Abstract 12087: Prevalence and Prognostic Implications of CMR Detected Myocardial Fibrosis in Patients With Mitral Valve Prolapse
Background: Mitral valve prolapse (MVP) is the most common cause of primary mitral regurgitation (MR). Arrhythmia and sudden cardiac death (SCD) have been associated with MVP; however, the mechanism is unclear. Prior studies suggested left ventricular (LV) fibrosis as an arrhythmic substrate.
Hypothesis: MVP patients have an increased prevalence of LV fibrosis which associated with adverse outcome.
Methods: Patients referred for CMR to assess mitral valve disease were enrolled. Confounding causes of LV fibrosis (CAD, LVEF < 50% etc.) and secondary MR were excluded. Primary MR patients were classified into MVP (>2 mm leaflet displacement) and a non-MVP group. Cine, phase contrast CMR were performed to assess cardiac morphology/function and MR severity. Late gadolinium enhancement (LGE) CMR was performed to identify LV fibrosis. Patients were followed for 1) arrhythmic events comprised of SCD/aborted SCD, or sustained/inducible ventricular arrhythmia requiring ICD and 2) composite outcome that included arrhythmic events or cardiovascular death.
Results: 356 primary MR patients (177 MVP, and 179 non-MVP) were enrolled. Baseline characteristics were relatively similar except MVP patients had more severe MR (MR fraction 42.1±14.3% vs. 32.8±12.2%, p<0.03). LGE representing LV fibrosis was more prevalent in MVP group (36.7% vs. 6.7%, p<0.001) and for each MR severity (figure 1A). On multivariate analysis, although lower LVEF, and increasing MR severity were associated with increased LV fibrosis, presence of MVP had the strongest association (OR 6.82, p < 0.001). During the follow up period (median 673 days), MVP patients with LV fibrosis had the highest annualized event rate for arrhythmic events and composite outcome (figure1B).
Conclusion: LV fibrosis is more prevalent in MVP than non-MVP patients with primary MR suggesting a unique pathophysiology in MVP. Presence of LV fibrosis in MVP may represent a risk marker of arrhythmic events and adverse clinical outcome.
Author Disclosures: D. Kitkungvan: None. F. Nabi: None. R.J. Kim: None. R. Bonow: None. J. Xu: None. S.H. Little: None. M. Quinones: None. G. Lawrie: None. W.A. Zoghbi: None. D.J. Shah: None.
- © 2016 by American Heart Association, Inc.