Understanding the cellular and hemodynamic mechanisms of myxomatous mitral valve disease, such as Lrp5 receptor regulation, may guide future targeted therapies.
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No immediate clinical implications for mitral valve disease; leaves open Lrp5-targeted therapies for future investigation.
The myxomatous mitral valve is the most common form of valvular heart disease. The pathologic presentation of myxomatous mitral valve disease varies between valve thickness, degree of leaflet prolapse and the presence or absence of flail leaflets. Recent molecular biology studies have confirmed that the myxomatous changes in mitral valve prolapse equals a cartilage phenotype, which is regulated by the Lrp5 receptor. Clinically, echocardiography defines the valve pathology to determine the surgical approach to valve repair or replacement. Furthermore, the timing of surgical valve repair is controversial and is the subject of a current multicenter trial. The results will resolve the timing of whether watchful waiting versus early surgical valve repair decreases morbidity and mortality of this disease process. This review will summarize the current understanding of the cellular and hemodynamic mechanisms of myxomatous mitral valve disease, which may have future implications in the targeted therapy of this disease process.
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Nalini M. Rajamannan (2014) studied this question.
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