INTRODUCTION

Cardiac magnetic resonance imaging (MRI) helps to identify scarring in patients with ischemic and nonischemic cardiomyopathy. Prior studies indicated that the location of scarring indicates the location of the arrhythmogenic substrate.^1–3 Its value is probably greatest for patients whose scar location is unknown and may involve the epicardium or the midmyocardium—hence, patients with nonischemic cardiomyopathy.

CARDIAC MAGNETIC RESONANCE METHODS

Cardiac MRI can characterize the myocardial tissue through multiple methods/contrasts, but the detection and mapping of arrhythmogenic substrates within the ventricles mostly relies on late gadolinium-enhanced imaging (LGE), which is the gold-standard method to image focal scars in patients. The method consists of acquiring T1-weighted images at the late phase (> 10 min) after the injection of gadolinium-based contrast agents. At this phase, the tracer is distributed within the extracellular space and therefore shows increased concentration in scar, which is a rather pauci-cellular fibrous tissue, as compared to the remaining myocardium composed mostly of myocytes. The key of LGE imaging methods is to further enhance the contrast between normal and diseased areas by applying a magnetization preparation scheme (called inversion-recovery) to artificially blacken the myocardium outside scar areas.⁴ This is both the strength of LGE imaging, providing unparalleled contrast between normal and diseased areas, and its weakness, giving access only to a relative contrast and preventing the assessment of diffuse fibrosis within the supposedly normal myocardium.

LGE imaging can be performed using multiple approaches: 2D, 3D, with or without fat-suppression schemes, and with highly variable spatial resolutions. In the context of ventricular arrhythmias, and particularly in patients with epicardial substrates, LGE ideally should be performed using 3D methods to enable the integration of 3D substrate maps during ablation procedures.⁵ Likewise, LGE methods should be performed at the highest spatial resolution, which requires the use of free-breathing techniques (voxel volume down to 1 mm³ vs. up to 32 mm³ using conventional breath-hold methods), in order to detect small or thin subepicardial scars.⁶ In addition, the suppression of fat signal should be optimized to distinguish subepicardial scars from the adjacent epicardial fat.

Besides LGE, other cardiac MRI contrasts can be of interest to characterize the structural substrate of epicardial ventricular arrhythmias. Precontrast T1-weighted imaging with and without preparation schemes to suppress the signal from fat has been used to identify intramyocardial fat, mostly in the context of arrhythmogenic right ventricular cardiomyopathy (ARVC).⁷ T1 mapping can be performed before and after contrast to quantify the extracellular volume fraction, which in the context of ventricular arrhythmias is mostly used to detect diffuse fibrosis, which has been shown to be associated with ventricular arrhythmias in nonischemic diseases, independent of LGE.^8,9 T2-weighted imaging and T2 mapping can be used to identify edema and may be valuable in the context of ventricular arrhythmias to detect an inflammatory state potentially amenable to medical therapy (e.g., sarcoid). Last, the spatial resolution of most tissue characterization methods remains somewhat limited to accurately image the right ventricular (RV) free wall, and in that context, cine imaging still plays an important role to detect RV substrates, particularly in ARVC patients—RV wall motion abnormalities often being the only sign of regional dysplasia.

The distribution of LGE throughout the myocardium is the cornerstone of the etiological diagnosis of structural heart disease on cardiac MRI. In the context of ventricular arrhythmias, LGE-MRI is particularly critical in nonischemic diseases, in which echocardiography and coronary angiography are often negative and do not provide accurate assessment of the transmural location of scar.6

Post-infarct Ventricular Tachycardia

Patients with post-infarction ventricular tachycardia (VT) show a LGE distribution matching a coronary artery territory. The extent of substrate can be highly variable across patients, both in terms of surface and transmurality. Even when transmural, the largest surface of the scar is most commonly located on the endocardial surface. Patients with nonischemic substrates will show a much broader range of LGE distribution patterns, depending on the underlying disease.

Idiopathic Dilated Cardiomyopathy

In idiopathic dilated cardiomyopathy (DCM), LGE can be negative in about 50% of the patients, although the LGE prevalence is much higher in those experiencing VT, reflecting the arrhythmogenic role of focal scar in DCM.¹⁰ Typical scars in DCM consist of intramural striae-like LGE, most commonly found on the basal septum and the inferolateral wall, potentially extending subepicardially on the anterior and inferolateral free wall.

Postmyocarditis VT

Patients with postmyocarditis VT will show variable LGE patterns, ranging from striae-like confluent scars to discontinuous patchy scars, both being of either intramural or subepicardial location. These mostly involve the LV free wall and less commonly the septum or the RV.

Cardiac Sarcoid

Patients with cardiac sarcoid will also show variable imaging presentation, and imaging findings will particularly depend on the disease stage. At the inflammatory phase, granulomas appear as thick, nodular LGE of intramural or subepicardial location, which can be distributed on the free walls of both ventricles as well as on the septum, the septo-basal location being quite suggestive. Also, a multifocal pattern of LGE involving parts of the left and right ventricle is not uncommon. Besides LGE, T2-weighted imaging or T2 mapping can show intense edema both at the site of granulomas and within the surrounding myocardium. At the chronic stage and in the absence of persisting inflammation, sarcoid lesions will shrink and evolve into less specific focal or striae-like scars following a similar distribution.

Hypertrophic Cardiomyopathy

Patients with hypertrophic cardiomyopathy (HCM) also have variable scar distribution. As in DCM, LGE is negative in many HCM patients, but LGE prevalence is much higher in those experiencing ventricular arrhythmias, reflecting the arrhythmogenic role of focal scar in HCM.¹¹ The most common LGE locations in HCM are (1) intramural patchy scars of highly variable density, most commonly found in hypertrophied segments and particularly on the septum, which can extend to the epicardial surface of the septum, (2) focal nodular scars on anterior and posterior RV insertions, (3) subendocardial scars suggestive of past ischemic events secondary to microvascular dysfunction, and (4) transmural apical scars in patients with apical aneurysms.

Arrhythmogenic Right Ventricular Cardiomyopathy

In patients with ARVC, conventional cardiac MRI methods still show spatial resolution limitations to directly image the RV substrate with tissue characterization techniques. Thus, the gold standard to assess the regional distribution of the disease on the RV remains the documentation of RV wall motion abnormalities with the use of cine imaging. The method can now be combined with feature tracking techniques, giving access to strain quantification.¹² However, tissue characterization techniques are also improving and the assessment of LGE distribution on the RV may become feasible using the most recent high-resolution free-breathing LGE techniques.¹³ In any case, LGE imaging remains critical in ARVC to detect LV involvement, which is present on cardiac MRI in a majority of patients and largely under-detected by other tests.¹⁴ Left ventricular LGE patterns in ARVC will typically consist of striae-like lesions of intramural or subepicardial location involving the left ventricular free wall, often mimicking postmyocarditis or sarcoid presentations. Of note, septal involvement is much less common in AVRC than in sarcoid. Figure 14.1 shows examples of LGE findings in patients presenting with epicardial arrhythmia secondary to various underlying etiologies.

The decision to access and map the epicardial space depends on the origin of the ventricular arrhythmia and on whether the arrhythmia can be reached from the endocardium. The location and extent of the arrhythmogenic substrate differs depending on the type of cardiac disease. It may be mainly confined to the endocardium in ischemic cardiomyopathy, to the intramural myocardium in idiopathic dilated cardiomyopathy, or to the epicardium in ARVC or postmyocarditis. Hence, the necessity to obtain epicardial access is rather low in patients with ischemic cardiomyopathy, while it is higher for patients with DCM, and even higher in patients with ARVC where the highest success and lowest recurrence rates have been reported in series that used both epicardial and endocardial mapping in a majority of the patients.15–17

In most centers, the decision to perform an epicardial access will be based on the underlying etiology and/or on a prior unsuccessful endocardial ablation procedure. However, several recent studies have investigated the use of cardiac MRI to make such a decision. Studying a cohort of 80 patients with scar-related VT of various etiologies, Andreu et al. reported that finding subepicardial LGE on cardiac MRI predicted an epicardial origin of the VT, defined as a successful ablation site on the epicardium, with 85% sensitivity and 100% specificity.³ This finding also seems to hold true in postmyocardial infarction VT, the same group reporting higher success rates in postmyocardial patients with prior infarctions with transmural scar on cardiac MRI when performing a first-line combined endo-epicardial approach as compared to an endocardial approach only.¹⁸ As expected, the presence of epicardial substrate on contact mapping in patients with transmural MI relates to the size of epicardial scar¹⁹ and to the degree of wall thinning on imaging.^19,20

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