Association between triglyceride–glucose index, inflammation, and mitral annular calcification

Mitral annular calcification (MAC), traditionally considered an age-related degenerative process, is now recognized as an active condition sharing pathophysiological features with atherosclerosis. While metabolic dysfunction and chronic inflammation are associated with cardiovascular calcification, their combined role in MAC remains unclear. This observational study enrolled 259 patients (130 MAC+, 129 MAC-) undergoing echocardiography. We calculated the triglyceride-glucose (TyG) index as Ln (fasting triglycerides [mg/dL] × fasting plasma glucose [mg/dL]/2) and derived inflammatory markers (neutrophil-to-lymphocyte [N/L] ratio, lymphocyte-to-monocyte [L/M] ratio, systemic immune-inflammation index) from complete blood counts. Multivariate logistic regression and receiver operating characteristic analyses were used to assess the predictors of MAC. MAC+ patients showed higher TyG index (9.02 ± 0.58 vs 8.76 ± 0.52, P < .001), N/L ratio (P < .001), and lower L/M ratio (P = .001). TyG index > 8.76 predicted MAC with 64.6% sensitivity (area under the curve = 0.621, P = .001), while N/L ratio > 2.08 showed 60.8% sensitivity (area under the curve = 0.615, P = .001). In multivariate analysis, age (odds ratio [OR], 1.09, P < .001), TyG index (OR, 2.76, P = .001), and L/M ratio (OR, 0.79, P = .008) independently predicted MAC. MAC is associated with insulin resistance (reflected by TyG index) and systemic inflammation (elevated N/L ratio, reduced L/M ratio). These findings position MAC as a multifactorial process linked to metabolic and inflammatory pathways. The TyG index, as a simple and cost-effective marker, could potentially be used alongside inflammatory markers in risk stratification for MAC. Future studies should investigate if modulating these factors can alter MAC progression.