INTRODUCTION

The anatomical substrate for ventricular tachycardia (VT) most commonly arises in the subendocardial segments of myocardium, particularly in those patients with postmyocardial infarction (MI) scar-related reentry.¹ VT circuits, however, are not exclusive to the subendocardium. In fact, the prevalence of epicardial VT has been reported to range from 14% to 33% among patients with a previous history of MI.^2,3 Furthermore, the prevalence of epicardial VT in patients with nonischemic cardiomyopathies tends to be higher compared to those with an ischemic VT substrate.^4–6

Since epicardial VT ablation with percutaneous subxiphoid access was first reported in patients with Chagas cardiomyopathy in 1996 by Sosa and colleagues, epicardial mapping and ablation have been widely performed for the treatment of scar-related VT, and endo- and epicardial ablation has been used to achieve improved outcomes, not only in the setting of nonischemic dilated cardiomyopathy (NICM)^5,7 and arrhythmogenic right ventricular cardiomyopathy (ARVC),^9,10 but also in ischemic cardiomyopathy (ICM).^11,12

However, the rate of major complications associated with epicardial VT ablation typically ranges between 5% and 10%, with hemopericardium representing the most common serious adverse event, followed by intra-abdominal bleeding and epicardial vascular and phrenic nerve injuries.^1,11,6,13 Other extracardiac complications such as pulmonary damage¹⁴ can also occur. Moreover, the pericardial fat that covers the epicardial ventricular surface¹⁵ may dramatically reduce the efficacy of epicardial ablation.¹⁶ Therefore, the indications for an epicardial approach should be carefully considered.

In light of this, we evaluated the feasibility and safety of elimination of epicardial substrate in the form of local abnormal ventricular activity (LAVA) through endocardial radiofrequency delivery in patients with scar-related VT as a result of ARVC, NICM, and ICM.¹⁷ Additionally, useful anatomic information based on contrast-enhanced multidetector computed tomography (MDCT), which might predict successful elimination of epicardial LAVA (Epi-LAVA) through an endocardial approach, was investigated.

We examined a total of 46 patients (Table 28.1), including 18 ICM, 13 NICM, and 15 ARVC who underwent combined endo- and epicardial mapping with a 3D navigation system, resulting in evidence of Epi-LAVA demonstrated by a multielectrode catheter. Four patients had previously failed ablation procedures (range 1 to 3).

Table 28.1 Characteristics of the Study Population

We commenced ablation with an endocardial approach when LAVA was detected on both the endo- and epicardium, aiming at elimination of both Endo- and Epi-LAVA. When LAVA was detected only epicardially in the absence of Endo-LAVA, endocardial ablation was performed at the site facing the Epi-LAVA, aiming to abolish the LAVA potentials transmurally. During endocardial ablation at the facing site, careful monitoring of transmural response and elimination of Epi-LAVA was possible with a multipolar high-density mapping catheter (PentaRay, Biosense Webster, Irvine, CA), which was placed at Epi-LAVA sites and stabilized by a steerable sheath (Agilis, Abbott, St. Paul, MN; Figure 28.1). This strategy was repeated at adjacent sites as needed to achieve complete Epi-LAVA elimination. After endocardial ablation, epicardial mapping of areas previously displaying LAVA was performed and used to guide further ablation as indicated by Epi-LAVA persistence. Radiofrequency energy was delivered with a 3.5-mm open-irrigation catheter (ThermoCool, Biosense Webster, Diamond Bar, CA) with a power of 30–45 W endocardially and 25–35 W epicardially.

RESULTS OF EPI-LAVA ELIMINATION THROUGH ENDOCARDIAL ABLATION

In total, 39 VTs (18 in ICM, 9 in NICM, 12 in ARVC) were hemodynamically tolerated and mapped with conventional activation and entrainment mapping approaches. Of these, in 23 (7 in ICM, 7 in NICM, 9 in ARVC) the critical site of the VT reentrant circuit was identified in the epicardium. Endocardial ablation at the facing site of the epicardial critical isthmus was performed, leading to successful termination of 5 VTs (2 [28%] ICM, 0 [0%] NICM, 3 [33%] ARVC). Figure 28.2 shows Epi-LAVA and the VT reentry circuit eliminated by ablation at the facing endocardial site in a patient with ARVC.

Overall, in 4/18 (22.2%) patients with ICM and 2/15 (13.3%) patients with ARVC, endocardial ablation could abolish all Epi-LAVA. These patients achieved complete elimination of both Endo- and Epi-LAVA with only endocardial ablation. By contrast, all patients with NICM required epicardial ablation. Incomplete Epi-LAVA elimination after endocardial ablation occurred in 22/48 patients (11/18 ICM, 2/15 NICM, 9/15 ARVC). However, in total, endocardial ablation had an impact on Epi-LAVA in 15/18 (83%) ICM, 2/13 (13%) NICM, and 11/15 (73%) ARVC patients, contributing to a potential reduction in epicardial radiofrequency applications.

In 8 (7 ICM and 1 NICM) of 21 patients undergoing MDCT, all identified Epi-LAVA were located within segments of LV wall thinning (< 5 mm). In all of these, endocardial ablation had an impact on Epi-LAVA (complete elimination in 2, and partial elimination in 6). The remaining 13 patients demonstrated presence of Epi-LAVA outside the wall thinning segments (Figure 28.3). None of these attained complete elimination of Epi-LAVA endocardially.

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