Successful LV Summit Ablation

Abstract

Background

Catheter ablation of arrhythmias from the left ventricular (LV) summit are often challenging because of anatomical inaccessibility and proximity to coronary arteries.

Case Summary

A 43-year-old man with recurrent arrhythmia-induced cardiomyopathy presented with the accelerated idioventricular rhythm. With earliest activation (preceding QRS onset by 63 ms) in the anterior interventricular vein, catheter ablation from the LV outflow tract and the left coronary cusp was unsuccessful. Catheter ablation using half-normal saline irrigation with an anterior dispersive patch successfully eliminated the accelerated idioventricular rhythm.

Discussion

This case illustrates the potential role of adjunctive approaches in overcoming anatomical barriers to LV summit ablation. The use of half-normal saline irrigation and anterior patch–assisted ablation demonstrated efficacy where conventional methods were insufficient.

Take-Home Message

Advanced radiofrequency ablation strategies, including modified irrigation and patch-assisted delivery, may enable safe and effective treatment of complex LV summit arrhythmias, thereby reducing reliance on more invasive or higher risk interventions.

Graphical Abstract

Visual Summary.

Successful LV Summit Ablation Using an Anterior Chest Wall Dispersive Patch and Half-Normal Saline Irrigation

The image shows the electroanatomical map of the LV summit region: RVOT, LVOT, LCC, and AIV. RF application from the LVOT and the LCC failed, but the use of half-normal saline irrigation and anterior patch-assisted ablation at the LVOT led to successful outcomes. AIV = anterior interventricular vein; LCC = left coronary cusp; LVOT = left ventricular outflow tract; RF = radiofrequency; RVOT = right ventricular outflow tract.

Case Report

A 43-year-old man with hypertension, dyslipidemia, and atrial fibrillation presented with recurrent heart failure. Four years earlier, he had developed tachycardia-induced cardiomyopathy from atrial fibrillation and had undergone catheter ablation, after which sinus rhythm was maintained and left ventricular (LV) ejection fraction improved. However, he developed recurrent heart failure with reduced LV ejection fraction and was referred to our hospital. A 12-lead electrocardiogram revealed a regular wide QRS complex rhythm at a ventricular rate of 95 beats/min, with atrioventricular dissociation, consistent with accelerated idioventricular rhythm. The QRS duration was 154 ms, with an inferior axis, early transition at V₂, QS pattern in lead I, absent S-wave in V₆, and a slurred initial upstroke of the QRS complex (Figure 1). The amplitude ratio of lead III/II was 1.20, and the Q-wave amplitude ratio of aVL/aVR was 1.46; these findings were consistent with an origin in the LV summit.¹ Transthoracic echocardiography demonstrated diffuse LV hypokinesis (LV ejection fraction: 38%). Coronary angiography revealed no significant coronary artery disease. Despite treatment with guideline-directed medical therapy, including carvedilol, accelerated idioventricular rhythm persisted, raising concern for arrhythmia-induced cardiomyopathy. Catheter ablation was therefore performed.

Take-Home Messages

• •This case demonstrates successful treatment of arrhythmia-induced cardiomyopathy from accelerated idioventricular rhythm at the challenging LV summit using innovative energy delivery, half-normal saline irrigation, and an anterior chest wall dispersive patch to enhance lesion depth.
• •It highlights the potential of these strategies to overcome anatomical limitations without epicardial access or ethanol infusion, although further validation is needed.

Figure 1.

12-Lead Surface Electrocardiogram

Electrocardiogram at baseline shows a wide QRS rhythm, consistent with an accelerated idioventricular rhythm with occasional sinus beats. The QRS morphology demonstrates an inferior axis, early precordial transition at V₂, a QS pattern in lead I, absence of an S-wave in V₆, and a slurred initial upstroke of the QRS complex, findings suggestive of an LV summit origin. LV = left ventricular.

Electrophysiology Mapping and Radiofrequency Ablation

The patient presented to the electrophysiology laboratory with accelerated idioventricular rhythm. Three-dimensional electroanatomic mapping was performed using the EnSite mapping system (Abbott). A 2-F microcatheter (EPstar Fix AIV, Japan Lifeline) was advanced into the anterior interventricular vein (AIV). The earliest ventricular activation of 63 ms with a spiky prepotential to the onset of QRS was recorded at the distal tip of the microcatheter (Figure 2A). Pace mapping at this site demonstrated a high match score of 98%, with an S-QRS interval of 56 ms (Figure 2B). Adjacent structures were mapped: the earliest activation was −35 ms at the right ventricular outflow tract, −56 ms at the subaortic LV outflow tract (LVOT), and −7 ms at the left coronary cusp (Figure 3). Based on the integration of all mapping data, the origin of the accelerated idioventricular rhythm appeared most consistent with the LV summit. However, because the endocardial LVOT also demonstrated early activation, the possibility of an intramural LVOT origin could not be excluded.

Figure 2.

Intracardiac Electrogram During Accelerated Idioventricular Rhythm

(A) The earliest ventricular activation, preceding QRS onset by 63 ms, was recorded at the distal tip of the microcatheter (path 1-2) in the AIV. (B) Pace mapping at the distal electrode pair (path 1-2) demonstrated a 98% pace match, with an S-QRS interval of 56 ms. AIV = anterior interventricular vein.

Figure 3.

Three-Dimensional Electroanatomical Activation Map of the RVOT, LVOT, Coronary Sinus, and Aortic Cusp During Accelerated Idioventricular Rhythm

The map, constructed using the EnSite mapping system, reveals the earliest activation site at the AIV, where the local electrogram preceded QRS onset by 63 ms. Local activation at the LVOT (−56 ms), RVOT (−35 ms), and LCC (−7 ms) are also shown. Color-coded mapping shows a centrifugal activation pattern, with the earliest site highlighted in the AIV. AIV = anterior interventricular vein; LCC = left coronary cusp; LVOT = left ventricular outflow tract; RVOT = right ventricular outflow tract.

During mapping, accelerated idioventricular rhythm became less frequent, and bigeminy premature ventricular contractions (PVCs) continued. Radiofrequency (RF) ablation at the LVOT site (25-35 W, 80-100 seconds) did not eliminate the PVCs. To direct the RF energy to the area, we attempted dispersive patch placement to the anterior chest wall, but the PVCs persisted. Although the AIV was the earliest activation site, RF ablation was not possible given the small diameter of the vein and its close proximity to the left anterior descending artery (Figure 4). RF application from the left coronary cusp also failed to eliminate the PVC. As an alternative strategy, RF energy was delivered using half-normal saline irrigation along with anterior patch placement to maximize lesion depth at the LVOT, the closest anatomical site to the earliest activation in the AIV; this led to the successful elimination of the PVC within 45 seconds of energy delivery (Figure 5). The power and impedance profiles during RF delivery of the 3 methods (conventional [posterior patch and normal saline irrigation], normal saline and anterior patch, and half-normal saline and anterior patch) are shown in Figure 6.

Figure 4.

Coronary Angiogram of the Left Coronary Artery

Fluoroscopic images showing (left) LAO and (right) RAO views. The ablation catheter was advanced into the AIV as close as possible to the distal tip of the microcatheter. The catheter tip was located in close proximity to the left anterior descending coronary artery, indicating that radiofrequency ablation in this area was not feasible. AIV = anterior interventricular vein; LAO = left anterior oblique; RAO = right anterior oblique.

Figure 5.

12-Lead Electrocardiogram Recorded During Radiofrequency Ablation

The disappearance of accelerated ventricular rhythm and PVC was observed after approximately 45 seconds of ablation. PVC = premature ventricular contraction; RF = radiofrequency.

Figure 6.

Graphs Illustrating Impedance and Power During Radiofrequency Ablation of the LVOT Under 3 Different Conditions

(A) Conventional: Posterior dispersive patch positioning with RF power delivery of 35 W, with baseline impedance of 99 Ω. (B) Anterior dispersive patch repositioning with 35 W applied for 50 seconds, with baseline impedance of 109 Ω. (C) Anterior patch positioning combined with half-normal saline irrigation during endocardial LVOT ablation using 35 W for 120 seconds. The initial impedance is higher than with normal saline irrigation and 16-Ω impedance drop, indicating improved lesion formation with the combination of anterior patch placement and half-normal saline irrigation.

After ablation, isoproterenol infusion and atrial burst pacing were performed, but neither induced PVCs or accelerated idioventricular rhythm. At the 3-month follow-up, the patient remained free of PVC recurrence, with improving LV function and no further episodes of heart failure hospitalization.

Discussion

This case illustrates a challenging and instructive approach to catheter ablation of arrhythmia originating from the LV summit, a region well known for its complex anatomy, close proximity to coronary arteries, and limited endocardial accessibility.² In this 43-year-old patient with recurrent heart failure, a rare yet clinically significant accelerated idioventricular rhythm originating from the LV summit was implicated in his arrhythmia-induced cardiomyopathy.

The success of the procedure hinged on innovative ablative techniques, notably the use of an anterior dispersive patch and half-normal saline irrigation to enhance lesion depth and effectiveness in an otherwise inaccessible target site. In this case, mapping revealed the earliest activation was at the distal AIV, with a close pace match (98%). However, direct ablation at this site was precluded because of the small size of the vessel, with high impedance and close proximity to coronary arteries. The LVOT endocardial sites showed relatively early activation. From an anatomical standpoint, the endocardial LVOT site represents one of the most suitable locations to initiate catheter ablation.² Unfortunately, we failed to achieve successful elimination of the arrhythmia from this area, likely owing to insufficient lesion depth. The anterior dispersive patch alters the current density vector to favor a more forward-directed energy delivery, theoretically extending lesion depth in an anterior trajectory.³ Although this method alone did not fully eliminate the PVCs initially, it played a critical role in focusing RF energy during the subsequent successful ablation.

The use of half-normal saline irrigation has been shown to decrease ionic concentration and charge density. Lowering ionic concentration results in electrical conduction at higher impedance and reduces losing RF current through dispersion to a lower impedance environment and facilitating the creation of larger lesions in the myocardial tissue.^4,5 This technique has been described in the context of epicardial ablation and inaccessible intramural arrhythmias, and its use here was pivotal in achieving a successful outcome without epicardial access or coronary artery injury.

Ethanol ablation, a potential option for epicardial LV summit arrhythmias, was not pursued owing to several concerns. It requires precise identification and cannulation of a suitable vein, often a small tributary of the great cardiac vein or AIV. In this case, the proximity of the target site to major coronary arteries posed a potential risk of coronary injury and unintended myocardial damage.^6,7 Moreover, ethanol ablation offers limited control over lesion size and spread, with irreversible effects and potential harm to adjacent structures. However, it may have been an alternative choice if half-normal saline irrigation and anterior patch-assisted RF ablation had been ineffective in this case.

Alternative energy sources such as pulsed-field ablation (PFA) and cryoablation offer potential options for LV summit ablation. PFA, a nonthermal technique using high-voltage electric fields for selective myocardial electroporation, shows promise for creating deep, transmural lesions while sparing nearby structures.⁸ However, in our case, PFA might not have been feasible given the proximity to a coronary artery. Cryoablation, while safer for adjacent structures because of controlled lesion formation, still carries some coronary risk.⁹ Given these limitations and the success with half-normal saline irrigation and anterior patch–assisted RF ablation in this case, neither PFA nor cryoablation were used. Nonetheless, both remain promising alternatives when conventional RF approaches fail.

Multiple studies have explored the use of half-normal saline irrigation during RF ablation,^4,5 particularly emphasizing its potential to enhance lesion depth and manage refractory arrhythmias, however, to our knowledge this is the first reported case to describe the combined use of half-normal saline irrigation and the anterior patch–assisted RF ablation technique. Although using this technique was effective in our patient, there are limited long-term data on its safety and efficacy. Risks such as steam pops, tissue overheating, or delayed myocardial injury must be weighed carefully. Future prospective studies or registries could help delineate the role of these adjunctive techniques in broader clinical practice.

Conclusions

This case demonstrates the successful use of adjunctive ablation techniques, specifically half-normal saline irrigation and anterior chest wall dispersive patch placement, for the treatment of accelerated idioventricular rhythm originating from the anatomically challenging LV summit. When conventional endocardial or epicardial approaches are limited by proximity to coronary arteries or insufficient lesion depth, these innovative strategies can offer a viable and effective alternative. Although the short-term outcome was favorable, further studies are needed to evaluate the long-term safety, efficacy, and broader applicability of these techniques in managing intramural ventricular arrhythmias.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.