Mitral Annulus Calcification

Abramowitz Y, Jilaihawi H, Chakravarty T, Mack MJ, Makkar RR.
Mitral Annulus Calcification. J Am Coll Cardiol 2015;66:1934-1941.

Mitral annulus calcification (MAC) is a commonly observed chronic, degenerative process of the base of the mitral valve. This review describes MAC, and reviews pathophysiological mechanisms contributing to its formation and clinical implications of its presence. The following are 10 points to remember:

  1. MAC is a chronic, degenerative process of the fibrous support of the mitral valve.
  2. MAC is usually visualized on echocardiography as an echo-dense shelf-like structure with an irregular, lumpy appearance involving the mitral valve annulus, with associated acoustic shadowing. In the Cardiovascular Health Study (Barasch E, et al. Am Heart J 2006;151:39-47), MAC was quantified as mild (focal, limited increase in echodensity of the mitral annulus), moderate (marked echodensity involving one third to one half of the ring circumference), or severe (marked echodensity involving more than half of the ring, or with intrusion into the left ventricular [LV] inflow tract).
  3. Electron-beam computed tomography (CT) and multislice (spiral) CT are effective, noninvasive means that can predict the extent and location of MAC, and objectively quantify the severity of MAC.
  4. The pathophysiological mechanisms contributing to MAC are not fully understood. Contributing factors include:
    • Degenerative, age-related factors.
    • Atherosclerosis. Many studies have shown a strong association between MAC and cardiovascular risk factors.
    • Increased mitral valve stress. MAC appears to be accelerated in association with hypertension, aortic stenosis, and hypertrophic cardiomyopathy.
    • Abnormal calcium-phosphorus metabolism. MAC is a common finding in patients with chronic kidney disease.
    • Congenital metabolic disorders. MAC can be seen in association with Marfan syndrome (it is unclear if the mitral annulus calcifies because of increased mitral valve stress caused by mitral valve prolapse, or due to an intrinsic abnormality of connective tissue) and Hurler syndrome (likely associated with abnormal fibroblasts and accelerated collagen degeneration).
    • Female sex.
  5. MAC is most often an incidental finding among patients being evaluated for cardiovascular or pulmonary disease.
  6. MAC is associated with cardiovascular risk factors, and appears to be associated with an increased risk of incident cardiovascular disease, cardiovascular death, and all-cause death.
  7. There are inconsistent findings with respect to any association between MAC and risk for clinical stroke.
  8. MAC generally has little or no impact on LV inflow hemodynamics or mitral valve function. There are limited data suggesting that MAC may exacerbate mitral regurgitation. Mitral stenosis due to MAC has been rarely reported.
  9. Patients with MAC have a higher prevalence of atrioventricular block, bundle branch block, intraventricular conduction delay, and atrial fibrillation.
  10. MAC can have implications at the time of surgical or transcatheter interventions:
    • Severe MAC can complicate mitral valve replacement. There is a risk of cardiac rupture at the atrioventricular junction or the LV free wall, or injury to the circumflex artery during debridement; and residual paraprosthetic mitral regurgitation with less aggressive debridement.
    • Severe MAC has been considered a contraindication for percutaneous mitral valve intervention with the MitraClip.
    • MAC is an independent predictor of permanent pacemaker implantation following transcatheter aortic valve replacement.

< Back to Listings