Few chronic disorders have altered the global health landscape as sharply as diabetes mellitus. What began as an urban illness of prosperity has now diffused across every social layer. Sedentary work, processed food habits, and easy calorie excess have together created an environment that favours persistent hyperglycaemia. Current international estimates place more than half a billion adults in the diabetic range, and India alone contributes a striking proportion of this burden (1,2). Cardiovascular disease continues to be the most serious companion of type 2 diabetes mellitus (T2DM). Among several metabolic disturbances that drive this risk, dyslipidaemia occupies a special position (3). It is rarely a simple rise in cholesterol; rather, it takes the form of high triglycerides, depressed high-density lipoprotein cholesterol (HDL-C), and the presence of smaller, denser low-density lipoprotein (LDL) particles. Together they produce a state often described as “atherogenic dyslipidaemia,” responsible for early and aggressive atherosclerosis (4,5). The process is biochemical as much as structural. Resistance to insulin increases the flow of free fatty acids from adipose tissue to the liver, prompting excess synthesis of very-low-density lipoprotein (VLDL) and slower clearance of triglyceride-rich remnants. Over time, HDL becomes depleted and vascular endothelium loses its protective tone, paving the way for plaque formation (6,7). Several long-term studies, including the UK Prospective Diabetes Study and the Framingham cohort, have shown that lipid disturbances in diabetes predict coronary events as strongly as in non-diabetic populations (8,9). Indian evidence tells a similar story: both community and hospital surveys report dyslipidaemia in nearly three-quarters of adults with T2DM, the majority presenting with raised triglycerides and low HDL-C (10,11). Yet, in many government and semi-urban settings, routine lipid screening and follow-up remain inconsistent, allowing silent progression toward ischaemic heart disease (12). The present work attempts to characterise this overlap between dyslipidaemia and ischaemic heart disease among adults with T2DM. By documenting the lipid pattern, clinical profile, and frequency of cardiac involvement in a cohort from a South-Indian tertiary hospital, the study hopes to generate locally relevant evidence that can reinforce preventive strategies in routine diabetic care.

Study Design and Setting This was a hospital-based, cross-sectional descriptive study conducted in the Department of General Medicine, Government Stanley Medical College and Hospital, Chennai. The study period extended from April 2024 to March 2025. Ethical clearance was obtained from the Institutional Ethics Committee before enrolment began. Sample Size and Selection Criteria A total of 100 patients with type 2 diabetes mellitus (T2DM) were included after obtaining informed written consent. Participants were selected from the diabetic outpatient clinic and general medicine wards through simple random sampling. Inclusion criteria comprised adults aged 30–70 years with a confirmed diagnosis of T2DM for at least one year. Exclusion criteria were type 1 diabetes, secondary diabetes, chronic kidney disease stage ≥ 3, hypothyroidism, nephrotic syndrome, chronic liver disease, and patients already on lipid-lowering therapy or steroids. Data Collection Each participant underwent a detailed history and clinical examination. Information recorded included age, sex, duration of diabetes, family history, smoking and alcohol status, body-mass index (BMI), waist-hip ratio, and blood pressure. Symptoms suggestive of ischaemic heart disease, such as exertional chest pain or dyspnoea, were noted. Laboratory Investigations After an overnight fast of at least eight hours, venous blood samples were collected for: ● Fasting and post-prandial plasma glucose, ● Glycated haemoglobin (HbA1c), ● Serum total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, and VLDL-cholesterol. All assays were performed in the central biochemistry laboratory using an enzymatic colorimetric method on a fully automated analyser (Erba EM-360). Lipid profiles were interpreted according to the NCEP-ATP III classification. Dyslipidaemia was defined by one or more of the following: total cholesterol ≥ 200 mg/dL, triglycerides ≥ 150 mg/dL, HDL-C < 40 mg/dL (men) or < 50 mg/dL (women), or LDL-C ≥ 130 mg/dL. Cardiovascular Evaluation All subjects underwent a resting 12-lead electrocardiogram. Patients with evidence of ischaemic changes (ST-segment depression, T-wave inversion, or Q-wave) were further evaluated by two-dimensional echocardiography. Ischaemic heart disease (IHD) was confirmed when either ECG or echocardiographic features indicated regional wall-motion abnormality, prior infarction, or reversible ischaemia. Statistical Analysis Data were entered in Microsoft Excel 2021 and analysed using SPSS version 28.0 (IBM Corp, USA). Continuous variables were expressed as mean ± standard deviation; categorical variables as proportions or percentages. The chi-square test assessed associations between categorical parameters, while Student’s t-test compared continuous means. Pearson’s correlation measured relationships among biochemical indices. Multivariate logistic regression identified independent predictors of IHD. A p-value < 0.05 was considered statistically significant.

Demographic and Clinical Characteristics Of the 100 adults with type 2 diabetes mellitus enrolled, 60 were males and 40 were females. The mean ± SD age of the cohort was 56.4 ± 8.6 years, and the mean duration of diabetes was 8.3 ± 4.7 years. Nearly half (48 %) were overweight (BMI 25–29.9 kg/m²), and another 26 % were obese (≥ 30 kg/m²). Hypertension co-existed in 58 % of participants, and 36 % were current or former smokers. Table 1. Demographic and baseline profile of study participants (n = 100) Parameter Mean ± SD / n (%) Age (years) 56.4 ± 8.6 Male: Female 60: 40 Duration of diabetes (years) 8.3 ± 4.7 BMI (kg/m²) 27.8 ± 3.9 Waist–hip ratio 0.94 ± 0.06 Hypertension present 58 (58 %) Smokers / ex-smokers 36 (36 %) Figure 1 illustrates the sex distribution and body-mass category among participants, showing a modest male predominance and higher overweight prevalence in both sexes. (Figure 1 – Bar chart: Distribution by gender and BMI category) Pattern of Dyslipidaemia Overall, dyslipidaemia (≥ 1 abnormal lipid parameter) was observed in 82 % of subjects. The most frequent abnormality was mixed dyslipidaemia (raised triglycerides + low HDL-C ± high LDL-C) seen in 37 cases, followed by isolated hypertriglyceridaemia (25 %), isolated low HDL-C (13 %), and isolated elevated LDL-C (7 %). Table 2. Lipid profile pattern among the study population Lipid abnormality n (%) Mean ± SD (mg/dL) Mixed dyslipidaemia 37 (37 %) TC 226 ± 37; TG 212 ± 64; HDL 38 ± 7 Isolated hypertriglyceridaemia 25 (25 %) TG 202 ± 55; HDL 43 ± 6 Isolated low HDL-C 13 (13 %) HDL 35 ± 5; TG 158 ± 41 Isolated high LDL-C 7 (7 %) LDL 148 ± 26 Normal lipid profile 18 (18 %) Within reference range Figure 2 (pie chart) displays the relative proportion of lipid-pattern categories, highlighting the dominance of mixed dyslipidaemia. (Figure 2 – Pie chart: Percentage distribution of lipid abnormalities) Association between Dyslipidaemia and Ischaemic Heart Disease Electrocardiographic or echocardiographic evidence of IHD was found in 36 patients. Among these, 32 (88.9 %) had dyslipidaemia. Triglyceride levels and low HDL-C showed significant correlation with IHD occurrence (p < 0.01), whereas total cholesterol and LDL-C alone did not reach statistical significance. Table 3. Comparison of lipid parameters between participants with and without IHD Parameter (mg/dL) IHD present (n = 36) No IHD (n = 64) p-value Total cholesterol 214 ± 39 204 ± 37 0.21 Triglycerides 212 ± 68 172 ± 54 0.001 HDL-C 38.6 ± 7.1 44.9 ± 8.3 0.004 LDL-C 132 ± 31 126 ± 29 0.26 VLDL-C 42.4 ± 10.8 34.6 ± 9.4 0.01 Figure 3 (stacked-bar graph) depicts the comparative mean lipid levels in subjects with and without IHD, clearly showing raised triglycerides and depressed HDL in the IHD subgroup. (Figure 3 – Stacked bar: Mean lipid values vs IHD status) Duration of Diabetes and Lipid Abnormalities Duration ≥ 10 years was significantly associated with higher triglycerides (mean 218 mg/dL) and lower HDL-C (mean 39 mg/dL) compared with those having diabetes < 10 years (TG 176 mg/dL; HDL 44 mg/dL; p < 0.05). Table 4. Relationship between duration of diabetes and mean lipid levels Duration of T2DM TG (mg/dL) HDL-C (mg/dL) LDL-C (mg/dL) < 5 years (n = 32) 168 ± 49 45.1 ± 8.2 121 ± 26 5–9 years (n = 28) 186 ± 55 42.3 ± 7.9 128 ± 29 ≥ 10 years (n = 40) 218 ± 63 39.4 ± 6.8 136 ± 32 Figure 4 (line graph) demonstrates a gradual increase in triglycerides and a fall in HDL-C with increasing duration of diabetes, underscoring a time-linked metabolic drift. (Figure 4 – Line graph: Lipid trends vs duration of diabetes) Multivariate Analysis On regression modelling, serum triglyceride (β = 0.42, p = 0.002) and HDL-C (β = – 0.31, p = 0.01) emerged as independent predictors of IHD after adjustment for age, sex, BMI, and duration of diabetes. Table 5. Multivariate logistic regression for predictors of ischaemic heart disease Variable β (coefficient) SE Odds ratio (95 % CI) p-value Age (> 55 years) 0.18 0.09 1.19 (0.98–1.43) 0.08 Male sex 0.26 0.12 1.30 (1.02–1.78) 0.04 BMI ≥ 25 kg/m² 0.15 0.07 1.16 (0.93–1.44) 0.11 Triglycerides > 200 mg/dL 0.42 0.13 1.52 (1.18–1.97) 0.002 HDL-C < 40 mg/dL – 0.31 0.12 0.73 (0.58–0.91) 0.01 Figure 5 (donut chart) visualises the proportion of independent lipid predictors contributing to IHD, highlighting triglycerides as the major factor. (Figure 5 – Donut chart: Relative weight of predictors of IHD) Summary of Findings In this cross-sectional study of 100 adults with type 2 diabetes mellitus, dyslipidaemia was identified in a striking 82 % of cases. The predominant pattern was mixed dyslipidaemia (37 %), followed by isolated hypertriglyceridaemia (25 %) and isolated low HDL-C (13 %). Ischaemic heart disease was documented in 36 % of participants and showed a strong association with elevated triglycerides and reduced HDL-C levels (p < 0.01). Individuals with diabetes for ten years or longer demonstrated higher triglycerides and lower HDL values compared with those of shorter duration, indicating a progressive metabolic shift over time. Multivariate regression confirmed that serum triglycerides above 200 mg/dL and HDL-C below 40 mg/dL were independent predictors of ischaemic heart disease after adjustment for age, sex, body-mass index, and disease duration. Altogether, the results underline the close biochemical and clinical interlink between lipid abnormalities and coronary risk among Indian patients with type 2 diabetes.

This study explored how disordered lipids contribute to ischaemic heart disease (IHD) among adults with type 2 diabetes mellitus. More than four out of every five participants had at least one lipid abnormality, and over one-third already showed electrocardiographic or echocardiographic signs of IHD. The numbers themselves tell a story: in diabetes, vascular risk begins long before any clinical event appears (13). The pattern we found, mainly mixed dyslipidaemia and hypertriglyceridaemia, is not unique to this cohort. Similar distributions have been reported in Indian community surveys and the ICMR-INDIAB project, where low HDL-C and high triglycerides remain the most stubborn abnormalities (14,15). Internationally, the UK Prospective Diabetes Study also underlined that triglycerides and HDL levels carry greater predictive weight for coronary events than total cholesterol (8). In that light, our own results seem to echo a broader biological rhythm shared across ethnicities: it is triglyceride excess, not total cholesterol, that quietly drives atherosclerosis in diabetes. Mechanistically, the explanation rests on insulin resistance and hepatic lipid oversupply. When insulin signalling falters, free fatty acids flood the liver and stimulate overproduction of very-low-density lipoprotein (VLDL). Lipoprotein-lipase activity drops, clearance slows, and the bloodstream fills with triglyceride-rich remnants. These remnants infiltrate arterial walls, generate reactive oxygen species, and encourage small, dense LDL particles to form (6,7). Low HDL-C adds a second hit; its protective role in reverse cholesterol transport weakens, and the endothelium loses its natural defence (16). Step by step, these changes convert a metabolic problem into a structural vascular one. Another notable finding here was the progressive deterioration in lipid values with longer diabetes duration. Those living with the condition for ten years or more had distinctly higher triglycerides and lower HDL-C. Pandya and colleagues observed a comparable drift, linking the length of diabetes to rising triglyceride-to-HDL ratios (15). Chronic hyperglycaemia may partly explain this pattern by glycation of apolipoproteins, impairing LDL-receptor binding and prolonging the circulation of atherogenic particles (17). Each additional year of poor glycaemic control seems to etch its own mark on the vascular wall. Clinical implications are clear. Lipid testing should not remain a yearly formality—it needs to be a central part of diabetic follow-up. Early detection of mixed dyslipidaemia allows timely introduction of statins, fibrates, or combination therapy. Indian recommendations from both the RSSDI and the Lipid Association of India now encourage clinicians to go beyond LDL-C control and to target triglycerides and HDL as well, particularly in patients with coexisting cardiovascular risk (18). In routine outpatient care, however, these goals often slip through gaps of awareness and resources. The strength of the current study lies in its simultaneous examination of biochemical and clinical evidence of IHD in a real-world hospital cohort. Limitations do exist. Being cross-sectional, it cannot establish temporal causality, and advanced lipid fractions like apolipoprotein B or Lp(a) were not assessed. Coronary angiographic correlation would also have strengthened the evidence. Even so, the trends mirror what larger epidemiological datasets have already signalled: lipid imbalance and insulin resistance travel hand in hand on the path to vascular damage. In sum, dyslipidaemia in diabetes emerges not as a bystander but as an active participant in coronary risk. The evidence argues for more vigilant lipid profiling and early, aggressive correction to prevent silent progression from metabolic disorder to overt heart disease. LIMITATIONS This study was cross-sectional and based in a single tertiary-care centre; hence, causal inference cannot be established. Coronary angiography was not performed to confirm ischaemic heart disease, and advanced lipid markers such as apolipoprotein B, Lp(a), or oxidised LDL were not measured. The relatively small sample size and absence of follow-up restrict generalisability. Nevertheless, the observed pattern of lipid derangement closely mirrors national data, supporting its clinical relevance. Future multicentric longitudinal studies incorporating broader biochemical panels and imaging correlation would help delineate the causal pathways more precisely.

Dyslipidaemia remains one of the most pervasive and modifiable risk factors in type 2 diabetes mellitus. In this hospital cohort, lipid abnormalities were almost universal, and their relationship with ischaemic heart disease was clear. Raised triglycerides and reduced HDL-cholesterol emerged as the two strongest markers of cardiovascular risk, independent of age, body-mass index, or duration of diabetes. These results highlight that focusing only on glycaemic control leaves a major part of the vascular threat unaddressed. Regular lipid monitoring, timely pharmacologic correction, and sustained lifestyle measures should therefore be viewed as essential extensions of diabetes management rather than optional add-ons. Early attention to this biochemical imbalance can prevent many of the irreversible cardiac complications that often define the later years of the disease.

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