Cardiac Magnetic Resonance in Primary Prevention of Sudden Cardiac Death

Abstract

Sudden death accounts for 400,000 deaths annually in the United States. Most sudden deaths are cardiac and are related to arrhythmias secondary to structural heart disease or primary electrical abnormalities of the heart. Implantable cardioverter defibrillator significantly improves survival in patients at increased risk of life-threatening arrhythmias, but better selection of eligible patients is required to avoid unnecessary implantation and identify those patients who may benefit most from this therapy. Left ventricular (LV) ejection fraction (EF) measured by echocardiography has been considered the most reliable parameter for long-term outcome in many cardiac diseases. However, LVEF is an inaccurate parameter for arrhythmic risk assessment as patients with normal or mildly reduced LV systolic function could experience sudden cardiac death (SCD). Among other tools for arrhythmic stratification, magnetic resonance (CMR) provides the most comprehensive cardiac evaluation including in vivo tissue characterization and significantly aids in the identification of patients at higher SCD risk. Most of the evidence are related to late gadolinium enhancement (LGE), which was proven to detect cardiac fibrosis. LGE has been reported to add incremental value for prognostic stratification and SCD prediction across a wide range of cardiac diseases, including both ischemic and nonischemic cardiomyopathies. In addition, T1, T2 mapping and extracellular volume assessment were reported to add incremental value for arrhythmic assessment despite suffering from several technical limitations. CMR should be part of a multiparametric approach for patients' evaluation, and it will play a pivotal role in prognostic stratification according to the current evidence.

Keywords: Cardiac magnetic resonance; late gadolinium enhancement; primary prevention; prognostic stratification; sudden cardiac death.

Figure 1

Examples of cardiac magnetic resonance applications in primary prevention: (a) Apical aneurysm of left ventricular with transmural late gadolinium enhancement positivity containing a stratified thrombus after acute myocardial infarction. (b) Diffuse intramyocardial and subepicardial late gadolinium enhancement positivity in a dilated left ventricular consistent with dilated cardiomyopathy. (c) Thickened left ventricular apex with mild late gadolinium enhancement positivity detecting apical hypertrophic cardiomyopathy. (d) Acute myocarditis with subepicardial and intramyocardial edema in a T2-weighted sequence revealing active inflammation. (e) Dilated right ventricular with bulging of the free wall in a patient with arrhythmogenic right ventricular dysplasia. (f) Transmural late gadolinium enhancement of the interventricular septum disclosing sarcoid lesions