Hybrid Positron Emission Tomography/Magnetic Resonance Imaging in Arrhythmic Mitral Valve Prolapse

Abstract

A subset of patients with mitral valve prolapse (MVP) may develop ventricular arrhythmias (VA) and/or sudden cardiac death at a young age, prior to any perceptible stigmata of myocardial dysfunction or symptoms.¹ Left ventricular (LV) fibrosis identified by cardiac magnetic resonance imaging (MRI) has been described as a consistent feature of MVP-related sustained VAs.² It has been hypothesized that repetitive traction by excess leaflet motion is the inciting stress stimulus that prompts activation of fibroblasts and recruitment of inflammatory cells, which leads to myocardial fibrosis.² Altered myocardial architecture (fibrosis) and electrotonic interactions between cardiomyocytes and myofibroblasts is thought to form the substrate for triggered and reentrant VAs.³ In addition to replacement fibrosis, subclinical myocardial inflammation or ischemia may be an additional proarrhythmic mechanism in patients with MVP.^4,5 We hypothesized that patients with significant degenerative mitral regurgitation (MR) owing to MVP and a history of ventricular ectopy have evidence of occult inflammation in addition to myocardial fibrosis, as detected by integrated fluorine 18–labeled fluorodeoxyglucose (¹⁸F-FDG) positron emission tomography (PET) and MRI (hybrid PET/MRI), an imaging modality that allows for simultaneous detection and quantification of functional, anatomic, and metabolic information.⁶