Cardiovascular risk factors and mitral annular calcification in type 2 diabetes

ObjectiveMitral annular calcification (MAC) is a degenerative process of the mitral annulus associated with cardiac disease and stroke. Although thought to be more prevalent in type 2 diabetes (T2DM), MAC remains poorly characterized in this population, due to confounding by renal and cardiac disease. Our goal was to study the risk factors for MAC in a sample of T2DM subjects without renal and cardiac disease.MethodsThe Penn Diabetes Heart Study (PDHS) is a cross-sectional study of diabetic individuals without clinical cardiovascular or renal disease. We quantified and analyzed MAC Agatston scores in baseline cardiac CTs from 1753 individuals. Logistic and tobit regression were used to assess MAC's relationship with risk factors and coronary artery calcium (CAC).ResultsMAC was present in 12.0% of subjects, with a median Agatston score of 72.3 [Interquartile range (22.2-256.9)]. Older age, female gender, Caucasian race, and longer diabetes duration were independently associated with both the presence and extent MAC even after controlling for CAC; however, hypertension, hyperlipidemia, tobacco use, CRP levels, and other comorbidities were not associated. CAC was strongly associated with MAC [OR of 4.0 (95% CI 2.4-6.6)] in multivariable models.ConclusionsAge, female gender, Caucasian race, and diabetes duration were associated with the presence and extent of MAC in T2DM subjects, independent of CAC, which was also strongly associated with MAC. These data suggest that additional mechanisms for MAC formation in diabetics may exist which are distinct from those related to generalized atherosclerosis and deserve further investigation.

► Mitral annular calcification (MAC) associates with adverse cardiovascular outcomes. ► We quantified MAC by CT in a large diabetic cohort without kidney or heart disease. ► MAC was not associated with traditional cardiovascular risk factors or CRP. ► Female sex, Caucasian race, and diabetes duration were associated independent of CAC. ► Mechanisms of MAC formation may differ from those of generalized atherosclerosis.