Hybrid PET/MRI in Arrhythmic Mitral Valve Prolapse
abstract
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Myocardial replacement fibrosis has been reported to occur in one-third of patients with mitral valve prolapse (MVP) and significant mitral regurgitation (MR). However, it remains unknown whether there are detectable changes in myocardial metabolism suggestive of inflammation or ischemia that accompany the development of fibrosis.
Objectives
To characterize the burden and distribution of fluorine 18-labeled (18F) fluorodeoxyglucose (FDG) uptake and late gadolinium enhancement (LGE) in patients with degenerative MVP and ventricular ectopy.
Design, Setting, and Participants
Prospective observational study of 20 patients with MVP and significant primary degenerative MR who were referred for mitral valve repair and underwent hybrid positron emission tomography/magnetic resonance imaging (PET/MRI). Ventricular arrhythmias were categorized as either complex (n = 12) or minor (n = 8). Coregistered hybrid 18F FDG-PET and MRI LGE images were assessed and categorized. Recruitment occurred in the new patient clinic of a mitral valve repair reference center. This study was conducted from January 11, 2018, to June 26, 2019.
Exposures
Simultaneous cardiac 18F FDG-PET and MRI with LGE imaging on a hybrid PET/MRI system and ambulatory rhythm monitoring.
Main Outcomes and Measures
Patients were categorized by the presence and pattern of FDG uptake and LGE, the severity of ventricular arrhythmias, and the indication for mitral valve surgery.
Results
In the cohort of 20 patients, the median age was 59.5 years (interquartile range, 52.5-63.2 years). Focal, or focal-on-diffuse uptake, of 18F-FDG (PET positive) was detected in 17 of 20 patients (85%). The FDG uptake coexisted with areas of LGE (PET/MRI positive) in 14 patients (70%). Of the 5 asymptomatic patients with normal ventricular indices and absence of any surgical indications, all were PET/MRI positive.
Conclusions and Relevance
In this pilot study, we demonstrate a novel association between degenerative MVP and FDG uptake, a surrogate for myocardial inflammation and/or ischemia. Such evidence of myocardial injury, even in asymptomatic patients, suggests an ongoing subclinical disease process. These findings warrant further investigation into whether imaging for myocardial inflammation, ischemia, and scar has a role in arrhythmic risk stratification and whether it provides incremental prognostic value in patients with chronic severe mitral regurgitation undergoing active surveillance.
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Additional Info
Hybrid Positron Emission Tomography/Magnetic Resonance Imaging in Arrhythmic Mitral Valve Prolapse
JAMA Cardiol 2020 May 27;[EPub Ahead of Print], MA Miller, DH Adams, D Pandis, PM Robson, A Pawale, R Pyzik, SL Liao, A El-Eshmawi, P Boateng, J Garg, S Waterford, MM Weiner, SR Dukkipati, VY Reddy, ZA Fayad, MG TrivieriFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Mitral valve prolapse (MVP) is a common disorder, affecting 1% to 3% of the general population. The clinical presentation is quite variable, from being totally benign to life-threatening, the latter often due to severe regurgitation and heart failure or ventricular arrhythmias. Left ventricular fibrosis, perhaps from inflammation and subsequent scarring caused by abnormal valve function, may underlie the development of sustained ventricular tachyarrhythmias, causing sudden cardiac death in 0.2% to 1.9%.1
The present authors tested whether MVP patients with significant degenerative mitral regurgitation and ventricular arrhythmias have evidence of occult inflammation as well as myocardial fibrosis by employing a hybrid approach using positron emission tomography (PET) (fluorine 18–labeled fluorodeoxyglucose; 18F-FDG) as a marker of inflammation and magnetic resonance imaging (MRI) with late gadolinium enhancement (LGE) to detect fibrosis.
In 17 of 20 patients about 60 years old, they found focal or diffuse uptake of 18F-FDG. In 14, the FDG uptake coexisted with areas of fibrosis detected by LGE. Overall, 5 asymptomatic patients with normal ventricular indices also showed these changes. The authors concluded that myocardial inflammation may be present in patients with MVP and degenerative regurgitation even in asymptomatic patients, potentially linking this process to myocardial fibrosis and the subsequent development of ventricular arrhythmias. This important observation raises the possibility that interrupting inflammation in the future may help reduce the risk of sudden cardiac death.
Reference