PO-684-06 ARRHYTHMIC MITRAL VALVE PROLAPSE WITH ONLY MILD OR MODERATE MITRAL REGURGITATION: CHARACTERIZATION BY PET/MRI

Abstract

Mitral valve prolapse (MVP) has been associated with ventricular arrhythmias and sudden cardiac death (SCD). A majority of MVP-related SCD occurs in patients with only mild or moderate MR. Replacement fibrosis, which is known to occur in the absence of severe MR, may be preceded and accompanied by an inflammatory response. We previously reported on a series of patients with severe MR planned for elective mitral valve surgery who underwent Hybrid PET-MRI imaging, and demonstrated that >90% of those patients with complex ventricular ectopy had evidence of FDG uptake, suggestive of ongoing subclinical inflammation. To evaluate the presence of myocardial inflammation/fibrosis and VA burden in a cohort of patients with MVP (Barlow’s) and less than severe MR. 10 patients with degenerative MVP and mild or moderate MR by transthoracic echocardiography underwent 18F-FDG PET/MRI (“Hybrid” PET/MRI). Focal 18F-FDG uptake was evaluated as a surrogate of inflammation, and LGE imaging was evaluated for myocardial fibrosis. Ambulatory extended ECG monitoring was performed to assess VA burden and severity. Mean age was 56.3 ±11.4 years, and 70% were female. Mean LVEF and LV end-diastolic diameter were 61.8 ±5.6% and 48.3±6.2 mm. Focal 18F-FDG uptake and LGE (PET+/MRI+) were present in 70% (n=7) of patients (Figure); 1 patient had focal 18F-FDG uptake and LGE was not performed. Only 2 patients had neither inflammation or fibrosis (PET-/MRI-). Complex ventricular ectopy was detected in 80% (n=8). In a cohort of patients with only mild or moderate MR, of which a majority had complex ventricular ectopy, 70% had evidence of myocardial inflammation and fibrosis. These findings may provide insight into the observation that a majority of sudden deaths in patients with MVP occur in patients with less than severe MR, as inflammation and fibrosis are both known to be pro-arrhythmic. Future studies are needed to determine whether the presence of myocardial inflammation impacts the natural history of degenerative MVP.