Author + information
- Received April 12, 2019
- Revision received April 29, 2019
- Accepted April 29, 2019
- Published online July 15, 2019.
- David F. Briceño, MDa,
- Andres Enriquez, MDb,
- Jackson J. Liang, DOa,
- Yasuhiro Shirai, MDa,
- Pasquale Santangeli, MD, PhDa,
- Gustavo Guandalini, MDa,
- Gregory E. Supple, MDa,
- Robert Schaller, DOa,
- Jeffrey Arkles, MDa,
- David S. Frankel, MDa,
- Carlos Tapias, MDc,
- Diego Rodriguez, MDc,
- Luis C. Saenz, MDc,
- David J. Callans, MDa,
- Francis Marchlinski, MDa and
- Fermin C. Garcia, MDa,c,∗ ()
- aElectrophysiology Section, Cardiovascular Division, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
- bFundación Cardioinfantil, Instituto de Cardiología, Centro Internacional de Arritmias Andrea Natale, Bogotá, Colombia
- cHeart Rhythm Service, Queen’s University, Kingston, Ontario, Canada
- ↵∗Address for correspondence:
Dr. Fermin C. Garcia, Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, 9 Founders Pavilion, 3400 Spruce Street, Philadelphia, Pennsylvania 19104.
Objectives This study describes the use of septal coronary venous mapping to facilitate substrate characterization and ablation of intramural septal ventricular arrhythmia (VA).
Background Intramural septal VA represents a challenge for substrate definition and catheter ablation.
Methods Between 2015 and 2018, 12 patients with structural heart disease, recurrent VA, and suspected intramural septal substrate underwent a septal coronary venous procedure in which mapping was performed by advancement of a wire into the septal perforator branches of the anterior interventricular vein. A total of 5 patients with idiopathic VA were also included as control subjects to compare substrate characteristics.
Results Patients were 63 ± 14 years of age, and 11 (92%) were men. Most patients with structural heart disease had nonischemic cardiomyopathy (83%). Six patients underwent ablation for premature ventricular contractions (PVC) and 6 for ventricular tachycardia. All patients had larger septal unipolar voltage abnormalities than bipolar voltage abnormalities (mean area 35.3 ± 16.8 cm2 vs. 10.7 ± 8.4 cm2, respectively; p = 0.01), Patients with idiopathic VA had normal voltage. Septal coronary venous mapping revealed low-voltage, fractionated, and multicomponent electrograms in sinus rhythm in all patients with substrate compared to that in patients with idiopathic VA (amplitude 0.9 ± 0.9 mV vs. 4.4 ± 3.7 mV, respectively; p = 0.007; and duration 147 ± 48 ms vs. 92 ± 10 ms, respectively; p = 0.03). Ablation targeted early activation, pace map match, and/or good entrainment sites from intraseptal recording. Over a mean follow-up of 339 ± 240 days, the PVC and insertable cardioverter-defibrillator therapies burden were significantly reduced (from a mean of 22 ± 11% to 4 ± 8%; p = 0.005; and a mean 5 ± 2 to 1 ± 1; p = 0.001, respectively). Most patients (80%) with idiopathic VA remained arrhythmia free.
Conclusions In patients with suspected intramural septal VA, mapping of the septal coronary veins may be helpful to characterize the arrhythmia substrate, identify ablation targets, and guide endocardial ablation.
Catheter ablation is an important therapeutic strategy for the management of ventricular arrhythmias (VA) (1). However, success varies and is often limited by imprecise substrate localization and arrhythmia mapping, specifically of septal VA in which intramural foci are protected deep from the endocardium (2). Isolated or predominant septal substrate for scar-related ventricular tachycardia (VT) represents a challenging clinical scenario in patients with nonischemic cardiomyopathy (NICM), often requiring the use of emergent technologies and experimental ablation approaches. Biventricular endocardial low-voltage zones extending from the basal septum (with or without patchy epicardial involvement) are characteristic of NICM in inferior or anterolateral substrates, but septal substrates may be purely intramural and best characterized by imaging (e.g., cardiac magnetic resonance [CMR] imaging) (2). Therefore, criteria to predict the presence of intramural VT substrate have been described, including septal unipolar voltage abnormalities and delayed transmural conduction time during septal pacing (2,3). Although mapping of the septal perforating branches of the coronary venous system has been previously described in limited numbers (4), direct assessment of the intramural septal substrate has not been described. The purpose of this study was to describe the use of septal coronary venous mapping to facilitate substrate characterization and ablation of intramural septal VA.
Consecutive patients with structural heart disease, recurrent sustained monomorphic ventricular tachycardia (VT), and premature ventricular contractions (PVC) who underwent catheter ablation at the Hospital of the University of Pennsylvania between 2015 and 2018 were assessed. Of these patients, we selected all patients with suspected septal intramural substrate who underwent septal coronary venous mapping. Five patients with idiopathic VA who underwent intramural septal mapping were also included as control subjects to compare the intramural septal characteristics. Septal intramural substrate was suspected based on voltage map size (abnormal unipolar voltage in the presence of mostly normal bipolar voltage or unipolar voltage that was larger than bipolar voltage abnormalities at the septum) or CMR imaging or positron emission tomography (PET).
Episodes of spontaneous recurrent VT or PVC were documented in all patients either by 12-lead electrocardiography or from stored electrograms (EGMs) recorded by an insertable cardioverter-defibrillator (ICD). All patients underwent detailed electrophysiologic evaluation after providing written informed consent, in accordance with University of Pennsylvania Health institutional guidelines.
Electrocardiograms of the patients in sinus rhythm and of the clinical VT when available were collected and analyzed. All patients underwent transthoracic echocardiography to evaluate left ventricular (LV) systolic function, wall motion abnormalities, and to exclude LV thrombus. CMR and PET were performed to further define the arrhythmogenic substrate in selected patients.
Endocardial electroanatomic substrate mapping
After providing informed consent, patients underwent electrophysiologic study and ablation in the post-absorptive state under conscious sedation. When feasible, beta-blockers, calcium channel blockers, and antiarrhythmic medications were discontinued at least 5 half-lives before the study, and intravenous anti-arrhythmic therapy was stopped 12 h before the procedure. In each case, an 8-F (SoundStar, Biosense Webster, Diamond Bar, California) intracardiac echocardiography probe was advanced into the right atrium and right ventricle (RV) to define anatomy, facilitate mapping, and assess contact during ablation. The CARTOsound module (Biosense Webster) was used in every patient to create a detailed anatomic reconstruction of the RV and left ventricle (LV), with particular attention to the septum, valvular structures, and the outflow tract regions. After patients received heparin, endocardial LV and RV mapping was performed when appropriate. An electroanatomic map was created using the CARTO system (Biosense Webster) and projected onto the anatomical map created using intracardiac echocardiography. A 3.5-mm tip open irrigated catheter (ThermoCool SmartTouch, Biosense Webster) was used for mapping and ablation. Bipolar EGMs were filtered at 30 to 500 Hz, displayed at 100 mm/s sweep speed, and stored for off-line analysis. Unipolar EGMs were filtered at 1 to 240 Hz. Activation and voltage maps were created using point-by-point mapping during intrinsic atrioventricular conduction or paced rhythm. Acquired EGMs were reconstructed into 3-dimensional voltage maps and area measurements made with the incorporated CARTO software. Mapping density was sufficient to allow complete surface representation with a fill threshold of 15 mm. Normal bipolar endocardial EGM voltage was defined as a peak-to-peak amplitude ≥1.5 mV; “dense scar” was defined as ≤0.5 mV (5). Unipolar voltage mapping was used to further assess for intramural substrate. Abnormal unipolar voltage was defined as <8.3 mV for the LV and <5.5 mV for the RV (<5.5 mV for RV free wall; <7.5 mV for the septal aspect of the RV with adjustment to <6.0 mV over the posterior RV outflow tract opposite to the aortic root) (6,7). Transseptal activation times were not uniformly measured.
When PVCs or sustained VT were not present spontaneously, induction was attempted by using an isoproterenol infusion (2 to 20 μg/min), burst pacing, or programmed electrical stimulation from multiple sites. The mechanism of VT (re-entrant versus automatic or triggered) was determined through pacing maneuvers during sustained VT. In the case of PVCs or automatic or triggered VT, detailed activation mapping and pace mapping were performed to approximate the site of origin.
Septal coronary venous mapping
Coronary venous mapping was performed by advancing a medium-curl steerable 71-cm Agilis sheath (St. Jude Medical, Sylmar, California) over a long guidewire into the coronary sinus through the right femoral vein (Figure 1). The sheath was advanced over a wire to the great cardiac vein. Coronary venography was then performed through the Agilis sheath to delineate the coronary venous branches. A 3-F decapolar catheter was inserted through the Agilis sheath and advanced into the anterior interventricular vein (Map-iT catheter, Access Point Technologies EP, Rogers, Minnesota). Selective cannulation of the septal perforator branches was achieved by introducing a Glidecath hydrophilic coated catheter (Terumo, Somerset, New Jersey) inside the Agilis sheath to guide the mapping guidewire. Activation and pace mapping from the selected septal perforator branch was performed along the depth of the branch to identify the best site, advancing a 0.014-inch VisionWire guidewire (Biotronik SE and Co. KG, Berlin, Germany) with its proximal end connected to an alligator clip in a unipolar configuration and the skin serving as the reference electrode (filtered at 30 to 150 Hz). This guidewire is insulated, 175 cm long, with a 15-mm noncoated straight and flexible tip, and a 40-mm noncoated end to allow recording from the tip. EGM characteristics were analyzed, and activation and pace maps were obtained.
Criteria to suspect intramural septal ventricular arrhythmia
After the adjacent structures of the LV outflow tract were mapped (anterior RV outflow tract, aortic cusps, subaortic area, endocardium opposite to the LV summit, and anterior mitral valve), the coronary venous septum was mapped when any of the following criteria suggested intramural “origin”:
1) Activation mapping showed isochronal (equally early or within 10 ms) local activation times in multiple anatomical sites without identification of an earlier site;
2) Best pace mapping intraseptally in cases in which the activation time was isochronic with other adjacent structures (but earlier than the great cardiac vein-anterior interventricular vein);
3) Absence of pre-systolic EGMs or concealed entrainment with return cycle within 30 ms from the tachycardia cycle length from adjacent structures of the LV outflow tract;
4) Failed ablation attempts from those adjacent structures.
Septal unipolar electrogram definitions
EGM analysis was performed by previously described methods and adapted to unipolar recordings (8). EGM amplitude (in millivolts) was defined as the peak-to-peak deflection measured in the 10-mm variable gain unipolar EGM. EGM duration (in milliseconds) was defined as the time from the earliest electrical activity that deviated from a stable baseline to the onset of the amplification signal decay artifact (an artifact caused by electronic decay of an amplified filtered signal) measured in the 10-mm fixed-gain unipolar EGM. The EGMs that were the most abnormal were defined as fractionated and were characterized by low-amplitude, high-frequency multicomponents of prolonged duration compared to a reference group of patients with idiopathic VA (see discussion later). All intracardiac recordings were displayed in the CardioLab IT Electrophysiology Recording System (General Electric, Boston, Massachusetts). EGMs were analyzed by using the same measuring scale (1/16) in the CardioLab recording system.
EGMs of patients with intramural septal substrate were compared to EGMs obtained from patients with idiopathic VA who underwent intramural mapping using the same septal coronary venous septal mapping technique described earlier. EGM characteristics (amplitude, duration, and fractionation) were compared between both groups.
Ablation was delivered using an open-irrigated 3.5-mm tip catheter (Thermocool SmartTouch, Biosense Webster) with a power of 20 to 50 W and a temperature limit of 42°C to achieve impedance drops of 10 to 15 Ω.
Radiofrequency energy application was sequentially attempted from the adjacent structures and aimed toward the region of interest previously identified in the intramural septum (earliest activation, best pace map, mid-diastolic activity, or VT isthmus), showing any of the described criteria supporting intramural “origin” of the mapped VA. The septal coronary venous guidewire was used as a fluoroscopic anatomic landmark to target these sites.
Ablation of automatic or triggered VT was deemed successful with immediate suppression and in the absence of spontaneous or inducible PVCs and VT episodes after repeating the induction protocol with isoproterenol and ventricular pacing. A minimum 60-min waiting period was observed after successful elimination of the VA. Ablation for re-entrant VTs was considered successful when the targeted VTs were rendered noninducible after ablation.
Following the procedure, patients were monitored using telemetry for recurrent VTs. For patients who had clinical VT was unable to be induced at the end of the ablation procedure and did not recur spontaneously after ablation, noninvasive programmed stimulation (NIPS) was typically performed within 1 to 3 days of ablation. For patients who had clinical or nonclinical VT was inducible at NIPS, repeat ablation, adjustment of antiarrhythmic drug therapy, or reprogramming of the ICD was performed according to the discretion of the physician and patient. The decision to continue, decrease, or discontinue antiarrhythmic drug therapy, 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.
For patients who chose to follow-up at the Penn Arrhythmia Center, outpatient appointments were conducted 6 weeks after ablation and then at 3- to 6-month intervals thereafter. For patients who chose to continue their clinical follow-up elsewhere, we contacted both the patient and the referring cardiologist at 6- to 12-month intervals and reviewed ICD interrogations to determine arrhythmia recurrence.
Continuous variables are expressed as mean ± SD and were compared by using Student’s t-tests. Categorical variables were expressed as frequencies and were compared using chi-square tests. Arrhythmia burdens (pre- and post-ablation) were compared by using a Student’s paired t-test. A p value <0.05 was considered statistically significant. Data were analyzed by using Stata version 12.1 software (Stata Corp., College Station, Texas).
A total of 12 patients with structural heart disease, septal VA, and suspected intramural substrate underwent septal coronary venous mapping at the Hospital of the University of Pennsylvania between January 2015 and May 2018. Baseline characteristics of all the patients are listed in Table 1. Mean age was 63 ± 14 years, and 11 patients (92%) were males. Mean LV ejection fraction was 37 ± 10%. Most patients had NICM (10 of 12 patients [83%]). The other 2 patients had ischemic cardiomyopathy. Six patients underwent ablation for PVCs and 6 for VT episodes. Six patients had previously undergone at least 1 ablation (range 1 to 2). Of these 6 patients, 1 had a prior ablation guided by septal coronary venous mapping. Antiarrhythmic drug therapy failed in all patients.
Five patients underwent pre-procedure imaging for further substrate characterization. CMR was available in 3 patients and revealed septal late gadolinium enhancement in 2 of them. Another 2 patients underwent PET scanning, which showed increased radiotracer uptake involving the septal wall in both cases.
Five consecutive patients with idiopathic VA who underwent septal intramural mapping were included (Table 1) as a comparison group. These patients were younger and had a higher LV ejection fraction than the patients with septal substrate. Two of the younger patients had CMR results that ruled out septal abnormalities. Three patients underwent ablation for PVCs and 2 for VTs. One patient had 2 prior ablations attempts.
Most patients with septal substrate had more than 1 VT or PVC morphology (67%). The mean number of morphologies was 1.7 ± 2.6. The predominant morphology was left bundle branch block (LBBB) with an inferior axis and a transition ≥V3. LBBB was present in 9 of 12 patients (75%) and RBBB in 3 patients (25%). Left axis was seen in 6 patients (50%). Most patients had a midline pattern with biphasic I, aVR, and aVL, or positive in I and more negative in aVL than in aVR.
Among the patients with idiopathic VA, only 1 had more than 1 VA morphology. The predominant morphology was LBBB with an inferior axis and an early transition ≤V2. RBBB was present in 3 of 5 patients (60%). Left axis was seen in 4 patients (80%). Most patients had a pattern more negative in aVL than in aVR.
Conscious sedation was used in all patients. Right- and left-sided mapping or ablation was performed in 10 patients (83%). For left-sided mapping and ablation, access was obtained through a retrograde aortic approach in 8 patients (67%), whereas the other 4 patients (33%) required a combination of trans-septal and retrograde approaches.
Contact force-based endocardial voltage mapping with adequate sampling density of the septal right and left ventricles was performed in all patients. Septal bipolar voltage was normal in 7 patients (58%), whereas 5 patients had small bipolar voltage abnormalities. All patients had moderate to large septal unipolar voltage abnormalities (mean bipolar voltage area was 10.7 ± 8.4 cm2 vs. 35.3 ± 16.8 cm2 unipolar voltage area, respectively; p = 0.01). The septal voltage map (bipolar and unipolar) of patients with idiopathic VA was normal.
All patients underwent detailed mapping of the coronary venous system as described earlier. Septal intramural activation was consistently early compared to that in the LV endocardium (mean 29 ± 12 ms pre-VA intramural vs. 17 ± 9 ms pre-VA LV endocardium, respectively; p = 0.009) and RV endocardium (mean 29 ± 12 ms pre-VA intramural vs. 8 ± 3 ms pre-VA RV endocardium, respectively; p = 0.0001). The pace maps with the best match to the clinical arrhythmia were always obtained within the intramural septum compared to that in the endocardium. In patients with VT, critical components of the circuits were also identified in the intramural septum based on intraseptal mid-diastolic activity and entrainment mapping. Entrainment mapping was feasible in 3 patients, and criteria for VT isthmus were demonstrated in 2 patients (Online Figure 1). Activation was explored across the length of the septal branch mapped to identify the best possible activation site and pace maps (more basal vs. more apical), to help guide the ablation targets (Online Figure 1). One patient had only occasional PVCs on the day of the procedure, but PVCs were triggered by intraseptal burst pacing (Online Figure 2).
Septal substrate characteristics
The intramural septal EGMs in patients with idiopathic VA had no fractionation. Recordings in these patients had rapid deflections and distinct components. In contrast, the intramural recordings in sinus rhythm in all patients with septal substrate were characterized by low amplitude and fractionated and multicomponent EGMs (Figure 2, Central Illustration).
Quantitative analysis of the EGMs in patients without septal substrate showed that mean EGM amplitude was 4.4 ± 3.7 mV and that 95% of the EGMs had an amplitude of 0.7 mV or greater. Mean EGM duration was 92 ± 10 ms; duration in 95% of the EGMs was 100 ms or less.
In patients with septal substrate, these EGMs exhibited significantly lower amplitude (0.9 ± 0.9 mV vs. 4.4 ± 3.7 mV, respectively; p = 0.007) and longer duration (147 ± 48 ms vs. 92 ± 10 ms, respectively; p = 0.03).
Most patients required extensive ablation from both the left and right endocardial septal surfaces (10 of 12 patients [83%]) targeting opposite areas of interest previously identified by intramural mapping (earliest activation, best pace maps, mid-diastolic activity during VT or documented VT isthmus) (Figure 3). In 4 patients (3 with VT and 1 with PVC) who had extensive septal ablation required from both ventricles, loss of capture from the septal coronary venous mapping guidewire was observed during ablation (Online Figure 2). This finding correlated with arrhythmia noninducibility.
Compared to patients with idiopathic VA, procedure and fluoroscopy times were similar (mean 431 ± 149 min vs. 340 ± 61 min, respectively; p = 0.09; 56 ± 34 min vs. 33 ± 19 min, respectively; p = 0.08); however, radiofrequency times were significantly longer in patients with septal substrate (mean 54 ± 33 min vs. 23 ± 12 min, respectively; p = 0.02).
Acute and long-term arrhythmia recurrence: Septal substrate
Among the 6 patients with PVCs, PVC was completely eliminated in 4 at the end of the procedure (67%), 1 had a reduction in PVC burden, and the other had no change in PVC burden. Two of the 6 patients with VT remained inducible for the clinical VT at the end of the procedure, whereas the clinical VT was eliminated in the other 4 patients.
Detailed follow-up information was available in all 12 patients. Over a mean follow-up of 339 ± 240 days, 8 patients (67%) were free of arrhythmia episodes. Among the patients with PVCs, the PVC burden was significantly reduced (mean 22 ± 11% to 4 ± 8%, respectively; p = 0.005). Similarly, in patients with VT, the number of ICD therapies (composite of antitachycardia pacing and shocks) was also significantly reduced (mean therapies 5 ± 2 to 1 ± 1; p = 0.001) (Figure 4). The 4 patients with loss of capture from the septal wire have remained free of arrhythmia episodes.
Patients with idiopathic conditions
Among the 5 patients, 4 had complete elimination of VA at the end of the procedure (80%). Detailed follow-up information was available in all 5 patients. Over a mean follow-up of 201 ± 264 days, 4 patients (80%) were free of arrhythmia episodes.
Electrophysiological characterization and ablation techniques
One of the major limitations of VT ablation is often the incomplete delineation of arrhythmogenic substrate, particularly the septum, and better mapping techniques may improve outcomes in these patients. This study provides more understanding of the intramural septal substrate. It was found that, in patients with suspected intramural septal VA, coronary venous mapping of the septal perforator branches using a unipolar guidewire may be helpful to better characterize this substrate by direct recordings. It was also found that abnormal EGMs in sinus rhythm are a hallmark of patients with intramural septal substrate, even when bipolar endocardial voltage is normal. These signals are characterized by fractionated, multicomponent, and low-voltage EGMs.
This mapping strategy facilitated the formulation of an ablation approach that targeted areas of septal interest from the adjacent endocardium. In all patients, intramural activation and pace maps were better than adjacent endocardial and epicardial sites. In addition, critical components of the VT isthmus were demonstrated in the intramural septum. The use of septal coronary venous mapping allowed for successful ablation in this complicated series of patients who had multiple prior ablations had failed. Similar short-term and long-term outcomes were seen in patients with septal intramural idiopathic VA.
Our group previously described the characteristics of patients with NICM who have an isolated septal substrate for VT (2). These patients represent almost 12% of NICM patients undergoing catheter ablation for VT and may have an exclusively intramural substrate deep within the interventricular septum that was until now evident only by indirect evaluation based on imaging, unipolar voltage mapping, or trans-septal activation (9). The long-term recurrence of arrhythmia after ablation is typically high in these patients, likely related to the presence of deep intramural substrate. In our previous report (2), VT recurred in 10 of 31 patients (32%) over a mean follow-up of 20 ± 28 months. As such, multiple procedures may be required in this patient population in order to achieve lasting VT elimination. Similar to the findings in the present study, those in the study by Yokokawa et al. (4) showed that idiopathic septal ventricular arrhythmia episodes can originate from intramural foci. They showed that activation mapping from within perforating branches in the interventricular septum can help localize the site of origin of intramural septal arrhythmias and suggested that ablation within the septum or from both sites of the septum may be required to eliminate the targeted arrhythmia.
In patients with septal substrate, VT recurrence is usually related to the technical limitations of delivering effective radiofrequency energy in this area, with incomplete or nontransmural lesion formation. Therefore, multiple bailout approaches have been described. Kreidieh et al. (10) reported 7 patients who underwent retrograde coronary venous ethanol ablation. Coronary venous mapping was performed targeting veins with early pre-systolic potentials and pace maps matching VT and PVCs. The clinical VT was successfully ablated acutely in all patients. Sapp et al. (11) described the use of intramyocardial infusion-needle catheter ablation for control of VTs that had been refractory to conventional catheter ablation therapy. More recently, Nguyen et al. (12) described their experience with ablation using a half-normal saline to target 94 patients with PVC and VT refractory to standard ablation, achieving immediate success in 78 of 94 patients (83%). They demonstrated that the use of a half-normal saline instead of a normal saline irrigant during high-power delivery targeting deep myocardial substrate was safe and effective. Other strategies, such as bipolar ablation, simultaneous unipolar ablation, transcoronary radiofrequency, and ethanol ablation or combinations of multiple strategies, have been described in cases when endocardial and epicardial ablation failed or a deep intramural substrate was likely, showing improvement in arrhythmia control (13–17). The present report also describes a strategy that may facilitate targeting these arrhythmias and potentially improve outcomes: the use of direct intramural mapping identifying critical VT circuits, local EGM characteristics consistent with VT substrate, early activation, and best pace maps to guide an anatomical ablation targeting opposing endocardial sites.
Generally, one must consider that, despite the added benefit of more detailed mapping, these adjunctive techniques (i.e., coronary venous mapping, alcohol ablation, intracoronary radiofrequency, needle ablation) are typically not necessary to achieve success in most patients; however, incorporating some of them may augment immediate and long-term success in certain patients.
Conventionally, acute ablation success has been assessed by the response to programmed stimulation at the end of the procedure; noninducibility represents a classic endpoint for VT ablation and the only endorsed endpoint by current practice guidelines (18). Despite this, with the evolution and dissemination of substrate-based ablation approaches, other procedural endpoints have been described to validate different ablation strategies (19). Herein, we also describe an ablation endpoint for patients with intramural septal VA. Septal wire noncapture after septal substrate modification is a feasible endpoint associated with acute procedural success. Further studies are needed to determine the short-term and long-term implications of this strategy. Interestingly, similar ablation endpoints for VT have been previously described. Di Biase et al. (20) used noncapture from the ablated area to determine whether the substrate was successfully homogenized. They showed increased VT free survival when this endpoint was achieved. Subsequently, our group reported that isolating the core of the VT substrate (the dense scar [<0.5 mV] region incorporating putative isthmus and early exit sites) may improve long-term VT-free survival (21).
Induction of arrhythmia
Successful activation mapping requires spontaneous presence of or ability to induce the clinical VA during the electrophysiology study. Therefore, stimulation protocols are typically used for arrhythmia induction. A potential additional use of the septal wire is arrhythmia induction, as seen in 1 of the patients, who had intraseptal burst pacing successfully induced PVCs, facilitating activation mapping, and was ultimately used as an ablation endpoint to prove noninducibility.
This study was a retrospective analysis of a small series of patients, with relatively limited follow-up in some patients (<1 year). The technique itself has several challenges and requires skilled and experienced operators, specific tools for vein cannulation, and suitable septal coronary venous branches. The substrate characterization is limited for some patients. In addition, many patients had previous ablations, which might have modified the EGM characteristics seen during septal mapping. VT circuits were defined using activation and pace mapping in most of the cases (only a minority were mappable with entrainment), and this might have led to inaccurate localization. Despite mapping the intramural space, extensive ablation was still required to successfully treat these patients, which could be related to the limitations of radiofrequency energy to successfully penetrate deeper tissue but could also be related to the limitations of unipolar mapping and anatomical restrictions. As such, it is important to mention the expected limitations of unipolar mapping to define activation, especially in scarred tissue with anisotropic effects because unipolar recordings are affected by far-field activation. Therefore, further studies to explore other ways to record inside the intramural space (e.g., advancing 2 wires and recording in bipolar configuration from both tips, and better wire technology) are needed. In addition, the anatomical limitations of wire mapping through septal perforator veins to identify the site of origin or critical part of the circuit are a major challenge. However, presently, this is the best method available for direct substrate assessment.
In patients with suspected intramural septal VA, mapping of the septal perforator branches of the coronary venous system using a unipolar guidewire may be helpful to characterize the arrhythmia substrate, identify ablation targets, and guide ablation from the adjacent endocardium.
COMPETENCY IN MEDICAL KNOWLEDGE 1: Abnormal electrograms of patients in sinus rhythm are a hallmark of intramural septal ventricular arrhythmia substrate even when bipolar endocardial voltage is normal. These signals are characterized by fractionated, multicomponent, and low-voltage electrograms.
COMPETENCY IN MEDICAL KNOWLEDGE 2: In patients with suspected intramural septal ventricular arrhythmias, mapping of the septal perforator branches of the coronary venous system using a unipolar guidewire may be helpful to guide ablation.
TRANSLATIONAL OUTLOOK 1: Further studies are needed to improve the tools for detailed direct characterization of the intramural space.
TRANSLATIONAL OUTLOOK 2: Considering the need for extensive ablation to successfully treat patients with intramural septal ventricular arrhythmias, continued development of different ablation strategies is a priority.
Supported in part by the Winkelman Family Fund in Cardiovascular Innovation. The 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
- cardiac magnetic resonance
- left bundle branch block
- left ventricle/ventricular
- nonischemic cardiomyopathy
- noninvasive programmed stimulation
- positron emission tomography
- premature ventricular contractions
- left bundle branch block
- right ventricle/ventricular
- ventricular arrhythmia
- ventricular tachycardia
- Received April 12, 2019.
- Revision received April 29, 2019.
- Accepted April 29, 2019.
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