Mitral annular calcification (MAC) is a degenerative process involving fibrous annulus of the mitral apparatus. Mitral annular calcification is associated with various clinical risk factors, such as diabetes mellitus, hypertension and hypercholesterolaemia. It is also known that patients with MAC have a higher prevalence of cardiovascular events and stroke. The atherosclerotic process as result of endothelial disruption at the foci of increased mechanical stress has been proposed as the pathophysiology of MAC. In their paper, Chan et al. investigated the possible impact of MAC on outcomes of myxomatous mitral valve repair. They also defined risk factors for MAC in severe mitral regurgitation due to myxomatous degeneration [1]. Severity of MAC is generally graded qualitatively, with calcification of less than one-third of the annulus reported as "mild", and greater than two-thirds reported as "severe." The thickness of the calcific band is another determinant of severity and can be echocardiographically measured from the parasternal long-axis view. In a subgroup analysis of the Framingham Heart Study, risks of incident cardiovascular disease (CVD), cardiovascular death, and all-cause death was found to increase by approximately 10% per 1-mm increase in MAC thickness [2]. The Northern Manhattan Study enrolled 1955 subjects without prior myocardial infarction or ischaemic stroke and followed up for a mean duration of 7.4 years. The severity of MAC was considered mild to moderate if calcification thickness was between 1-4 mm and severe if >4 mm. MAC was associated with increased risk of MI (adjusted HR 1.75, 95% CI 1.13-2.69) and vascular death (adjusted HR 1.53, 95% CI 1.09-2.15). Increasing MAC severity was associated with worsening study outcomes [3].
In conclusion, the link between MAC and CVD risk is gradual upon calcification severity. When dealing with MAC, qualitative assessment of the calcification should be done specifically.
Conflict of interest: none declared.
References
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