# Relationship Between Mitral Annular Calcification and Inflammatory Indices in Patients with Cardiometabolic Risk Factors

## TL;DR

This study finds that inflammatory markers are not independently linked to mitral annular calcification once cardiometabolic factors are considered, suggesting metabolic issues are more central to its development.

## Contribution

The study clarifies that inflammatory indices reflect cardiometabolic context rather than being directly linked to mitral annular calcification.

## Key findings

- Inflammatory markers like CRP and NLR differ between patients with and without MAC in unadjusted comparisons.
- After adjusting for cardiometabolic factors, inflammatory markers do not independently associate with MAC.
- Age and glucose metabolism abnormalities are the strongest independent predictors of MAC.

## Abstract

Background: Mitral annular calcification (MAC) is associated with systemic atherosclerosis and cardiometabolic risk factors. Although hematologic inflammatory indices have been reported to be correlated with MAC, whether these associations persist after accounting for the cardiometabolic context in which MAC occurs remains unclear. Methods: In a prospective, cross-sectional study of consecutive adults, patients with mild MAC were compared to those without MAC. Individuals with major inflammatory conditions, advanced chronic kidney disease, cirrhosis, malignancy, autoimmune/acute inflammatory disorders, significant valvular disease, prosthetic valves/pacing devices, psychiatric disorders, or moderate-severe MAC were excluded. C-reactive protein (CRP) and hematological inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR), Systemic Inflammatory Response Index (SIRI), and lymphocyte-to-leukocyte ratio (LLR), were analyzed in relation to MAC status. Results: Among 205 patients, 134 had mild MAC and 71 had no MAC. Patients with MAC were older and displayed higher cardiometabolic burden, including more frequent dysglycemia, higher blood pressure, and greater adiposity. In unadjusted comparisons, inflammatory markers differed according to MAC status: CRP (0.31 mg/dL vs. 0.18 mg/dL, p = 0.002), NLR (2.52 vs. 1.99, p = 0.032), SIRI (1.27 vs. 1.04, p = 0.039), and LLR (0.26 vs. 0.29, p = 0.032). In multivariable logistic regression models, none of the inflammatory markers remained independently associated with MAC. In contrast, age (ORs 1.056–1.063 per year increase, p ≤ 0.001), prediabetes (ORs 2.43–3.63, p ≤ 0.001), and type 2 diabetes (OR 5.91 and 6.19, p ≤ 0.001) demonstrated consistent independent associations with MAC across all models. Conclusions: In this cardiometabolic population with mild MAC, inflammatory indices showed unadjusted differences but no independent associations with MAC after comprehensive cardiometabolic adjustment. These findings are most compatible with inflammatory markers primarily reflecting the cardiometabolic milieu in which MAC occurs rather than representing MAC-specific processes. Age and glucose metabolism abnormalities emerged as the dominant independent factors associated with mild MAC, reinforcing the central role of metabolic dysfunction in MAC pathogenesis.