Assessment of Valvular Oxidative Stress in a Young Patient with Primary Severe Mitral Regurgitation

Abstract

Mitral valve regurgitation (MR) is the most common valvular heart disease. Diagnosing and managing mitral regurgitation is often challenging and requires a structured approach, integrating findings on history, physical examination and imaging. A common cardiac anomaly is myxomatous mitral valve prolapse. Excess myxomatous leaflet tissue, bileaflet prolapse or billowing, chordae elongation and annular dilatation are all features of Barlow’s disease. Currently, there is no successful pharmacological treatment available to prevent or slow its progression. Here, we report the case of a 30-year-old male patient, with no previous significant medical background and no medication at home, who was diagnosed with severe mitral regurgitation at a regular check-up and was admitted to our clinic with mild exertion dyspnea and fatigue. Transthoracic echocardiography showed intensely thickened mitral leaflets with a myxomatous appearance, prolapse of the middle scallop of the posterior leaflet (P2), apparently with ruptured chordae, and severe mitral regurgitation with a holosystolic eccentric jet. While oxidative stress is a central pathomechanism of cardiovascular disease, information regarding valvular oxidative stress in the literature is rather scarce. In this respect, we assessed oxidative stress through confocal microscopy in a sample of a mitral valve harvested during valvular surgery. We found an increased production of reactive oxygen species in the mitral valve sample that was alleviated after incubation with the angiotensin 2 receptor type I (AT1) antagonist irbesartan. This case is worth mentioning as a starting point for a prospective study aimed at assessing the role of valvular oxidative stress and mitochondrial dysfunction in patients with various degrees of primary and secondary mitral regurgitation.