Valvular & structural heart diseaseCohort study
Left Ventricular Remodelling in Mitral Valve Prolapse: More Than Volume Overload
- Prospective inclusion of patients with nonsyndromic mitral valve prolapse (MVP) at 3 centers
Authors' conclusion
LV remodeling in MVP is a multifactorial process, where, especially in patients with Barlow disease, the associated mitral annular dilatation and larger prolapse volume drive LV dilatation beyond MR severity. In addition, a burden of ≥3% ventricular ectopy is strongly correlated with LV dilatation and dysfunction. Finally, a monogenic cardiomyopathy substrate appears unlikely.
Study context
- Population
- Patients with nonsyndromic mitral valve prolapse (MVP)patients with MVP included (58% males, age 52±17 years)
- Participants
- 103 patients
- Exposure
- Determinants of left ventricular (LV) remodeling in patients with MVP beyond mitral regurgitation (MR) volume load
Main finding
As reported in the abstract
Disproportionate LV remodeling present
37%
Observational data: associations, not effects.
Further findings
LV end-systolic volume index, Barlow disease phenotypic features (mitral annular dilatation)
- Independently associated with LV dilatation
- P < 0.001
- R 2
- 0.518
- after correction for age, sex, and MR volume load
- multivariable regression analysis
Total volume load (MR volume+prolapse volume) vs MR volume alone
- Stronger correlation with LV remodeling than MR volume alone
Ventricular arrhythmia (≥3% premature ventricular contractions) and LV end-systolic volume index
- Independently associated with increased LV end-systolic volume index
- P = 0.024
- R 2
- 0.518
- even after correction for other classical risk factors
Likely pathogenic or pathogenic variant in cardiomyopathy-associated genes
- None of the patients carried a variant
Original publication
Summarised from the published abstract; every number is checked against it