INTRODUCTION

Epicardial mapping and ablation of post-ischemic/myocardial infarction (post-MI) ventricular tachycardia (VT) has been traditionally considered second-line therapy, although its use has been variably reported in post-MI VT ablation, ranging from to 13% to 38%, in early experiences,^1,2 large series,³ and multicenter studies.^4–6

EPICARDIAL VT SUBSTRATE IN ISCHEMIC HEART DISEASE

The histopathological substrate of post-MI VT was described in the late 1980s. The subendocardial necrosis, with relative sparing of the endocardial rim, defined a unique substrate and did correlate with electrophysiological substrate in animal models and clinical studies^7,8 and resulted in high efficacy of endocardial ablation, either surgically or percutaneously.^1,9

Patterns of transmural necrosis extending from subendocardium to epicardial layers have been also described.¹⁰ Regional differences between anterior versus inferior infarct have been postulated in remote studies, with greater involvement of transmural/epicardial layers in right coronary and left circumflex artery-related MI.^2,10–14 In the autoptic studies from Duke University, a gradient of transmurality was also shown by some inferior infarcts, with the necrosis extending to the epicardium at the apex against subendocardial involvement at the base; in contrast, anterior MIs are not necessarily transmural throughout the affected wall.^15,16 All this evidence came before the modern era of aggressive reperfusion strategies of acute and subacute MI, which could have changed the aforementioned VT substrate, making the characterization no longer reliable for present-day circumstances.¹⁷

The role of epicardial layers into the VT mechanism was investigated early.^1,18,19 Simultaneous endo-epicardial intraoperative mapping with multipolar catheters in post-MI patients highlighted a more complex scenario of VT substrates, with almost 25% of patients showing complete or partial epicardial substrate of VT.¹⁸

An inherent functional role has also been suggested for the epicardial fiber orientation, as the functional blocks have been shown to occur parallel to the orientation of the muscle bundles, so the transverse conduction is sufficiently slow to favor the occurrence of reentry.⁸

INDICATIONS TO EPICARDIAL APPROACH AND ABLATION: EVIDENCE FROM THE LITERATURE

Ablation series and consensus documents^20–23 reported the epicardial approach to be largely reasonable after a failed endocardial ablation or LV thrombus/inaccessible LV. The favorable outcomes of endocardial ablation in post-MI VTs (up to 80%) reported in high-volume centers strengthens the statement and suggests that epicardial access to be considered only after a failure of endocardial ablation.^24–26 Whether an overlooked epicardial component may be partially responsible for recurrent VTs is still subject to debate.

In our experience, not even a previous failed endocardial ablation is a sufficient criterion per se to perform an epicardial puncture, since the incomplete endocardial mapping/ablation could be responsible for the procedure failure. In a population of post-MI patients referred to our VT Unit to perform a combined endo-epicardial approach because of a previous endocardial ablation failure, the VT reentry circuit was still defined endocardially in about 31% of patients. However, we do believe that the implementation of high-density mapping techniques might help to characterize the complex substrate of ischemic VTs in the years ahead to optimize the strategy.

Despite having data primarily provided by patients with nonischemic etiologies, some ECG criteria have been tested to predict an epicardial VT origin in ischemic patients.27 They are mainly based on the concept that the activation wavefront proceeds slowly from the epicardial surface through the myocardial wall to finally reach the Purkinje system. As a consequence, the QRS shows an initial slow deflection. The proposed criteria are (Figure 34.1):

1.Pseudodelta wave ≥ 34 ms

2.Intrinsicoid deflection time ≥ 85 ms

3.RS complex duration ≥ 121 ms

4.Q wave in lead I

5.Maximum deflection index (from earliest time to maximum deflection divided by the total QRS duration, in any precordial lead)

Overall, these criteria failed to identify VTs requiring epicardial ablation,²⁸ especially in the basal segments of the LV, and they were tested mainly in right bundle branch block (RBBB) VT morphologies.

In addition, the QRS morphology merely describes a VT exit site that could be spatially distant from the isthmus²⁹; scar extension, slow conduction inside the diseased tissue, and the partial extension of VT isthmus across the layers might also hamper the ECG’s ability to detect the effective ablation target. Finally, 12-lead VT morphology is not always available, and patients could have multiple VTs, which limit significantly the role of ECG analysis to set the indication to epicardial approach.

Figure 34.1 Left Panel: 12-lead ECG of epicardial VT in a 48-year-old male with previous inferolateral MI, showing a RBBB morphology and superior axis (cycle length, 380 ms). AV dissociation can be detected in V1; QS complex is also present in lead I. Right Panel: Magnified box to show the ECG criteria for epicardial VTs. The QRS beginning (black vertical line) is marked in lead II. Pink arrow shows pseudodelta wave (lead V1, 45 ms); blue arrow shows intrinsicoid deflection time to the peak of R wave in lead V2 (98 ms); red arrow shows the shortest RS complex duration (lead V4, 122 ms). Procedural data are shown in Figures 34.4–34.6.

Imaging Techniques

Identification of scar tissue, either by late gadolinium enhancement (LGE) magnetic resonance imaging (MRI) or multidetector computed tomography (MDCT), has shown to match the histology of the myocardial infarction30–32 in animal models and is correlated with 3D voltage maps.^33–36 Cardiac MRI allows characterization of the scar in core and border zone and can identify VT isthmuses as border zone corridors.^37–39

In a different series, LGE MRI and MDCT have proven to be useful in detecting the arrhythmogenic substrate extension and improving preprocedure planning.^40–45 Infarct transmurality (IT defined as hyperenhancement involving 75% of myocardial wall thickness) has been associated with epicardial substrates,^43,44 and a combined approach has shown to improve the ablation outcome⁴⁴; nevertheless, the epicardial approach could be useless in up to 30% of patients with IT.

The wall thinning, either detected by CT scan⁴⁵ or LGE-MRI,⁴⁰ has been also associated with the presence of epicardial substrate in ischemic cardiomyopathy (Figure 34.2).

Recently, an epicardial scar area of > 14% on LGE MRI and/or wall-thinning of < 3.59 mm has shown to have very high sensitivity (respectively 1 and 0.91) and specificity (1 and 0.93) to detect epicardial arrhythmogenic substrate in post-MI patients.⁴⁰

The systematic implementation of imaging techniques in VT ablation procedures has shown to be feasible in a large cohort of VT patients; however, the impact on the procedure management appears to be significant in nonischemic etiologies and the decision to perform pericardial approach is still based on multiple criteria.⁴²

From a conceptual standpoint, however, as important as preoperative imaging can be, the main limitation is the lack of any functional assessment of the residual viable tissue; an epicardial extension of the scarring process, indeed, does not imply an epicardial VT substrate, by default, and the characterization of conduction properties inside the scar, so critical to the reentry genesis, cannot be provided.

Because of the limitations of MRI-device compatibility and artifacts generated by the intracavitary leads, imaging findings appeared to be insufficient to plan the epicardial approach in ischemic heart disease.

Intraoperative mapping findings

Endocardial mapping findings are the clue to definitely prove the absence of endocardial VT origin and to indicate the need for epicardial approach, although it requires reversing any anticoagulation to perform the subxiphoid puncture or the surgical access.

The extension of endocardial bipolar scar as a marker of epicardial substrate has been addressed. In our previous experience,⁴⁶ endocardial bipolar dense scar area > 22.5 cm² best predicted scar transmurality; endocardial bipolar dense scar area ≥ 7 cm² and endocardial bipolar scar density > 0.35 (the ratio of the bipolar DS area to total LVA, an index assumed to reflect the density of the myocardial fibrosis within the infarct region) were associated with the presence of epicardial late potentials (sensitivity: 0.88; specificity: 0.67) in patients with post-MI VT. Interestingly, 18% of post-MI patients did not show any dense scar area at endocardial mapping.

Figure 34.2 Cardiac CT angiography of 76-year-old male with a postischemic dilated cardiomyopathy and LV aneurysm. Panel A: Axial CT scan. Panel B: Two-chamber long axis CT scan. Panel C: Two-chamber short axis CT scan. CT images show an enlarged left ventricle with anterior aneurysm (arrows) characterized by bulging of the anterior mid-wall, significantly thinned, related to a postischemic scar. (Courtesy of Prof. Antonio Esposito and Dr. Anna Palmisano.)

Recently, other authors showed that post-MI patients who had undergone epicardial ablation had significantly smaller endocardial bipolar scar area as compared to those with endo-only ablation (54.0 vs 86.7 cm2); the same authors found an epicardial VT substrate even in the absence of endocardial scar in a small number of patients.⁴⁷

The role of unipolar voltage mapping has been also assessed. In patients with VT recurrences after endocardial ablation, deep epicardial substrates were found in the surrounding area of unipolar low voltage encompassing the bipolar LV area,⁴⁸

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