Use of three-dimensional electroanatomic mapping for epicardial access: needle tracking, electrographic characteristics, and clinical application.

AIMS: Pericardiocentesis is usually completed under fluoroscopy. The electroanatomic mapping (EAM) system allows visualizing puncture needle tip (NT) while displaying the electrogram recorded from NT, making it possible to obtain epicardial access (EA) independent of fluoroscopy. This study was designed to establish and validate a technique by which EA is obtained under guidance of three-dimensional (3D) EAM combined with NT electrogram. METHODS AND RESULTS: 3D shell of the heart was generated, and the NT was made trackable in the EAM system. Unipolar NT electrogram was continuously monitored. Penetration into pericardial sac was determined by an increase in NT potential amplitude and an injury current. A long guidewire of which the tip was also visible in the EAM system was advanced to confirm EA. Epicardial access was successfully obtained without complication in 13 pigs and 22 patients. In the animals, NT potential amplitude was 3.2 ± 1.0 mV when it was located in mediastinum, 5.2 ± 1.6 mV when in contact with fibrous pericardium, and 9.8 ± 2.8 mV after penetrating into pericardial sac (all P ≤ 0.001). In human subjects, it measured 1.54 ± 0.40 mV, 3.61 ± 1.08 mV, and 7.15 ± 2.88 mV, respectively (all P < 0.001). Fluoroscopy time decreased in every 4-5 cases (64 ± 15, 23 ± 17, and 0 s for animals 1-4, 5-8, 9-13, respectively, P = 0.01; 44 ± 23, 31 ± 18, 4±7 s for patients 1-7, 8-14, 15-22, respectively, P < 0.001). In five pigs and seven patients, EA was obtained without X-ray exposure. CONCLUSION: By tracking NT in the 3D EAM system and continuously monitoring the NT electrogram, it is feasible and safe to obtain EA with minimum or no fluoroscopic guidance.

Biatrial arrhythmogenic substrate in patients with hypertrophic obstructive cardiomyopathy.

BACKGROUND: Atrial fibrillation (AF) in patients with hypertrophic obstructive cardiomyopathy (HOCM) may be caused by a primary atrial myopathy. Whether HOCM-related atrial myopathy affects mainly electrophysiological properties of the left atrium (LA) or also the right atrium (RA) has never been investigated. OBJECTIVE: The purpose of this study was to characterize atrial conduction and explore differences in the prevalence of conduction disorders, potential fractionation, and low-voltage areas (LVAs) between the RA and LA during sinus rhythm (SR) as indicators of potential arrhythmogenic areas. METHODS: Intraoperative epicardial mapping of both atria during SR was performed in 15 HOCM patients (age 50 ± 12 years). Conduction delay (CD) and conductin block (CB), unipolar potential characteristics (voltages, fractionation), and LVA were quantified. RESULTS: Conduction disorders and LVA were found scattered throughout both atria in all patients and did not differ between the RA and LA (CD: 2.9% [1.9%-3.6%] vs 2.6% [2.1%-6.4%], P = .541; CB: 1.7% [0.9%-3.1%] vs 1.5% [0.5%-2.8%], P = .600; LVA: 4.7% [1.6%-7.7%] vs 2.9% [2.1%-7.1%], P = .793). Compared to the RA, unipolar voltages of single potentials (SPs) and fractionated potentials (FPs) were higher in the LA (SP: P75 7.3 mV vs 10.9 mV; FP: P75 2.0 mV vs 3.7 mV). FP contained low-voltage components in only 18% of all LA sites compared to 36% of all RA sites. CONCLUSION: In patients with HOCM, conduction disorders, LVA, and FP are equally present in both atria, supporting the hypothesis of a primary atrial myopathy. Conceptually, the presence of a biatrial substrate and high-voltage FP may contribute to failure of ablative therapy of atrial tachyarrhythmias in this population.

Epicardial Ventricular Tachycardia Ablation: Patient Selection, Access, and Ablation Techniques and Strategies to Manage Complications.

Epicardial ventricular tachycardia ablation is an important treatment modality for refractory ventricular tachycardia. This comprehensive review guides clinicians through optimized strategies for improved procedural outcomes and patient safety during epicardial ventricular tachycardia ablation. Patient selection criteria, including cardiomyopathy type, electrocardiogram findings, and prior ablation history, are discussed. Detailed techniques for safe pericardial access are provided. Potential complications and strategies for prevention and management are explored. The review also addresses challenges and pitfalls of epicardial mapping and ablation.

Feasibility of Transatrial Access for Epicardial Ablation: Evaluation of 2 Different Techniques in Swine.

BACKGROUND: The subxiphoid pericardial access is technically difficult and has a considerable rate of complications, thus transatrial access may be an alternative. OBJECTIVES: This study sought to assess the feasibility and safety of this strategy regarding periprocedural period and after 1-week follow-up. METHODS: The investigators performed epicardial mapping through transatrial puncture in 20 swine. Animals were divided into group A, in which aspiration of the sheath was performed to maintain negative pressure after the withdraw of the catheters, and group B, in which a device (Konar-MF VSD Occluder) was delivered to occlude the right atrial appendage perforation. Bleeding was investigated immediately and 1 week after. RESULTS: Access was safe in 19 of 20 animals (95%) with small amount of bleeding (6.4 ± 6 mL). In group A (n = 10), 1 animal presented hemopericardium right after the puncture. In the other 9, epicardial ablation was performed and 60.0 ± 28.0 mL of blood was aspirated without events. After 1 week, fibrin-hemorrhagic pericarditis was identified in 3 animals. In group B (n = 10), reaching the epicardial surface was possible in all animals. An adequate position of the prosthesis was obtained in 90% (9 of 10). One death occurred in the immediate postoperative period, secondary to pneumothorax. After 1 week, postmortem analysis showed absence of pericardial bleeding and a normal-appearing pericardium in the 8 animals with adequate prosthesis position. CONCLUSIONS: Transatrial access allows epicardial mapping and ablation. Sheath removal after negative pressure contributes to achieving acute bleeding control but does not prevent its occurrence. The use of the device prevents bleeding and hemorrhagic pericarditis.

Dry suction water seal system for management of pericardial fluid during epicardial ablation.

INTRODUCTION: Epicardial ablation is an important approach in the management of patients with complex ventricular arrhythmias. Irrigated ablation catheters present a challenge in this potential space due to fluid accumulation that can cause hemodynamic compromise, requiring frequent manual fluid aspiration. In this series, we report our initial experience with the use of a dry suction water seal system for pericardial fluid management during epicardial ablation. METHODS: Consecutive patients undergoing epicardial ventricular tachycardia (VT) ablation at a single center were included. All patients underwent epicardial access via a subxiphoid approach with a single operator. A deflectable sheath was advanced into the pericardial space, and the side port was attached to a dry suction water seal system attached to wall suction at -20 mmHg. Procedural information including patient characteristics, outcomes, and adverse events. After a period of initial experience, pericardial fluid infusion and aspiration volumes were recorded. RESULTS: Eleven patients were included in this series. All patients underwent epicardial ablation with complete success achieved in 8 of the 11 patients and partial success in the remaining patients. Pericardial fluid intake ranging from 485 to 3050 mL with aspiration of 350-3050 mL using the dry suction water seal system. No adverse events occurred. CONCLUSION: Dry suction water seal drainage systems can provide a safe strategy for efficient pericardial fluid management during epicardial VT ablation, potentially shortening procedure duration.

High-density and high coverage composite mapping of repetitive atrial activation patterns.

BACKGROUND: Repetitive atrial activation patterns (RAAPs) during atrial fibrillation (AF) may be associated with localized mechanisms that maintain AF. Current electro-anatomical mapping systems are unsuitable for analyzing RAAPs due to the trade-off between spatial coverage and electrode density in clinical catheters. This work proposes a technique to overcome this trade-off by constructing composite maps from spatially overlapping sequential recordings. METHODS: High-density epicardial contact mapping was performed during open-chest surgery in goats (n=16, left and right atria) with 3 or 22 weeks of sustained AF (249-electrode array, electrode distance 2.4 mm). A dataset mimicking sequential recordings was generated by segmenting the grid into four spatially overlapping regions (each region 6.5 cm2, 48±10% overlap) without temporal overlap. RAAPs were detected in each region using recurrence plots of activation times. RAAPs in two different regions were joined in case of RAAP cross-recurrence between overlapping electrodes. We quantified the reconstruction success rate and quality of the composite maps. RESULTS: Of 1021 RAAPs found in the full mapping array (32±13 per recording), 328 spatiotemporally stable RAAPs were analyzed. 247 composite maps were generated (75% success) with a quality of 0.86±0.21 (Pearson correlation). Success was significantly affected by the RAAP area. Quality was weakly correlated with the number of repetitions of RAAPs (r=0.13, p<0.05) and not affected by the atrial side (left or right) or AF duration (3 or 22 weeks of AF). CONCLUSIONS: Constructing composite maps by combining spatially overlapping sequential recordings is feasible. Interpretation of these maps can play a central role in ablation planning.

Unipolar voltage mapping in right ventricular cardiomyopathy: pitfalls, solutions and advantages.

AIMS: Endocardial unipolar and bipolar voltage mapping (UVM/BVM) of the right ventricle (RV) are used for transmural substrate delineation. However, far-field electrograms (EGMs) and EGM changes due to injury current may influence automatically generated UVM. Epicardial BVM is considered less accurate due to the impact of fat thickness (FT). Data on epicardial UVM are sparse. The aim of the study is two-fold: to assess the influence of the manually corrected window-of-interest on UVM and the potential role of epicardial UVM in RV cardiomyopathies. METHODS AND RESULTS: Consecutive patients who underwent endo-epicardial RV mapping with computed-tomography (CT) integration were included. Mapping points were superimposed on short-axis CT slices and correlated with local FT. All points were manually re-analysed and the window-of-interest was adjusted to correct for false high unipolar voltage (UV). For opposite endo-epicardial point-pairs, endo-epicardial bipolar voltage (BV) and UV were correlated for different FT categories. A total of 3791 point-pairs of 33 patients were analysed. In 69% of endocardial points and 63% of epicardial points, the window-of-interest needed to be adjusted due to the inclusion of far-field EGMs, injury current components, or RV-pacing artifacts. The Pearson correlation between corrected endo-epicardial BV and UV was lower for point-pairs with greater FT; however, this correlation was much stronger and less influenced by fat for UV. CONCLUSION: At the majority of mapping sites, the window-of-interest needs to be manually adjusted for correct UVM. Unadjusted UVM underestimates low UV regions. Unipolar voltage seems to be less influenced by epicardial fat, suggesting a promising role for UVM in epicardial substrate delineation.

The transmural activation interval: a new mapping tool to identify ventricular tachycardia substrates in right ventricular cardiomyopathy.

AIMS: In right ventricular cardiomyopathy (RVCM), intramural scar may prevent rapid transmural activation, which may facilitate subepicardial ventricular tachycardia (VT) circuits. A critical transmural activation delay determined during sinus rhythm (SR) may identify VT substrates in RVCM. METHODS AND RESULTS: Consecutive patients with RVCM who underwent detailed endocardial-epicardial mapping and ablation for scar-related VT were enrolled. The transmural activation interval (TAI, first endocardial to first epicardial activation) and maximal activation interval (MAI, first endocardial to last epicardial activation) were determined in endocardial-epicardial point pairs located <10 mm apart. VT-related sites were determined by conventional substrate mapping and limited activation mapping when possible. Nineteen patients (46 ± 16 years, 84% male, 63% arrhythmogenic right ventricular cardiomyopathy, 37% exercise-induced arrhythmogenic remodelling) were inducible for 44 VT [CL 283 (interquartile range, IQR 240-325)ms]. A total of 2569 endocardial-epicardial coupled point pairs were analysed, including 98 (4%) epicardial VT-related sites.The TAI and MAI were significantly longer at VT-related sites compared with other electroanatomical scar sites [TAI median 31 (IQR 11-50) vs. 2 (-7-11)ms, P < 0.001; MAI median 65 (IQR 45-87) vs. 23 (13-39)ms, P < 0.001]. TAI and MAI allowed highly accurate identification of epicardial VT-related sites (optimal cut-off TAI 17 ms and MAI 45 ms, both AUC 0.81). Both TAI and MAI had a better predictive accuracy for VT-related sites than endocardial and epicardial voltage and electrogram (EGM) duration (AUC 0.51-0.73). CONCLUSION: The transmural activation delay in SR can be used to identify VT substrates in patients with RVCM and predominantly hemodynamically non-tolerated VT, and may be an important new mapping tool for substrate-based ablation.

Epicardial mapping and ablation of ventricular tachycardia from the coronary venous system in post-coronary bypass patients.

BACKGROUND: Ventricular tachycardia (VT) ablation of mid- or epicardial substrate is difficult and requires a creative approach in patients with a history of coronary bypass that precludes percutaneous epicardial catheter manipulation. The coronary venous system (CVS) provides limited access to the epicardial surface of the heart. The objective of this study is to assess the feasibility, safety, and efficacy of epicardial mapping and ablation of VT substrates from the CVS in patients with history of coronary bypass. METHODS: Patients undergoing VT ablation at our institution were retrospectively reviewed. Those who had basal to mid ventricular substrate based on computed tomography imaging and history of coronary bypass were included. Endocardial and CVS mapping and ablation was performed in standard fashion using 3D electroanatomic mapping. The primary endpoint was defined as VT circuit elimination, termination, non-inducibility, or perturbation of the circuit. RESULTS: Of 192 consecutive VT ablations from 2017 to 2020, 35 (18%) had a history of coronary bypass and basal to the mid-ventricular substrate by imaging. There were no significant characteristic differences between the endocardial only (n = 19) vs endocardial + CVS (n = 16) groups. In 14 (88%) of patients undergoing CVS mapping, the VT circuit was identified to be within access from the epicardial surface. Ablation was attempted in 8 (57%) of these patients, and the primary endpoint was reached in 88% of those undergoing CVS ablation. There were no complications related to CVS ablation. CONCLUSION: Mapping and ablation of mid- or epicardial VT circuits from the CVS branches are feasible and safe and may be helpful in the treatment of VT in patients who are otherwise not candidates for percutaneous epicardial ablation.

Dexmedetomidine for sedation during epicardial ablation for ventricular tachycardia: a single-center experience.

BACKGROUND: Epicardial approach to ventricular tachycardia (VT) ablation is mainly performed under general anesthesia (GA). Although catheter manipulation and ablation in the epicardial space could be painful, GA lowers blood pressure and may interfere with arrhythmia induction and mapping, and the use of muscle relaxants precludes identification of the phrenic nerve (PN). Moreover, an anesthesiologist's presence is required during GA for the whole procedure, which may not always be possible. Therefore, we evaluated the feasibility and safety of epicardial VT ablations performed under conscious sedation using dexmedetomidine in our center. METHODS: Between January 2018 and January 2022, all patients who underwent epicardial VT ablation under continuous dexmedetomidine infusion were prospectively included in the study. All patients received premedication 30 min before the epicardial puncture with paracetamol (acetaminophen 10 mg/ml) 1000 mg and ketorolac 30 mg. Sedation protocol included an intravenous bolus of midazolam hydrochloride (0.03-0.05 mg/kg) followed by continuous infusion of dexmedetomidine (0.2-0.7 mcg/kg/h). In addition, an intravenous fentanyl citrate bolus (0.7-1.4 mcg/kg) was given for short-term analgesia, followed by a second dose repeated after 30 to 45 min. Sedation-related complications were defined in case of respiratory failure, severe hypotension, and bradycardia requiring treatment. RESULTS: Sixty-nine patients underwent epicardial or endo-epi VT ablation under conscious sedation and were included in the analysis. The mean age was 65.4 ± 12.1 years; forty-six patients were males (66.6%). All patients had drug-refractory recurrent VT. Forty-seven patients (68.1%) had non-ischemic cardiomyopathy (NICM), 13 patients (18.9%) had ischemic-cardiomyopathy (ICM), and 9 patients (13%) had myocarditis. Standard percutaneous sub-xiphoid access was attempted in all patients. Non-inducibility of any VT was achieved in 82.6% (9/9 myocarditis, 10/13 ICM, 38/47 NICM, n = 57/69 patients), inducibility of non-clinical VT in 13% (3/13 ICM, 6/38 NICM, n = 9/69 patients), and failure in 4.3% (3/38 NICM, n = 3/69 patients). Although we observed procedural-related complications in five patients (7.2%), one transient PN palsy, two pericarditis, and two vascular complications, those were not related to the conscious sedation protocol. No respiratory failure, severe hypotension, or bradycardia requiring treatment has been observed among the patients. CONCLUSIONS: Prompt availability of anesthesiology support remains crucial for complex procedures such as epicardial VT ablation. Continuous infusion of dexmedetomidine and administration of midazolam and fentanyl seem to be a safe and effective sedation protocol in patients undergoing epicardial VT ablation.

Epicardial access facilitated by carbon dioxide insufflation via intentional coronary vein exit: step-by-step description of the technique and review of the literature.

Pericardial access from a subxiphoid approach is often necessary to gain access to a critical epicardial substrate that is inaccessible from the endocardium. Although relatively safe, a rate of up to 5% of acute and 2% delayed complications has been reported. Intentional perforation of a distal coronary vein branch with pericardial insufflation of CO2 to create a negative contrast space anterior to the right ventricle is an emerging approach to facilitate pericardial access. In this report, we describe the technique of intentional coronary vein exit with CO2 insufflation to perform epicardial mapping and ablation of ventricular tachycardia (VT) in a step-by-step approach and review the published literature on this topic.

'Vanishing' fragmented potential at the epicardium in a patient with Brugada syndrome.

A man in his 40s with Brugada syndrome underwent catheter ablation for ventricular fibrillation. When we performed epicardial mapping again to check for residual ablation sites after ablation, a remarkable reproducible fragmented potential was observed at the anterior aspect of the right ventricle using an Advisor HD Grid (Abbott), which had not been detected during the initial mapping before ablation, and which was invisible to the ablation catheter. Fluoroscopic imaging demonstrated a shiny area anterior to the heart, suggesting trapped air, presumed to have arisen when the sheath was inserted into the pericardial space. The air trapped between the heart and pericardium prevented the HD grid from contacting the epicardium, resulting in the recording of a fragmented potential. The trapped air was removed manually via the sheath, and the potential vanished. When fragmented potentials are observed at the anterior right ventricle (RV) in the epicardium, air trapping should be ruled out by fluoroscopy.

Assessing Noninvasive Delineation of Low-Voltage Zones Using ECG Imaging in Patients With Structural Heart Disease.

OBJECTIVES: This study sought to assess the association between electrocardiographic imaging (ECGI) parameters and voltage from simultaneous electroanatomic mapping (EAM). BACKGROUND: ECGI offers noninvasive assessment of electrophysiologic features relevant for mapping ventricular arrhythmia and its substrate, but the accuracy of ECGI in the delineation of scar is unclear. METHODS: Sixteen patients with structural heart disease underwent simultaneous ECGI (CardioInsight, Medtronic) and contact EAM (CARTO, Biosense-Webster) during ventricular tachycardia catheter ablation, with 7 mapped epicardially. ECGI and EAM geometries were coregistered using anatomic landmarks. ECGI points were paired to the closest site on the EAM within 10 mm. The association between EAM voltage and ECGI features from reconstructed epicardial unipolar electrograms was assessed by mixed-effects regression models. The classification of low-voltage regions was performed using receiver-operating characteristic analysis. RESULTS: A total of 9,541 ECGI points (median: 596; interquartile range: 377-737 across patients) were paired to an EAM site. Epicardial EAM voltage was associated with ECGI features of signal fractionation and local repolarization dispersion (N = 7; P < 0.05), but they poorly classified sites with bipolar voltage of <1.5 mV or <0.5 mV thresholds (median area under the curve across patients: 0.50-0.62). No association was found between bipolar EAM voltage and low-amplitude reconstructed epicardial unipolar electrograms or ECGI-derived bipolar electrograms. Similar results were found in the combined cohort (n = 16), including endocardial EAM voltage compared to epicardial ECGI features (n = 9). CONCLUSIONS: Despite a statistically significant association between ECGI features and EAM voltage, the accuracy of the delineation of low-voltage zones was modest. This may limit ECGI use for pr-procedural substrate analysis in ventricular tachycardia ablation, but it could provide value in risk assessment for ventricular arrhythmias.

High-density epicardial mapping in Brugada syndrome: Depolarization and repolarization abnormalities.

BACKGROUND: The pathogenesis of Brugada syndrome (BrS) and consequently of abnormal electrograms (aEGMs) found in the epicardium of the right ventricular outflow tract (RVOT-EPI) is controversial. OBJECTIVE: The purpose of this study was to analyze aEGM from high-density RVOT-EPI electroanatomic mapping (EAM). METHODS: All patients undergoing RVOT-EPI EAM with the HD-Grid catheter for BrS were retrospectively included. Maps were acquired before and after ajmaline, and all patients had concomitant noninvasive electrocardiographic imaging with annotation of RVOT-EPI latest activation time (RVOTat). High-frequency potentials (HFPs) were defined as ventricular potentials occurring during or after the far-field ventricular EGM showing a local activation time (HFPat). Low-frequency potentials (LFPs) were defined as aEGMs occurring after near-field ventricular activation showing fractionation or delayed components. Their activation time from surface ECG was defined as LFPat. RESULTS: Fifteen consecutive patients were included in the study. At EAM before ajmaline, 7 patients (46.7%) showed LFPs. All patients showed HFPs before and after ajmaline and LFPs after ajmaline. Mean HFPat (134.4 vs 65.3 ms, P <.001), mean LFPat (224.6 vs 113.6 ms, P <.001), and mean RVOTat (124.8 vs 55.9 ms, P <.001) increased after ajmaline. RVOTat correlated with HFPat before (ρ = 0.76) and after ajmaline (ρ = 0.82), while RVOTat was shorter than LFPat before (P <.001) and after ajmaline (P <.001). BrS patients with history of aborted sudden cardiac death had longer aEGMs after ajmaline. CONCLUSION: Two different types of aEGMs are described from BrS high-density epicardial mapping. This might correlate with depolarization and repolarization abnormalities.

An improved procedure for isolating adult mouse cardiomyocytes for epicardial activation mapping.

Cardiovascular disease is a leading cause of death and disability worldwide. Although genetically modified mouse models offer great potential for robust research in vivo, in vitro studies using isolated cardiomyocytes also provide an important approach for investigating the mechanisms underlying cardiovascular disease pathogenesis and drug actions. Currently, isolation of mouse adult cardiomyocytes often relies on aortic retrograde intubation under a stereoscopic microscope, which poses considerable technical barriers and requires extensive training. Although a simplified, Langendorff-free method has been used to isolate viable cardiomyocytes from the adult mouse heart, the system requires enzymatic digestions and continuous manual technical operation. This study established an optimized approach that allows isolation of adult mouse cardiomyocytes and epicardial activation mapping of mouse hearts using a Langendorff device. We used retrograde puncture through the abdominal aorta in vivo and enzymatic digestion on the Langendorff perfusion device to isolate adult mouse cardiomyocytes without using a microscope. The yields of isolated cardiomyocytes were amenable to patch clamp techniques. Furthermore, this approach allowed epicardial activation mapping. We used a novel, simplified method to isolate viable cardiomyocytes from adult mouse hearts and to map epicardial activation. This novel approach could be beneficial in more extensive research in the cardiac field.

Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?

Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts depolarized when coupled myocytes produced action potentials. This review also introduces another non-myocyte which may modulate both myocardial (myo)fibroblasts and myocytes: epicardial adipose tissue. Epicardial adipocytes are in intimate contact with myocytes and (myo)fibroblasts and may infiltrate the myocardium. Adipocytes secrete numerous adipokines which modulate (myo)fibroblast and myocyte physiology. These adipokines are protective in healthy hearts, preventing inflammation and fibrosis. However, adipokines secreted from adipocytes may switch to pro-inflammatory and pro-fibrotic, associated with reactive oxygen species generation. Pro-fibrotic adipokines stimulate myofibroblast differentiation, causing pronounced fibrosis in the epicardial adipose tissue and the myocardium. Adipose tissue also influences myocyte electrophysiology, via the adipokines and/or through electrotonic interactions. Deeper understanding of the interactions between myocytes and non-myocytes is important to understand and manage atrial fibrillation.

Role of endocardial ablation in eliminating an epicardial arrhythmogenic substrate in patients with Brugada syndrome.

BACKGROUND: Epicardial ablation is occasionally limited by coronary artery (CA) injuries or epicardial fat (EF). OBJECTIVE: The purpose of this study was to evaluate the anatomic obstacles that prevent ablation of epicardial abnormal potentials (EAPs) in patients with Brugada syndrome (BrS) and to investigate the feasibility of EAP elimination by endocardial right ventricular (RV) ablation. METHODS: This study included 16 BrS patients with previous ventricular fibrillation (VF), including 10 with an electrical storm. Data from multidetector computed tomography were assessed, and the proximity of the CA and EF was correlated with EAPs. RESULTS: EAPs were present in the epicardial RV outflow tract and RV inferior wall in all patients and 12 patients (75%), respectively. These EAPs were present within 5 mm of the main body and branches of the right CA in 14 patients (87.5%). However, only 1.4% ± 2.9% of the EAP area was covered with thick EF (≥8 mm). Partial EAP elimination by endocardial RV ablation was feasible in all 10 patients, with 53.3% successful endocardial RV radiofrequency applications for eliminating EAPs. After the procedure, VF remained inducible in 37.5% of the patients. During the 25.1 ± 29.1 months of follow-up, no patients experienced an electrical storm, and VF burden significantly decreased (median VF episodes before and after ablation: 7 and 0, respectively). CONCLUSION: EAPs are near the CA in most BrS patients, thereby requiring caution during epicardial ablation, whereas EF is less of an issue. Endocardial ablation is feasible to eliminate some EAPs and may be combined with epicardial ablation.

Landing on the spot: Approaches to outflow tract PVCs; from ECG to EGMs to intracardiac echocardiography.

Premature ventricular complexes (PVCs) are increasingly recognized, as the use of ECG wearables becomes more widespread. In particular, PVCs arising from both the right ventricular outflow tract (RVOT) and left ventricular outflow tract (LVOT) comprise the majority of these arrhythmias and form a significant component of an electrophysiology practice. A keen understanding of the correlative anatomy of the outflow tracts, in addition to recognizing key ECG indices illustrating PVC sites of origin, are fundamental in preparing for a successful ablation. Patient selection, incorporating symptomatology, structural disease, and PVC burden can pose a challenge, though tools such as the ABC-VT risk score may help identify those patients with a higher risk of clinical deterioration. Utilizing intracardiac echocardiography to highlight salient anatomic features not visible with fluoroscopy allows for a more precise and safer ablation. Interpretation of intracardiac EGMs, and the careful examination for low amplitude highly fractionated pre-potentials, enhanced by the advent of new developed mapping/ablation catheters, remains crucial. Utilizing these tools will guide the electrophysiologist to an efficient and effective outflow tract PVC ablation.

Advanced Therapies for Ventricular Arrhythmias in Patients With Chagasic Cardiomyopathy: JACC State-of-the-Art Review.

Chagas disease is caused by infection from the protozoan parasite Trypanosoma cruzi. Although it is endemic to Latin America, global migration has led to an increased incidence of Chagas in Europe, Asia, Australia, and North America. Following acute infection, up to 30% of patients will develop chronic Chagas disease, with most patients developing Chagasic cardiomyopathy. Chronic Chagas cardiomyopathy is highly arrhythmogenic, with estimated annual rates of appropriate implantable cardioverter-defibrillator therapies and electrical storm of 25% and 9.1%, respectively. Managing arrhythmias in patients with Chagasic cardiomyopathy is a major challenge for the clinical electrophysiologist, requiring intimate knowledge of cardiac anatomy, advanced training, and expertise. Endocardial-epicardial mapping and ablation strategy is needed to treat arrhythmias in this patient population, owing to the suboptimal long-term success rate of endocardial mapping and ablation alone. We also describe innovative approaches to improve acute and long-term clinical outcomes in patients with refractory ventricular arrhythmias following catheter ablation, such as bilateral cervicothoracic sympathectomy and bilateral renal denervation, among others.

Spatial and transmural properties of the reentrant ventricular tachycardia circuit in arrhythmogenic right ventricular cardiomyopathy: Simultaneous epicardial and endocardial recordings.

BACKGROUND: While advances in the characterization of the structural substrate in arrhythmogenic right ventricular cardiomyopathy (ARVC) have been made, the ventricular tachycardia (VT) circuit remains incompletely described. OBJECTIVE: The purpose of this study was to delineate the reentrant VT circuit with simultaneous epicardial and endocardial mapping (SEEM) in ARVC. METHODS: Twenty-three consecutive patients with ARVC and VT underwent SEEM at 4 centers between 2014 and 2020. Retrospective analysis was performed on combined isochronal activation maps. RESULTS: Of the 30 VT circuits, 24 were delineated with SEEM (956 [341-1843] endocardial points and 1763 [882-3054] epicardial points). The apex and outflow tract rarely harbored VT circuits, with 50% distributed in the inferior wall and 43% in the free wall. The entire tachycardia cycle length was recorded from the epicardium in 71% of circuits. In all circuits, a large proportion of the tachycardia cycle length was recorded from the epicardium relative to the endocardium. Localized epicardial reentry was observed in 35% of patients (14 mm × 15 mm), which was associated with smaller endocardial low voltage area (39 cm2 vs 104 cm2; P = .002) and preserved right ventricular ejection fraction (35% vs 25%; P = .046) compared with those with larger circuit dimensions. Seventy percent of termination sites were achieved from the epicardium. CONCLUSION: High-resolution recordings from both myocardial surfaces confirm a consistent predominance of epicardial participation during reentry in ARVC. Only the perivalvular inflow region of the "triangle of dysplasia" had a strong propensity to harbor VT circuits, with the greatest proportion located in the inferior wall. Localized epicardial reentry may be a manifestation of earlier stage disease with a relative paucity of endocardial substrate.