European Journal of Cardiovascular Medicine

Diabetes mellitus (DM) is a complex group of metabolic disorders arising from multifactorial interactions between genetic predisposition and environmental influences, characterized by abnormalities in insulin secretion, insulin action, or both [1-3]. It is a chronic condition involving disturbances in carbohydrate metabolism, wherein insufficient insulin availability or diminished insulin activity results in persistent hyperglycemia, ultimately affecting protein and lipid metabolism. In Type I DM, autoimmune-mediated destruction of pancreatic β-cells leads to absolute insulin deficiency, whereas in Type II DM, insulin production is inadequate and its biological effectiveness is impaired [4]. Although Type I DM remains clinically important, Type II DM constitutes more than 90% of all cases, primarily due to insulin receptor downregulation, insulin resistance, and progressive pancreatic β-cell dysfunction. Lifestyle-related factors significantly contribute to its rising prevalence.

Cardiovascular disease (CVD) represents one of the most significant complications of Type II DM, with affected individuals experiencing nearly double the risk compared to the general population [5]. Importantly, diabetes can lead to early subclinical cardiac dysfunction, marked by structural and functional abnormalities that arise even in asymptomatic patients. These changes are largely driven by metabolic risk factors—including obesity, dyslipidemia, and inadequate glycemic control—which accelerate the development of diabetic cardiomyopathy. Echocardiography serves as a key non-invasive diagnostic modality, enabling early detection of myocardial alterations such as diastolic dysfunction, left ventricular hypertrophy, and subtle systolic impairment, often preceding the onset of overt heart failure [6].

Dyslipidemia is a frequent metabolic abnormality in DM, affecting nearly 50% of patients, with higher incidence among those with poorly controlled glycemia. Abnormal lipid metabolism plays a pivotal role in the development of microvascular complications, coronary artery disease (CAD), cerebrovascular accidents, and peripheral vascular disease. Cardiovascular causes account for approximately 75–80% of mortality among diabetic patients. South Asians, particularly Indians, exhibit a higher genetic susceptibility to both DM and CAD, with diabetic individuals experiencing a 2–3-fold higher risk of CAD, a fourfold increase in mortality from acute myocardial infarction (MI), and double the risk of post-MI morbidity compared to their non-diabetic counterparts [7,8].

Given the significant overlap between dyslipidemia, cardiac structural and functional abnormalities, and glycemic control, the present study aims to assess the prevalence of lipid abnormalities in patients with Type II DM and investigate whether echocardiographic changes suggestive of ischemia correlate with glycemic parameters. Furthermore, it seeks to determine the association between dyslipidemia and echocardiographic findings in this population, thereby contributing to early risk stratification and targeted interventions.

After obtaining approval from the Institutional Ethics Committee (IEC), a cross-sectional study was carried out at Sri Aurobindo Medical College and Post Graduate Institute, Indore. The study included male and female patients from the Outpatient Department (OPD), Inpatient Department (IPD), and Intensive Care Unit (ICU) who had a confirmed diagnosis of diabetes mellitus (DM) and met the eligibility criteria. A total of 136 participants were recruited through voluntary consent. Given that the hospital manages over 200 diabetic cases annually, the selected sample size was considered both practical and representative of the target population.

Inclusion and Exclusion Criteria: The study included patients aged 20–70 years, those predisposed to diabetes, and those at high risk for cardiac disease who were willing to participate. Patients younger than 20 years, those with significant comorbidities such as sepsis, organ failure, or malignancy, and pregnant women were excluded.

Methodology

Patients meeting the inclusion criteria were approached during their hospital visits and informed in detail about the purpose, methodology, and significance of the study. Written informed consent was obtained from all willing participants. Data were recorded using a pre-structured proforma that included demographic information, detailed medical history, clinical examination findings, and results of laboratory and echocardiographic investigations.

All patients underwent thorough clinical evaluation followed by relevant biochemical and echocardiographic assessments.  Baseline demographic and anthropometric data, including age, gender, height, weight, body mass index (BMI), and relevant medical history, were recorded for all participants through a questionnaire-based interview and physical examination.

Determination of Blood Glucose

Blood samples were collected from the antecubital vein under aseptic precautions. For fasting blood glucose estimation, 4 ml of venous blood was drawn after an overnight fast. Postprandial blood sugar (PPBS) was measured from a second sample taken two hours after a standardized breakfast. Blood glucose levels were determined using the glucose oxidase–peroxidase enzymatic method (end-point, kit method) on an ERBA-CHEM-7 semi-autoanalyzer. Glycosylated hemoglobin (HbA1c) was measured using the ion-exchange resin method (end-point).

Lipid Profile Assessment

Serum lipid profile was analyzed for the following parameters:

• Total Cholesterol (TC): Measured by the cholesterol oxidase enzymatic method (end-point, kit method) using a TURBO CHEM 100 fully automated analyzer.
• High-Density Lipoprotein (HDL) Cholesterol: Estimated by the phosphotungstic acid precipitation method (end-point, kit method).
• Low-Density Lipoprotein (LDL) Cholesterol: Calculated using Friedewald’s formula.
• Triglycerides (TG): Measured by the glycerol phosphate kinase enzymatic method (end-point, kit method).

Echocardiographic Evaluation

All patients underwent 2D echocardiography using a Philips/GE echocardiography system equipped with a standard transducer probe. The examinations were conducted by a qualified cardiologist who was blinded to the patients’ clinical details, in accordance with the recommendations of the American Society of Echocardiography (ASE). To strengthen the study’s statistical validity, the following echocardiographic parameters were recorded:

• Left Ventricular Ejection Fraction (LVEF): for evaluation of systolic function.
• Left Ventricular Mass Index (LVMI): to assess cardiac structural remodeling.
• E/A ratio (Early-to-Late ventricular filling): as a marker of diastolic dysfunction.
• Global Longitudinal Strain (GLS) measured by speckle-tracking echocardiography: for detection of early or subclinical myocardial dysfunction.

Statistical Analysis

Laboratory results were transcribed directly from official reports into the proforma. The collected data were entered into Microsoft Excel 2010 and analyzed using appropriate statistical software. Quantitative variables were summarized as mean ± standard deviation (SD), while qualitative variables were presented as frequencies and percentages. Graphical representation using pie charts and bar diagrams was employed for demographic variables. Associations between categorical variables were analyzed using the Chi-square test, while correlations between quantitative variables were assessed using Pearson’s correlation or Spearman’s rank correlation coefficient with scatter plot analysis. A p-value less than 0.05 was considered statistically significant, whereas values equal to or greater than 0.05 were deemed insignificant.

In the present study, a total of 136 patients with Type II diabetes mellitus were evaluated, with a mean age of 52.18 ± 9.62 years. In this study of 136 Type II diabetic patients, males constituted a slightly higher proportion (55.88%) compared to females (44.12%). The largest age groups were 35–40 years and 46–50 years, each accounting for 21.32% of participants, followed by 51–55 years (16.91%) and 61–65 years (14.71%). Fewer patients were in the 41–45 years (7.35%) and 66–70 years (7.35%) age ranges. This distribution indicates a predominance of middle-aged individuals, reflecting the typical onset pattern of Type II diabetes in the productive age group. [Table 1]

Table 1: Gender-wise and Age-wise Distribution of Study Subjects (n = 136)

Among the 136 T2DM patients, the mean BMI was 27.9 ± 3.6 kg/m², with more than half (51.5%) categorized as overweight and one-third (32.4%) as obese, reflecting a high prevalence of excess body weight. Mean systolic and diastolic blood pressures were 133.2 ± 12.1 mmHg and 84.6 ± 7.9 mmHg, respectively, indicating a trend toward prehypertension and early hypertensive changes in the cohort.

Table 2: Anthropometric and Hemodynamic Profile of the Study Population (n = 136)

Analysis of biochemical parameters and electrocardiographic findings revealed several noteworthy associations. Low-density lipoprotein (LDL) cholesterol levels showed a statistically significant relationship with P wave abnormalities on ECG (P < 0.0002). Both total cholesterol and serum triglyceride (TG) levels were found to be significantly elevated (P < 0.0003). A similar significant association was noted between QRS complex variations and raised TG levels (P < 0.0002). Total cholesterol values also demonstrated a strong correlation with P wave changes (P < 0.0003). [Table 2]

Table 3: Mean Values of Sugar and Lipid Parameters (n = 136)

The echocardiographic assessment of 136 asymptomatic T2DM patients revealed a preserved mean LVEF (56.2%), though slightly lower than expected in healthy individuals, suggesting subtle systolic impairment. An elevated LVMI (178.4 g/m²) indicated structural remodeling, while a reduced E/A ratio (0.85) reflected early diastolic dysfunction. Additionally, the mean GLS (–18.5%) pointed toward subclinical myocardial dysfunction despite normal ejection fraction, underscoring the value of advanced echocardiographic parameters in detecting early diabetic cardiomyopathy. [Table 3]

Table 3: Echocardiographic Parameters of the Study Population

When correlating biochemical and electrocardiographic parameters, the most prominent negative correlation was found between HbA1c and the E/A ratio (r = –0.792), signifying that poor glycemic control is strongly associated with impaired diastolic function. This underlines the role of chronic hyperglycemia in the pathogenesis of diabetic cardiomyopathy and its progression toward HFpEF. A moderate positive correlation was observed between total cholesterol and LVMI (r = 0.541, p < 0.001), indicating that elevated cholesterol levels contribute significantly to left ventricular hypertrophy and remodeling. BMI showed weak but positive correlations with both LVEF (r = 0.118) and LVMI (r = 0.091), suggesting that excess body weight may predispose patients to subtle structural changes. Correlations between triglycerides and echocardiographic parameters were weak, though LDL demonstrated a minor positive association with LVMI (r = 0.122), reinforcing its role in promoting ventricular remodeling. HDL levels exhibited negligible relationships with cardiac function, highlighting the greater clinical relevance of LDL and total cholesterol in this population. [Table 4]

Table 4: Correlation Between Metabolic Risk Factors and Echocardiographic Parameters (n = 136)

Type II diabetes mellitus (DM) is a chronic metabolic disorder that disrupts glucose homeostasis and profoundly affects lipid metabolism, thereby predisposing patients to cardiovascular disease (CVD). Echocardiographic changes, even in asymptomatic individuals, can serve as early markers of subclinical myocardial involvement. Given the established association between DM, dyslipidemia, and CVD, early detection of both metabolic and electrical abnormalities is crucial to preventing long-term complications. While biochemical parameters provide insight into metabolic derangements, 2D Echo remains a simple, non-invasive, and cost-effective tool for detecting early cardiac changes, especially in resource-limited settings. The combined use of biochemical and Echo assessment may enhance cardiovascular risk stratification in diabetic patients.

Although previous studies have independently evaluated lipid abnormalities or echocardiographic changes in diabetic populations, limited research has explored their direct correlation in asymptomatic Type II DM. Moreover, earlier investigations often involved smaller sample sizes, lacked simultaneous biochemical–ECG assessment, or did not examine the strength of correlations between glycemic indices, lipid parameters, and echocardiographic findings. The present study addresses this gap by concurrently analyzing these variables in a cohort of 136 diabetic patients.

Globally, the prevalence of DM and its complications has risen dramatically. According to the World Health Organization, approximately 347 million people are currently living with diabetes, and in 2004 alone, 3.4 million deaths were attributed to its complications. By 2030, DM is projected to rank as the seventh leading cause of death worldwide. Dyslipidemia is a frequent comorbidity in Type II DM, arising from both overproduction of lipoproteins and reduced clearance due to diminished receptor expression on endothelial cells. Such disturbances often reflect the combined effects of impaired nutrition and metabolic dysfunction. The inverse relationship between high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) observed in this study aligns with earlier findings, supporting the concept of atherogenic dyslipidemia—characterized by moderate TG elevation, low HDL-C, and high low-density lipoprotein cholesterol (LDL-C)—as a key contributor to CVD [9,10].

In our cohort, total cholesterol (TC), LDL-C, and TG were significantly elevated, whereas HDL-C was reduced (P < 0.0002). Echocardiographic changes were prominent, with LVMI significantly increased and GLS reduced compared to reference values (P < 0.0002). Evidence of diastolic dysfunction was reflected in the marked reduction of the E/A ratio (P < 0.0002), whereas LVEF, though within normal limits, showed a mild downward trend. Strong inverse correlations were noted between HbA1c and both the E/A ratio (r = –0.792) and GLS (r = –0.681), underscoring the impact of poor glycemic control on diastolic and subclinical systolic function. Additionally, a moderate positive association was observed between total cholesterol and LVMI (r = 0.541), suggesting that dyslipidemia contributes to structural cardiac remodeling. In contrast, correlations between BMI and echocardiographic indices were weak, indicating a lesser influence of body mass on early myocardial changes in this cohort.

HbA1c was found to have a strong negative correlation with the E/A ratio, which suggests that poor glycemic control significantly affects diastolic function. This finding is consistent with earlier studies by Fang ZY et al. [11] and Poornima IG et al. [12], which reported a high prevalence of diastolic dysfunction in poorly controlled diabetics. The proposed mechanism is increased myocardial fibrosis and impaired relaxation due to chronic hyperglycemia and oxidative stress.

Previous reports have documented similar biochemical patterns, with fasting blood glucose >125 mg/dL and postprandial glucose >200 mg/dL, along with significantly higher TC, TG, LDL-C, and very LDL-C compared to non-diabetic controls [13–16]. Obese diabetics tend to exhibit more severe dyslipidemia [14,16], and elevated TC levels have been associated with higher BMI and waist circumference [17,18]. Dyslipidemia also represents a core component of metabolic syndrome (MS), often involving multiple lipid abnormalities in the same individual [19–21]. In our study, TG levels were higher in overweight and obese diabetics, echoing earlier reports [16]. This pattern—raised TG, low HDL-C, and moderately increased LDL-C—was consistently observed and supports its recognition as a hallmark lipid abnormality in Type II DM.

HDL-C was significantly lower in overweight and obese diabetics compared to their normal-BMI counterparts [16], and our findings concur with studies showing reduced HDL-C in obese diabetics versus obese controls [17]. Furthermore, as in Patel et al.’s work [20], our results demonstrated that HbA1c positively correlated with LDL-C, TG, and TC, while negatively correlating with HDL-C. Similar to Pandya’s findings [19], uncontrolled diabetes was associated with higher TG and LDL-C, underscoring the need for simultaneous glycemic and lipid control.

Type II DM is an independent risk factor for CVD, with premature atherosclerosis driven by endothelial dysfunction, advanced glycation end products, and elevated free fatty acids—all markers of chronic systemic inflammation [22]. Diabetic patients may present with coronary artery disease (CAD), heart failure, or arrhythmias; however, silent ischemia due to autonomic neuropathy is common. Lee et al. reported a comparatively weaker association between metabolic markers and diastolic dysfunction, a finding likely influenced by the smaller sample size of their study [23]. In contrast, our results are consistent with those of Patil et al., who emphasized the role of BMI and HbA1c in the development of early cardiac dysfunction; however, their study did not incorporate GLS assessment through speckle-tracking echocardiography, which is a valuable parameter for identifying subclinical myocardial changes [24].

In our cohort, LVEF values were slightly below optimal but still within the preserved range, supporting earlier observations that systolic dysfunction in diabetes may present subtly and remain undetected by conventional ejection fraction measurement [25]. The reduced GLS values in our study provide further confirmation of early impairment in myocardial strain, a result also highlighted by the META-DIA trial [26].

Overall, our findings corroborate and extend prior research linking metabolic risk factors with subclinical cardiac dysfunction in asymptomatic patients with type 2 diabetes mellitus. For instance, Li et al. described a moderate correlation between HbA1c and diastolic function [27], whereas our results demonstrated a stronger relationship, underscoring the detrimental effect of poor glycemic control on ventricular relaxation. Similarly, while Patil et al. noted BMI and HbA1c as contributors to increased LVMI, their analysis did not evaluate GLS; by including it, we were able to identify an additional role of triglycerides in subclinical myocardial impairment.

Schillaci et al. associated LDL with left ventricular hypertrophy, whereas our findings indicated a stronger correlation between total cholesterol and LVMI, highlighting the contribution of dyslipidemia to structural remodeling [28]. Range et al. emphasized GLS as a sensitive marker for early cardiac dysfunction, which is consistent with our results [29]. Likewise, Sara et al. observed subtle reductions in LVEF among diabetic individuals, a pattern also evident in our study, suggesting the presence of early systolic impairment [30]. Collectively, these findings emphasize the importance of early cardiovascular assessment in asymptomatic T2DM patients to detect and address subclinical dysfunction at a reversible stage.

The present study highlights the value of 2D Echo as a low-cost, non-invasive screening tool for early cardiovascular risk detection in asymptomatic Type II diabetics. By concurrently assessing glycemic indices, lipid profiles, and echocardiographic changes, it contributes to the limited literature on this topic. However, limitations include the moderate sample size, lack of a control group, and absence of gender- and age-stratified analyses. Future multicenter studies with larger cohorts and longitudinal follow-up are warranted to establish causality and determine the prognostic implications of these findings.

Dyslipidemia and echocardiographic abnormalities are frequently observed in type 2 diabetes mellitus (T2DM), even in the absence of clinically overt cardiovascular disease. In this study, asymptomatic T2DM patients demonstrated significant subclinical cardiac changes, including increased LVMI, reduced E/A ratio, and impaired GLS, indicating structural remodeling, early diastolic dysfunction, and subtle systolic strain abnormalities despite preserved LVEF. Poor glycemic control, reflected by elevated HbA1c, showed the strongest association with diastolic and strain abnormalities, while dyslipidemia, particularly elevated total cholesterol, correlated moderately with ventricular hypertrophy. BMI had weaker associations, suggesting a lesser role compared to metabolic markers. These findings emphasize the utility of advanced echocardiographic modalities for early detection of diabetic cardiomyopathy and reinforce the need for comprehensive management strategies. Optimal diabetes care requires strict glycemic and lipid control, weight regulation, lifestyle modifications, and cardiovascular risk reduction, which together may delay progression to overt heart failure and improve long-term outcomes.

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