INTRODUCTION

The interventional treatment of ventricular tachycardia (VT) in the setting of nonischemic cardiomyopathy (NICM) is challenging due to the complexity of the underlying arrhythmic substrate typically involving the basal perivalvular regions and the interventricular septum, with a high prevalence of midmyocardial and subepicardial substrates frequently requiring a combined endocardial–epicardial approach.¹ In these terms, accurate preprocedural identification of the abnormal substrate is of great value both for planning the ablation strategy (i.e., need for epicardial approach) and to improve the outcome of ablation.

A catheter ablation approach aided by noninvasive imaging techniques such as cardiac magnetic resonance (cardiac MRI) and computed tomography (CT) to accurately define the anatomy of the cardiac chambers, course of coronary vessels and phrenic nerve, and to identify areas of scar has been shown to significantly impact the acute procedural strategy, leading to additional mapping focused on the anatomical substrate area and eventually to epicardial access in about one-third of NICM patients.² Moreover, it has been correlated with higher VT-free survival rates at long-term follow-up.³ However, these imaging modalities can be cost-prohibitive, are not widely available, may be relatively contraindicated in patients with implantable cardiac electronic devices or advanced renal disease, and typically require time-consuming postprocessing in order to obtain images that can be implemented on the electroanatomic mapping (EAM) systems. From this perspective, it is extremely important to gain all the possible information from the 12-lead surface electrocardiogram (ECG).

Sweveral ECG parameters have been correlated with the presence and amount of scar in different forms of cardiomyopathy with a high degree of accuracy.⁴ Furthermore, specific ECG patterns are associated with specific etiologies of structural heart disease and characteristics scar distribution patterns.^5–7 These make the ECG an indispensable tool for providing diagnostic information in patients with NICM and VT that potentially contributes to the development of the catheter ablation strategy.

COMMON ECG FINDINGS IN NONISCHEMIC DILATED CARDIOMYOPATHY

While there are no specific ECG features unique to NICM, several ECG findings reflect the left ventricular (LV) adverse remodeling taking place in patients with NICM as well as the presence of various amounts of myocardial fibrosis. Typical ECG abnormalities include atrioventricular and interventricular conduction delays, reduced voltage and fragmentation of QRS complexes (particularly in the limb leads), and presence of abnormal Q waves.

A certain degree of PR interval prolongation is commonly seen in patients with NICM, as is QRS prolongation related either to the involvement of the conduction system by the cardiomyopathic process and to the presence of diffuse interstitial fibrosis with delayed intraventricular activation. Even in the absence of established bundle branch block, lead-specific prolongation of the QRS complex, such as increased S-wave duration in inferior leads and in V6, may be observed as a result of delayed propagation through the abnormal basal-lateral myocardium or delayed transmural activation from the endocardium to epicardium due to the predominant involvement of the intramural myocardial layers commonly observed in NICM.6 Low-voltage QRS complexes can be found in up to 70% of NICM cases and reflect the diffuse LV interstitial fibrosis with loss of excitable myocardium; they are typically observed in the limb leads, and they may present a discrepancy with precordial QRS voltages that appear to be normal.⁸ Specifically, the amplitude of the R wave in the bipolar limb leads decreases with the increase of LV end-diastolic volume, in contrast to the unipolar precordial leads, which remain unaffected.⁹ Fragmentation or notching of the QRS is a marker of delayed and asynchronous activation of diseased myocardium and is commonly observed in the inferior and lateral leads. Abnormal Q waves are infrequent, but if present, are mostly seen in leads V1 to V4 as poor R-wave progression mimicking the appearance of a myocardial infarction (“pseudoinfarction” pattern).

Scar Patterns in Nonischemic Cardiomyopathy

In the majority (75%) of patients with NICM referred to catheter ablation for recurrent VT, only a modest (< 25%) area of endocardial bipolar voltage abnormality, mostly involving the basal perivalvular region, can be found on EAM voltage mapping. The substrate typically involves the midmyocardium and epicardium, as evidenced by the presence of larger unipolar voltage abnormality correlating with epicardial bipolar low-voltage areas.^3,11,12

On the basis of noninvasive imaging techniques such as late gadolinium enhancement (LGE) cardiac MRI and invasive EAM mapping, two distinct scar patterns have been described in these patients. A predominant anteroseptal scar distribution can be identified in half of the cases, while a predominant inferolateral scar can be found in the remaining half.^13,14 Patients with predominant anteroseptal scar usually have more extensive endocardial scarring, a higher degree of LV dysfunction, and a high prevalence of deep intraseptal substrates. Critical VT sites can be found in the left ventricular outflow tract (LVOT) or anteroseptal LV endocardium in up to 90% of these cases, and VT recurrence rates after ablation are higher in these patients (Figure 25.1).^13,14 On the other hand, patients with a predominant inferolateral scar frequently have an epicardial substrate with critical VT sites located in the inferolateral epicardium in 63%.¹³

Figure 25.1 Patient with advanced nonischemic dilated cardiomyopathy and septal scar. Panel A: The baseline 12-lead ECG shows prolonged PR interval (> 230 ms), complete left bundle branch block with a QRS duration about 170 ms, and presence of a small r wave in V3 (≤ 0.3 mV) consistent with septal substrate. The patient had multiple ventricular tachycardias arising from the interventricular septum. Panel B: Voltage maps confirmed the presence of a large bipolar (Panel C) and unipolar (Panel D) voltage abnormality involving the left ventricular septum.

Although the course of the epicardial coronary vessels and phrenic nerve may complicate VT ablation in up to half of patients with inferolateral scar, these patients typically have better procedural outcomes with reported VT-free survival rates reaching 75% at almost 2 years follow-up, compared to only 26% in the anteroseptal group.14 Patients with predominantly inferolateral substrate are also less likely to require repeat ablation (7% vs. 59%) compared to the anteroseptal group.¹⁴ While a predominant anteroseptal or inferolateral scar pattern can be identified in the majority of patients with NICM, these two groups are not mutually exclusive. In more advanced forms of NICM, the extent of abnormal substrate is greater, spreading beyond the corresponding anteroseptal or inferolateral area.⁷ A significant negative correlation has been found between the extension of the endocardial unipolar low-voltage area, left ventricular ejection fraction (LVEF), wider QRS duration, with a higher incidence of VT recurrence and mortality after catheter ablation.^7,15

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