Advances in Arrhythmia and Electrophysiology Applications of Cardiac Magnetic Resonance in Electrophysiology

Because of its wide availability, echocardiography is the most frequently used modality for diagnosis of the underlying substrate for cardiac arrhythmia. However, echocardiography is unable to visualize intramyocardial substrates for reentrant arrhythmia such as fat or scar fibrosis. Replacement of myocytes with nonviable tissue results in hypertrophy of the remaining viable cells and is associated with altered ion channel and gap junction expression. These changes affect myocardial mechanical function and promote arrhythmia.1 Because of its soft-tissue resolution, multiplanar imaging capabilities, and specialized techniques uniquely suited for diagnosis of various structural changes,2 cardiac magnetic resonance (CMR) offers significant advantages for identification of arrhythmic substrates. Ischemic cardiomyopathy (ICM) is ventricular dysfunction resulting from coronary artery disease and myocardial infarction and is a common substrate of ventricular arrhythmia. Techniques to visualize infarcted myocardium in the acute3–7 and chronic8–11 settings have been well described and rely primarily on steady-state free precession cine CMR for evaluation of function, and late gadolinium enhancement (LGE) imaging to assess scar burden and distribution. The steady-state free precession cine technique relies on short repetition times and electrocardiographic gating to provide dynamic visualization of the heart during the full cardiac cycle. The LGE technique uses an inversion recovery gradient echo sequence with optimization of the inversion time set to null the signal of normal myocardium. In the setting of ICM, images are acquired 10 to 15 minutes after intravenous administration of 0.2 mmol/kg gadolinium chelate. Gadolinium chelates are hydrophilic and have low molecular weights thereby concentrating into the extracellular fluid space. The extent of LGE is primarily determined by expansion of the extracellular space in fibrotic tissue, which slows washout of the gadolinium chelates.12 This “delayed” time period from contrast administration to scan acquisition allows clearance of the contrast medium from the normal myocardium, whereas nonviable myocardium shows LGE due to enhanced relaxivity of excited protons adjacent to retained gadolinium, which increases the signal on T1-weighted images. Hypertrophic cardiomyopathy (HCM) is characterized by myocardial hypertrophy resulting from an inherited defect in the protein components of the cardiac sarcomere. In cases where hypertrophy occurs at the basal septum, subaortic outflow obstruction and mitral regurgitation due to systolic anterior motion of the anterior leaflet of the mitral valve can be present. Echocardiography is the standard technique for evaluation of HCM.13 CMR is an appropriate alternative to confirm the diagnosis or identify atypical cases,14,15 and is most useful when the echocardiography acoustic window is limited.16 LGE can detect midwall and patchy scar in regions with hypertrophy (Figure 1A).17 Necropsy studies have revealed good correlation between the LGE pattern of enhancement and the distribution of scar.16,18 Nonischemic cardiomyopathy (NICM) is characterized by ventricular dilatation and impaired contraction in the absence of flow limiting coronary disease. Although some cases are due to viral, genetic, toxic, or immune causes, many are of unknown etiology. The anatomic and functional abnormalities of NICM are readily assessed by cine CMR.19 Midwall striae or patches of LGE can be identified in approximately one third of patients (Figure 1B).20–22 Compared with ICM, the pattern and location of LGE in NICM is often atypical, making it difficult to distinguish artifact from true scar. The presence of scar should, therefore, be verified by use of multiple image planes and optimized inversion times. Sarcoidosis with cardiac involvement is relatively uncommon ( 5% of patients with pulmonary sarcoidosis). Currently used techniques, including echocardiography,23 scintigraphy,24 and myocardial biopsy25 are often inadequate for early diagnosis. In patients with systemic sarcoidosis suspected of cardiac involvement, CMR may provide a diagnostic alternative and a method by which disease activity can be followed.26–29 Because of increased T2 relaxation time, inflammatory sarcoid granules present as high signal intensity regions on T2-weighted images. Focal areas of LGE likely representing fibrosis can be noted (Figure 1C), most commonly in the basal segments of the left ventricle (LV).30 Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by enlargement, dysfunction, and fibro-fatty infiltration of the right ventricle (RV). Given its ability to comprehensively image the RV31 and characterize fibro-fatty infiltration, CMR has emerged as an important adjunct for the diagnosis of ARVD.32–34 CMR abnormalities in ARVD can