INTRODUCTION

Substrate mapping is recognized as an important step in ventricular tachycardia (VT) ablation strategy. The ability to discern the depth and extent of scar is cornerstone in VT ablation. Electroanatomic mapping (EAM) helps to characterize scars. The presence, precise location, and extent of scar can be reliably identified by detailed voltage mapping. Bipolar and unipolar voltage maps are widely used to distinguish scar tissue from healthy myocardium. Unipolar voltage mapping from the endocardial surface gives invaluable insight into possible deep myocardial substrate abnormalities. This suggestion of transmural extent of a scar is critical information which, when corroborated with other electrophysiological characteristics, enables the operator to make decisive clinical decisions such as shifting to epicardium or focus on septal/midmyocardial substrate.

TYPES OF SCAR: PRESENCE, EXTENT, AND TRANSMURALITY

A myocardial scar can be of variable depth. A transmural scar can involve the entire thickness of the ventricular wall, often seen with ischemic cardiomyopathies (ICM). In contrast, a nontransmural scar is confined to the subendocardium or may involve deeper regions of the myocardium (intramural/epicardial).¹ In nonischemic cardiomyopathy (NICM), the substrate is often heterogenous, patchy, and nontransmural (intramural or epicardial). These scars are classically seen in basal septal, inferior, lateral, and perivalvular regions of the left ventricle (LV).^1,2 With advancement and early access of percutaneous coronary interventions, such patchy scars are now increasingly seen in ICM.^2,3 Therefore, patients with mixed cardiomyopathy may have confluent scar due to ischemia along with patchy scar of nonischemic pattern.⁴

Additionally, even in ICM with confluent scar, while the central core has a dense transmural fibrous tissue, it is generally surrounded by a zone of heterogeneous scar with bundles of viable myocardium interspersed within.⁵ These surviving myocardial cells surrounded by fibrotic tissue in the border zone are responsible for the slow conduction and anisotropy leading to reentrant ventricular arrythmias. During EAM, an endocardial bipolar voltage amplitude of > 1.5 mV has been defined as normal tissue and a voltage amplitude of < 0.5 mV as dense scar.⁶ However, a mismatch has been described in up to one-third of infarct zones, and there are often patches of fibrosis within the endocardium.⁷

Of note, transmural scars can also be seen in NICM. Chagas cardiomyopathy is an example of transmural scar in NICM. However, unlike ICM, the scar in Chagas cardiomyopathy is primarily in LV epicardium with variable endocardial extensions.⁸ Similarly, transmural scar can be seen extending from epicardium to endocardium predominantly in the right ventricle (RV) in arrhthmogenic right ventricular cardiomyopathy (ARVC). In end-stage cardiomyopathies, such as burnt-out hypertrophic cardiomyopathy (HCM) and idiopathic dilated cardiomyopathy, the scar may have a transmural extent. However, the scarring usually emerges epicardially or intramurally and extends to variable depths.¹

Figure 17.1 Panel A: Delayed contrast enhancement with transmural involvement of the basal lateral wall of the LV in a 64-year-old male with a history of a lateral wall myocardial infarction presenting with multiple shocks from the implanted cardioverter-defibrillator. Panel B: Endocardial bipolar voltage map (< 0.5 mV) showing evidence of scar in the basal lateral wall. Panel C: Late systolic potentials in sinus rhythm corresponding to the region of bipolar abnormality (yellow arrow). Panel D: Mid-diastolic potentials in the same region during the ventricular tachycardia. Panel E: Corresponding region of transmural scar as seen on the intracardiac echocardiogram. Panel F: Endocardial unipolar voltage map (< 8.3 mV) revealing a wider area of abnormal substrate. Panel G: Epicardial bipolar map showing a wide and large zone of abnormality. Successful substrate modification was performed in this patient.

Reduced voltage amplitudes of uni- and bipolar electrograms, fractionation, and slowing of conduction with late potentials are some of the characteristic electrophysiological changes seen in areas of scar.9 Detailed EAM can help to delineate these changes and identify the region of scar. Bipolar voltage mapping can give information about the local myocardium and unipolar voltage mapping with a wider field of view can give information about the deeper myocardial substrates like midmyocardium and the epicardium.⁹ However, the characteristic of the uni- and bipolar electrograms depend not only on the transmurality and heterogeneity of the scar but also a number of other variables such as catheter orientation, wall thickness, etc., which have to be accounted for before interpretation of the voltage maps.¹⁰ Table 17.1 shows the variables that may affect endocardial unipolar voltage.^11,12

Conventionally, the normal LV endocardial unipolar voltage is defined as voltage amplitude greater than 8.27 mV.⁹ In NICM, a unipolar voltage amplitude of < 8.27 mV in a setting of normal bipolar voltage may suggest an epicardial substrate.⁹ However, this cutoff value was derived in a cohort with nontransmural scars,⁹ and its utility in presence of any myocardial scar remains unclear. Similarly, the ability of endocardial unipolar voltage abnormalities to pick up epicardial scars in the RV has been shown in multiple studies, though the proposed cutoffs have been variable.^13,14 In fact, since the proposition of unipolar cutoffs of < 8.27 mV in the LV and < 5.5 mV in the RV to define an epicardial scar, multiple cutoffs have been proposed. In Chagas cardiomyopathy, unipolar voltage ≤ 4 mV can identify the epicardial scar.⁸

Table 17.1 Variables That May Affect Endocardial Unipolar Voltage

Additionally, due to wider field of view, other factors can also affect the unipolar voltage amplitude. In areas with endocardial bipolar voltage > 1.5 mV and epicardial fat < 1 mm, a unipolar cutoff of < 3.9 mV could be better in predicting epicardial scars.15

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