous or inducible VT and mean cycle length was 423 ± 111 ms. Of the 11 patients in whom a retrograde aortic approach was utilized, 81-cm SL-1 sheaths (St. Jude Medical, St. Paul, Minnesota) were used in 3, 65-cm Arrow sheaths (Teleflex Inc., Wayne, Pennsylvania) was used in 2, a 21-cm Arrow sheath was used in 1, and short 11-cm Arrow sheaths were used in the remaining 6 cases.
Endocardial voltage mapping with adequate sampling density of the periaortic region (within 1 cm beneath the aortic valve) to identify the presence of scar was performed in 24 patients (82.8%). Periaortic bipolar or unipolar voltage abnormalities (using voltage cutoffs of <1.5 mV for bipolar and <8.3 mV for unipolar mapping) with abnormal electrograms extending beyond 1 cm from the aortic valve annulus were detected in all 24 of these patients (Figure 2). Bipolar periaortic voltage abnormalities were seen in 20 patients, whereas 4 additional patients had normal bipolar but abnormal unipolar voltages in the periaortic region. These periaortic voltage abnormalities persisted after lowering the unipolar voltage scar cutoff to <6.0 mV (6). In the remaining 5 patients, the clinical VT were unrelated to the periaortic region and the presence of periaortic scar could not be excluded due to inadequate sampling of the region. Clinical VT was felt to originate from or involve regions of periaortic scar in 13 patients, as confirmed by pace mapping and entrainment mapping (for re-entrant VT) or pace mapping and activation mapping (for automatic/triggered VT) (Figure 3).
Twenty-four patients had VT due to re-entry (myocardial re-entrant VT in 22, BBR VT only in 1, and both myocardial re-entrant VT and BBR VT in 1). Seven patients had VT due to triggered/automatic mechanism (successfully ablated from the periaortic LV in 3, aortic cusp region in 1, posteromedial papillary muscle in 1, anterolateral papillary muscle in 1, and apical septum in 1). Two patients had VT of both re-entrant and triggered/automatic mechanisms that were targeted. One patient underwent 3 ablations over the course of 30 months for 2 different VT mechanisms (BBR VT in the first 2 ablations and periaortic scar-related re-entrant VT in the third ablation). Of the 4 patients who underwent VT ablation within 7 days of AVR, 1 patient had atypical BBR VT and the other 3 patients had myocardial VT not originating from the periaortic region. Of the 10 patients with NICM, VT was targeted from the periaortic region in 7 (70%). VT was targeted from regions of prior infarction in all 13 patients with ICM. Of the 6 patients with mixed ICM/NICM, in 3 (50%), the VT substrate was related to prior infarction, whereas in the remaining 3, it was unrelated (basal septal substrate in 2, BBR VT in 1).
One patient underwent epicardial mapping and ablation during 1 of his procedures. In that patient, epicardial access was obtained using percutaneous subxiphoid puncture. Of note, due to prior cardiac surgery, the patient had surgical adhesions and there was difficulty in passing the guidewire freely in the epicardial space. As such, only the epicardial aspect of the septum and free wall of the LV to the superior and lateral margin were able to be mapped in this patient. Ablation was performed on the LV basal free wall 3 to 4 cm lateral to the left anterior descending artery.
Details about the procedural aspects of the VT ablation procedures are listed in Table 2. The median total procedure time was 360 (IQR: 206, 296) min and median fluoroscopy time was 52.4 (IQR: 31.9, 61) min. A median of 44 (IQR: 15.25, 64.5) radiofrequency lesions were delivered per procedure (median total radiofrequency ablation duration of 56.5 [IQR: 20.2, 71.0] min per procedure). At the end of the first ablation procedure, all 29 patients were noninducible for clinical VT, whereas 10 patients (34.5%) were inducible only for nonclinical VT at the end of the procedure. Overall (including repeat procedures), repeat induction was attempted after ablation in 37 procedures (92.5%). Of these, complete noninducibility was achieved acutely after 24 procedures and only nonclinical VT remained inducible at the end of the remaining 13 procedures. NIPS was performed after 16 of the ablation procedures (mean 2.6 ± 1.2 days post-ablation), and post-ablation NIPS showed no inducible VT in 7, inducible nonclinical VT only in 6, and inducible clinical VT in 3.
After last ablation, 21 patients (72.4%) were discharged on AAD, 16 (55.2%) of whom were discharged on amiodarone. Among the 21 patients who were taking amiodarone prior to last ablation, amiodarone dosage at time of discharge was either decreased or discontinued altogether in 13 (61.9%).
Follow-up data regarding VT recurrence status after hospital discharge post-ablation was available in 22 patients. Long-term freedom from recurrent VT was achieved in 16 patients (72.7%) after a single procedure. Meanwhile, allowing for multiple procedures, only 2 patients (9.1%) experienced VT recurrence after their last ablation (1,617 days and 177 days after last ablation). Figure 4 shows the Kaplan-Meier survival curve for VT recurrence after a single (Figure 4A) and multiple (Figure 4B) procedures. Vital status was able to be assessed in 26 patients, 11 (42.3%) of whom have died since their last ablation, as assessed by a combination of clinical medical records and querying of the Social Security Death Index, over a median follow-up duration of 12.8 (IQR: 2.2, 36.5) months for mortality. Cause of death was noncardiac in 1 patient, cardiac in 3, and unknown in the remaining 7. All 3 cardiac deaths were due to progressive heart failure rather than ventricular arrhythmias. Figure 4C shows the Kaplan-Meier survival curve for overall survival after last VT ablation. AAD use at last follow-up was able to be assessed in 24 patients. Of these, 15 (62.5%) remained on any AAD at last follow-up, 9 (37.5%) of whom remained on amiodarone.
All patients survived to hospital discharge after VT ablation. Overall, there were 2 (5%) major complications related to the ablation procedure, both of which were vascular access complications: right common iliac artery dissection in 1 patient (treated conservatively) and femoral pseudoaneurysm in another (requiring surgical repair). There were no cerebral or systemic noncerebral arterial embolic complications. Pre- and post-ablation transthoracic echocardiography showed no change in aortic valve function after ablation and no worsening of aortic regurgitation. Importantly, in cases where retrograde aortic access was attempted, careful intracardiac echocardiography assessment of aortic valve gradients and degree of regurgitation with color flow Doppler was performed immediately before retrograde access and at the end of the procedure to ensure no change in aortic valve function or worsening of aortic regurgitation.
The major findings of our study is that in patients with prior AVR referred for VT ablation, ablation can be performed safely with excellent freedom from VT during long-term follow-up. Regarding the underlying substrate, the presence of abnormal electrograms in the periaortic region with bipolar or unipolar voltage abnormalities consistent with scar are universally present, but these regions of scar are not always related to the clinical VT circuits. In fact, in the majority of patients in our series, the VT substrate was usually unrelated to the AVR, such as scar from prior myocardial infarction or another underlying nonischemic process (i.e., cardiac sarcoidosis).
Substrate and VT mechanisms
Eckart et al. (1) previously reported mechanisms of VT in 20 patients with prior valve surgery, 12 of whom had prior AVR and 2 more with dual aortic and mitral valve surgery. In their study, the investigators excluded patients with prior myocardial infarction. They demonstrated that VT related to valve surgery presented in a bimodal manner—occurring either days post-surgery or years later. In their series, VT in 70% of patients was attributed to scar-related re-entry, whereas 10% had BBR VT. In their study (which included 3 patients with lone mitral valve surgery), 9 of 14 patients (64%) had periaortic bipolar scar, and only 8 of 14 patients had bipolar voltage abnormalities seen adjacent to the valve that had been operated on. Their results are slightly different than our experience, because we detected either bipolar or unipolar scar in all 24 patients who underwent detailed voltage mapping of the periaortic region—even among several patients whose VT was presumed to be unrelated to the prior AVR. In recent years, it has become well accepted that unipolar voltage mapping can be helpful in identifying mid-myocardial or epicardial substrate in patients without endocardial scar (3). Thus, our findings would suggest that aortic valve surgery can injure the myocardium in the left ventricular outflow tract (LVOT) resulting in electrophysiologic scar, which in rare cases can be the substrate for re-entrant VT. Nagashima et al. (7) have reported that in patients with VT from the LVOT in the absence of structural heart disease, the presence of abnormal, low-voltage electrograms in the periaortic region consistent with scar can be the underlying VT substrate. In their series, the inducibility of multiple VT morphologies suggested a re-entrant mechanism associated with periaortic scar. Interestingly, all 8 patients with multiple VT morphologies in whom ICE was used to define the aortic annulus in their study had evidence of periaortic scar (bipolar voltages <1.5 mV) at both 1.0 and 1.5 cm from the AV annulus, whereas periaortic bipolar voltages at these sites were >1.5 mV in the 2 patients with single VT morphologies as well as all patients with idiopathic premature ventricular complexes (7).
Access to the LV
CA of VT in patients with prior AVR can be technically difficult, especially in patients with periaortic VT substrate. In patients with mechanical AVR, retrograde aortic access is prohibited and a transseptal approach must be taken, as was previously described by Yamada et al. (8). Meanwhile, in the presence of bioprosthetic AVR or TAVR, it remains unclear whether retrograde aortic access is feasible and can be safely performed. Srivatsa et al. (9) recently reported a case of periaortic ventricular arrhythmias in a patient with prior TAVR that were successfully eliminated with ablation utilizing a retrograde aortic approach using the Stereotaxis magnetic navigational system (Stereotaxis Inc., St. Louis, Missouri). In our series, ablation was safely performed via transseptal access in patients with mechanical AVR and TAVR, whereas retrograde access was performed in several patients with bioprosthetic AVR without any evidence of acute damage to the valve or worsening of aortic regurgitation. There was only 1 patient with a bioprosthetic AVR in whom retrograde aortic access failed due to inability to cross the valve, and a transseptal approach was therefore necessary to access the LV. In another patient, the bioprosthetic AVR was unable to be crossed in the standard fashion (with the catheter tip looped), but the LV was able to be accessed retrogradely when the catheter tip was straightened and carefully passed directly through the aortic valve under ICE guidance. In 1 patient with dual mechanical aortic and mitral valves (“no-access LV”), access was successfully obtained via transventricular septal approach facilitated by a radiofrequency wire, as reported by Santangeli et al. (10).
The use of ICE allows for visualization of the aortic valve to assess for calcification as well as degree of aortic stenosis and insufficiency before the decision is made to access the LV via a retrograde versus transseptal approach. In cases where there is any concern about bioprosthetic valve function, a transseptal approach should be considered. In cases where retrograde access is pursued, ICE (including with CARTOSOUND; Biosense Webster) can aid in visualizing the aortic cusps to facilitate passage of the ablation catheter through the valve into the LV. Additionally, ICE can visualize the ascending aorta to assess for calcification and atheroma.
Mechanical hemodynamic support devices are often utilized in high-risk patients undergoing VT ablation, either prophylactically or as rescue therapy after acute hemodynamic decline (11–14). We did not use hemodynamic support devices in any procedures in this series. The presence of a mechanical aortic valve is an absolute contraindication for the use of the Impella (Abiomed, Danvers, Massachusetts) device, and whereas the uncomplicated use of Impella after bioprosthetic AVR has been reported, the safety of doing so remains unknown (15). For these patients, if mechanical hemodynamic support is felt to be appropriate, extracorporeal membrane oxygenation or TandemHeart (Cardiac Assist Inc., Pittsburgh, Pennsylvania) may be more suitable alternatives.
Safety and efficacy
When VT ablation was performed by experienced operators, under ICE guidance, it can be safely performed with low rates of serious complications. As previously reported to be the most common complication after VT ablation, vascular access complications comprised the only two major complications in our series (16). It is important to note that we did not attempt retrograde aortic access in any patients with mechanical AVR or TAVR. Theoretically, a retrograde aortic approach in patients with a bioprosthetic aortic valve could damage the valve leaflets and result in aortic regurgitation if not performed carefully. Thus, ablation and catheter manipulation across a bioprosthetic valve should always be done carefully under ICE guidance and operators should perform imaging with transthoracic echocardiogram and/or ICE both pre- and post-ablation to evaluate for iatrogenic aortic regurgitation or damage to the aortic valve apparatus. Furthermore, in no patients did we perform ablation in the aortic cusp region, so whether aortic cusp ablation in patients after AVR can be safely performed remains unclear.
Of note, Whitman et al. (17) recently reported high rates (58%) of new silent cerebral emboli detected on post-procedural brain magnetic resonance imaging in a small prospective series, including a 63% incidence of cerebral emboli in patients in whom a retrograde aortic approach was performed. Although we did not perform brain imaging before and after ablation in patients to rule out silent cerebral emboli, there were no clinically significant cerebrovascular or systemic noncerebral arterial emboli associated with any of the ablation procedures. Whereas the clinical significance and persistence of silent cerebral emboli detected shortly after the procedure remain unknown, we are unable to quantify the risk of such events in patients with AVR undergoing VT ablation, especially those with a bioprosthetic valve in whom a retrograde aortic approach is performed.
This was a retrospective, single-center study and is thus subject to bias. The procedures were performed by experienced operators at a high-volume VT ablation center, thus safety and efficacy outcomes may not be generalizable to less experienced centers. Our institution is a tertiary care referral center and due to concern for damaging the aortic valve in patients with prior AVR, many providers may consider CA to be a treatment of last resort in this patient population. Thus, these patients are frequently referred to us late in the course of their disease, which may affect likelihood of success with CA. Also, because we are a tertiary care center, many patients were referred urgently for their VT ablation and chose to follow-up after the procedure with their local providers. As such, long-term follow-up to assess for VT recurrence was unavailable for 7 patients after last ablation. We were unable to ascertain cause of death in 7 patients who were followed up elsewhere and are therefore unable to exclude whether their deaths were related to recurrent ventricular arrhythmias. Finally, in our series we identified 9 patients who had VT that we thought to be due to a triggered/automatic VT mechanism, in 3 of whom VT was successfully ablated from the periaortic region. As discussed previously (7), “idiopathic” VT from the LVOT in patients with structurally normal hearts has been demonstrated in some cases to actually originate from regions of periaortic scar and be due to reentrant mechanisms. Even though we were able to successfully eliminate VT with focal ablation in the LVOT region in all patients with triggered/automatic VT, we were unable to completely exclude micro–re-entry as the underlying VT mechanism.
In patients with prior AVR and symptomatic VT, catheter ablation is a safe and effective treatment option. A retrograde approach can be utilized safely under ICE guidance in patients with bioprosthetic AVR, whereas a transseptal approach is necessary in those with mechanical AVR. Although the majority of patients referred for VT ablation after AVR had VT from substrate unrelated to prior AVR, a significant percentage (41.4%) had VT involving periaortic substrate or BBR. Periaortic bipolar or unipolar scar was universally present in patients after AVR in patients with adequate periaortic sampling density. Catheter ablation can be safely performed in patients after AVR with excellent long-term VT elimination allowing for multiple ablations.
COMPETENCY IN MEDICAL KNOWLEDGE: In patients with AVR and VT who undergo CA, periaortic voltage abnormalities on electroanatomic mapping are universally present. The VT substrate can involve the periaortic region or be unrelated to prior AVR, and BBR can be the VT mechanism in some patients. CA can be safely performed with excellent long-term VT elimination. A retrograde approach can be utilized safely under ICE guidance in patients with bioprosthetic AVR, whereas a transseptal approach is necessary in those with mechanical AVR.
TRANSLATIONAL OUTLOOK: Larger series are necessary to confirm the safety and efficacy of VT ablation in patients after AVR and to further define the periaortic substrate in these patients. Further studies should also examine the safety and feasibility of nontraditional methods to achieve LV access, as in patients with mechanical mitral and aortic valves (“no-entry” LV).
Dr. Arkles provides consulting services to Biosense Webster. Dr. Nazarian provides consulting services to Siemens, Biosense Webster, and CardioSolv; and has received research grants from Biosense Webster and ImriCor. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Abbreviations and Acronyms
- antiarrhythmic drugs
- aortic valve replacement
- bundle branch re-entry
- catheter ablation
- implantable cardioverter-defibrillator
- intracardiac echocardiography
- interquartile range
- left ventricle
- left ventricular outflow tract
- noninvasive programmed stimulation
- transcatheter aortic valve replacement
- ventricular tachycardia
- Received April 9, 2018.
- Revision received August 13, 2018.
- Accepted August 14, 2018.
- 2018 American College of Cardiology Foundation
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