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Severe mitral annular calcification is associated with increased cardiovascular risks and presents significant challenges for surgical intervention.
What happens to individuals with severe mitral annular calcification (MAC) over time and how many might be eligible for treatment is of interest as hospitals plan to implement or expand their mitral valve structural heart programs. There is no medical therapy for MAC, nor any well-established biomarkers of progression or cell or animal models of the disease.1 MAC is associated with increased risk of stroke, myocardial infarction, heart failure, and mortality.2,3 Surgical valve replacement or repair of the mitral valve in the presence of MAC is risky and challenging.
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Gonzalez et al. (2025) studied this question.
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