Mitral valve calcification (MVC), particularly mitral annular calcification (MAC), is a chronic degenerative process commonly observed in elderly individuals and is increasingly recognized as a marker of cardiovascular morbidity and mortality (1). The prevalence of MVC rises with advancing age, and it is often associated with conditions such as hypertension, chronic kidney disease, dyslipidemia, and notably, diabetes mellitus (DM) (2,3). MVC not only contributes to valvular dysfunction, including mitral stenosis or regurgitation, but is also linked to an elevated risk of arrhythmias, thromboembolic events, and adverse cardiovascular outcomes (4).

Diabetes mellitus, a global health concern characterized by chronic hyperglycemia, is known to accelerate atherosclerosis and vascular calcification through complex metabolic and inflammatory pathways (5). Hyperglycemia promotes endothelial dysfunction, oxidative stress, and the activation of pro-calcific signaling cascades, all of which contribute to ectopic calcification in both vascular and valvular tissues (6,7). Several studies have demonstrated that patients with DM are predisposed to more severe calcific changes in various cardiovascular structures, including coronary arteries and heart valves (8).

The interplay between DM and MVC is of particular concern in elderly populations, where both conditions frequently coexist. While previous research has highlighted an association between DM and valvular calcification, the extent to which diabetes influences the severity of MVC remains underexplored (9). Moreover, poor glycemic control has been implicated in accelerating degenerative valvular changes, suggesting that metabolic management may play a role in mitigating disease progression (10).

Given the increasing burden of diabetes in aging populations and the clinical implications of MVC, it is essential to understand this association better. This study aims to evaluate the relationship between diabetes mellitus and the severity of mitral valve calcification in elderly patients, with a focus on the impact of glycemic control on calcification severity

This cross-sectional observational study was conducted at the Department of Cardiology of a tertiary care hospital between January 2024 and December 2024. The study included elderly patients aged 65 years and above who underwent transthoracic echocardiography (TTE) for various clinical indications during the study period.

Inclusion Criteria:

Patients aged ≥65 years with available echocardiographic data were included. The diabetic group comprised individuals with a confirmed diagnosis of Type 2 Diabetes Mellitus based on American Diabetes Association (ADA) criteria, either through medical records or ongoing antidiabetic treatment.

Exclusion Criteria:

Patients with rheumatic heart disease, prior mitral valve surgery, infective endocarditis, congenital heart defects, chronic inflammatory diseases, or advanced chronic kidney disease (stage 4 or higher) were excluded to eliminate confounding factors influencing calcification.

Echocardiographic Assessment:

All participants underwent standardized transthoracic echocardiography using a Philips iE33 system equipped with a 2.5–3.5 MHz transducer. Mitral valve calcification (MVC) was identified and graded by experienced cardiologists blinded to the patients' diabetic status. The severity of MVC was categorized as mild, moderate, or severe based on echogenicity, extent of calcification along the annulus, and involvement of leaflets, following established echocardiographic criteria.

Clinical and Biochemical Data Collection:

Demographic details, medical history, duration of diabetes, hypertension status, and lipid profile were recorded. Glycemic control was assessed using the most recent glycated hemoglobin (HbA1c) levels within three months of the echocardiographic evaluation.

Statistical Analysis:

Data were analyzed using SPSS version 26. Continuous variables were expressed as mean ± standard deviation, while categorical variables were presented as frequencies and percentages. The association between diabetes mellitus and MVC severity was evaluated using the chi-square test for categorical variables. Logistic regression analysis was performed to adjust for potential confounders such as age, hypertension, and dyslipidemia. A p-value of less than 0.05 was considered statistically significant.

A total of 150 elderly patients were enrolled in the study, comprising 80 individuals with Type 2 Diabetes Mellitus (DM group) and 70 non-diabetic controls (Non-DM group). The mean age of participants was 71.4 ± 5.2 years, with no significant difference in age or gender distribution between the two groups (p>0.05).

Severity of Mitral Valve Calcification in Study Groups

The distribution of mitral valve calcification (MVC) severity differed significantly between diabetic and non-diabetic patients. In the DM group, 45% of patients exhibited severe MVC, compared to only 20% in the Non-DM group. Mild calcification was more prevalent among non-diabetics (50%) than diabetics (20%) (Table 1). The association between diabetes and higher MVC severity was statistically significant (p=0.002).

Table 1: Distribution of Mitral Valve Calcification Severity in Diabetic and Non-Diabetic Patients

*Statistically significant

Impact of Glycemic Control on MVC Severity

Among diabetic patients, those with poor glycemic control (HbA1c ≥8%) demonstrated a higher prevalence of severe MVC compared to patients with HbA1c <7%. Specifically, 52% of poorly controlled diabetics had severe MVC, while only 30% of well-controlled diabetics showed similar severity (Table 2). This difference was significant (p=0.01).

Table 2: Association of Glycemic Control (HbA1c Levels) with MVC Severity in Diabetic Patients (n=80)

*Statistically significant

Multivariate Analysis

Logistic regression analysis revealed that diabetes mellitus was independently associated with severe MVC (Odds Ratio [OR]: 2.8; 95% Confidence Interval [CI]: 1.5–5.3; p=0.001) after adjusting for age, hypertension, and dyslipidemia (Table 3).

Table 3: Multivariate Logistic Regression Analysis for Predictors of Severe Mitral Valve Calcification

*Statistically significant

In summary, diabetic patients exhibited a significantly higher severity of mitral valve calcification compared to non-diabetics (Table 1). Poor glycemic control further increased the risk of severe calcification (Table 2). Diabetes remained an independent predictor of severe MVC even after adjusting for common cardiovascular risk factors (Table 3).

This study demonstrates a significant association between diabetes mellitus (DM) and increased severity of mitral valve calcification (MVC) in elderly patients. Our findings indicate that individuals with DM, particularly those with poor glycemic control, are more likely to develop severe MVC compared to non-diabetic counterparts. These results are consistent with previous research highlighting the role of metabolic disorders in promoting valvular calcification (1,2).

MVC, particularly mitral annular calcification (MAC), has long been recognized as a degenerative process linked to aging and cardiovascular risk factors (3). Diabetes mellitus contributes to this pathophysiology through mechanisms such as chronic inflammation, oxidative stress, and endothelial dysfunction, all of which facilitate calcific deposition in cardiovascular structures (4,5). Hyperglycemia-induced activation of pro-calcific pathways, including advanced glycation end products (AGEs) and transforming growth factor-beta (TGF-β) signaling, has been implicated in accelerating calcification of both vascular and valvular tissues (6,7).

Our study observed that 45% of diabetic patients exhibited severe MVC, a significantly higher proportion compared to 20% in non-diabetics. Similar trends have been reported by Elmariah et al., where DM was identified as an independent risk factor for advanced MAC (8). Furthermore, poor glycemic control, reflected by elevated HbA1c levels, showed a strong correlation with severe calcification, supporting the hypothesis that sustained hyperglycemia exacerbates valvular degeneration (9,10). These findings emphasize the importance of optimal metabolic control in preventing or slowing the progression of MVC.

In addition to diabetes, traditional cardiovascular risk factors such as hypertension and dyslipidemia are known contributors to MVC development (11). However, in our multivariate analysis, DM remained an independent predictor of severe MVC after adjusting for these confounders, aligning with prior studies that highlight the unique impact of diabetes on calcific processes (12).

The clinical implications of MVC are substantial, as severe calcification is associated with increased risks of mitral valve dysfunction, atrial fibrillation, conduction abnormalities, and cardiovascular mortality (13). Diabetic patients with MVC may therefore represent a high-risk group requiring closer cardiovascular monitoring. Moreover, emerging evidence suggests that MVC serves not only as a marker of localized valvular disease but also as a surrogate indicator of systemic atherosclerosis and calcific burden (14,15).

While our study provides valuable insights, certain limitations should be acknowledged. The cross-sectional design precludes establishing causality between DM and MVC progression. Additionally, we relied on echocardiographic assessment, which, despite being non-invasive and widely used, may have interobserver variability in grading calcification severity. Future longitudinal studies with larger cohorts and advanced imaging modalities, such as cardiac CT, could offer a more detailed evaluation of calcific progression in diabetic populations.

In conclusion, our findings reinforce the association between diabetes mellitus and increased severity of mitral valve calcification in elderly patients. Poor glycemic control further amplifies this risk, underscoring the need for stringent metabolic management. Early identification of MVC in diabetic individuals could aid in risk stratification and guide preventive cardiovascular strategies.

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