Abstract

This editorial refers to ‘Prognostic and therapeutic implications of pulmonary hypertension complicating degenerative mitral regurgitation due to flail leaflet: A Multicentre Long-term International Study’ by A. Barbieri et al., doi:10.1093/eurheartj/ehq294 Lack of normal mitral leaflet apposition and abnormal pointing of the flail component into the left atrium (LA) during systole are typical features of mitral leaflet flail which generate haemodynamically relevant mitral regurgitation (MR). The most common reason for mitral leaflet flail is chord rupture.1 Rarely, severe prolapse with the leaflet tip bulging into the LA causing severe MR can also occur without chord rupture.2 The flow direction impacting the mitral leaflets and anatomical features of the leaflets in patients with mitral valve prolapse (MVP) may facilitate chord rupture. Rupture of the chord or papillary muscle is the major cause of acute severe MR due to mitral leaflet flail. Flail mitral leaflet is associated with significant risk of developing left ventricular (LV) dysfunction, atrial fibrillation, pulmonary hypertension, tricuspid regurgitation (TR), heart failure, and sudden death.1–3 Although MVP has a higher prevalence in younger women, mitral leaflet flail often affects males >50 years of age.1,2 The aetiology of mitral leaflet flail is complex. Prolapsed myxomatous mitral valves show collagen and elastic tissue alterations, and in spontaneously ruptured mitral chords the myxomatous process often involves mitral chords and papillary muscles. In spontaneously ruptured chords, collagen types III and AB are often absent. Impaired mechanical properties due to collagen alterations and acid mucopolysaccharide accumulation in the mitral leaflets and chords may lead to spontaneous chord rupture. Myxoid chords are more extensible and weaker than normal chords and the failure resistance is more likely to be compromised in the chord than in the leaflet.2,4 Relevant fibrosis of the myxoid chords, particularly near their …

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