Mitral valve prolapse (MVP) is the most common valvular heart disease in developed countries, with a prevalence of 2-3% across the general population (1). It is associated with connective tissue diseases and a genetic component has been described; the presence of parental MVP has been found to increase risk 5-fold (2). It is clinically defined as a systolic superior displacement of one or both mitral valve leaflets, >2mm above the plane of the mitral annulus. MVP is heterogenous but two distinct phenotypic subsets are defined: (i) myxomatous (Barlow’s) disease, characterised by excess tissue and chordal thickening/elongation, as a result of a non-inflammatory, progressive disarray of valve structure and (ii) fibroblastic deficiency, characterised by chordal thinning and a higher probability of chordae rupture (1).