Coronary artery disease (CAD) remains one of the leading causes of morbidity and mortality worldwide and poses a major public health challenge, particularly in developing countries such as India. The disease is characterized by atherosclerotic narrowing of the coronary arteries, leading to myocardial ischemia and adverse cardiovascular events. Despite significant advances in prevention and treatment, the burden of CAD continues to increase due to the growing prevalence of diabetes mellitus, hypertension, dyslipidemia, obesity, smoking, and sedentary lifestyles. Recently, attention has shifted toward identifying novel and potentially modifiable risk factors that may influence the development and progression of CAD. Among these, vitamin D deficiency has emerged as an important area of research because of its widespread prevalence and possible association with cardiovascular health.^[1]

Vitamin D is a fat-soluble vitamin synthesized in the skin following exposure to ultraviolet B radiation and obtained in smaller quantities from dietary sources. Beyond its established role in calcium and phosphorus metabolism and maintenance of bone health, vitamin D exerts several extra-skeletal effects through vitamin D receptors present in endothelial cells, vascular smooth muscle cells, cardiomyocytes, and immune cells. Experimental studies have demonstrated that vitamin D possesses anti-inflammatory, antioxidant, immunomodulatory, and anti-proliferative properties, suggesting a potential protective role against the development of atherosclerosis and cardiovascular disease.^[2]

Several biological mechanisms have been proposed to explain the relationship between vitamin D deficiency and CAD. Low vitamin D levels have been associated with endothelial dysfunction, increased arterial stiffness, activation of the renin-angiotensin-aldosterone system, vascular inflammation, insulin resistance, and enhanced thrombogenicity. Vitamin D deficiency may also contribute to dyslipidemia, hypertension, diabetes mellitus, and obesity, all of which are well-recognized cardiovascular risk factors. Consequently, inadequate vitamin D status may accelerate atherosclerotic plaque formation and increase the risk of myocardial infarction and adverse cardiovascular outcomes.^[3]

Vitamin D deficiency is highly prevalent worldwide, affecting nearly one billion individuals, with particularly high rates reported in South Asian countries despite abundant sunlight. In India, lifestyle changes, limited sun exposure, skin pigmentation, dietary inadequacy, urbanization, and cultural practices contribute to widespread vitamin D deficiency across all age groups. Several observational studies have reported a higher prevalence of vitamin D deficiency among patients with CAD compared to healthy individuals. However, findings regarding the strength and independence of this association remain inconsistent because of variations in study design, patient characteristics, geographic location, and confounding risk factors.^[4]

Understanding the prevalence and determinants of vitamin D deficiency among patients with CAD is important for identifying high-risk individuals who may benefit from early screening and targeted interventions. Identification of demographic, clinical, and lifestyle factors associated with vitamin D deficiency may help clinicians develop comprehensive cardiovascular risk assessment strategies. Therefore, the present cross-sectional study was conducted to determine the prevalence of vitamin D deficiency in patients with coronary artery disease and to identify the demographic and clinical determinants associated with deficient vitamin D status in a tertiary care hospital.[5]

AIM

To determine the prevalence and determinants of vitamin D deficiency among patients with coronary artery disease.

OBJECTIVES

1. To estimate the prevalence of vitamin D deficiency among patients diagnosed with coronary artery disease.
2. To assess the association between vitamin D deficiency and demographic and clinical characteristics of patients with coronary artery disease.
3. To identify the independent determinants of vitamin D deficiency among patients with coronary artery disease.

Source of Data The data were collected from patients diagnosed with coronary artery disease who attended the Department of Cardiology and were admitted to the tertiary care teaching hospital during the study period. Clinical information, laboratory findings, and serum vitamin D levels were obtained from patient interviews, medical records, physical examination, and laboratory investigations. Study Design A hospital-based cross-sectional observational study was conducted. Study Location The study was conducted in the Department of Cardiology & Department of Medicine, MGM Medical College, Chh Sambhajinagar, Maharashtra, INDIA. Study Duration The study was conducted over a period of 12 months, including patient recruitment, laboratory investigations, data collection, statistical analysis, and interpretation of results. Sample Size A total of 200 patients with confirmed coronary artery disease were included in the study. Inclusion Criteria • Patients aged 18 years and above. • Patients diagnosed with coronary artery disease based on clinical evaluation, electrocardiography, cardiac biomarkers, coronary angiography, or previous documented CAD. • Patients who provided written informed consent. • Patients willing to undergo serum vitamin D estimation. Exclusion Criteria • Patients receiving vitamin D supplementation within the previous six months. • Patients with chronic kidney disease stage IV or V. • Patients with chronic liver disease. • Patients with malabsorption syndromes. • Patients with known parathyroid disorders. • Patients with active malignancy. • Pregnant or lactating women. • Patients unwilling to participate. Procedure and Methodology After obtaining approval from the Institutional Ethics Committee, eligible patients fulfilling the inclusion criteria were enrolled consecutively after obtaining written informed consent. A detailed history was obtained regarding age, sex, occupation, residence, smoking, alcohol consumption, physical activity, dietary habits, sunlight exposure, diabetes mellitus, hypertension, dyslipidemia, obesity, family history of coronary artery disease, and current medications. A comprehensive clinical examination was performed, including measurement of height, weight, body mass index (BMI), waist circumference, blood pressure, and cardiovascular examination. Relevant clinical information regarding the diagnosis and severity of coronary artery disease was recorded from hospital records. Venous blood samples were collected under aseptic precautions for estimation of serum 25-hydroxyvitamin D [25(OH)D] levels along with routine biochemical investigations, including fasting blood glucose, HbA1c (where applicable), lipid profile, serum calcium, phosphorus, creatinine, and other investigations as indicated. Vitamin D status was classified according to Endocrine Society guidelines as: • Deficient: <20 ng/mL • Insufficient: 20–29 ng/mL • Sufficient: ≥30 ng/mL Patients were categorized accordingly, and associations between vitamin D deficiency and demographic, clinical, anthropometric, and biochemical variables were evaluated. Sample Processing Approximately 5 mL of fasting venous blood was collected under aseptic conditions in plain and EDTA vacutainers. Samples were allowed to clot, and serum was separated by centrifugation at 3000 rpm for 10 minutes. Serum 25-hydroxyvitamin D [25(OH)D] concentrations were measured using a standardized chemiluminescent immunoassay (CLIA) or electrochemiluminescence immunoassay (ECLIA), following the manufacturer's protocol. Internal quality control procedures were maintained throughout the laboratory analysis to ensure accuracy and precision. Statistical Methods The collected data were entered into Microsoft Excel and analyzed using SPSS version 26.0. • Continuous variables were expressed as mean ± standard deviation (SD) or median (interquartile range), depending on data distribution. • Categorical variables were presented as frequencies and percentages. • Normality of continuous variables was assessed using the Shapiro-Wilk test. • Differences between groups were analyzed using the Independent Student's t-test or Mann-Whitney U test. • Associations between categorical variables were evaluated using the Chi-square test or Fisher's exact test. • Variables showing statistical significance in univariate analysis were entered into multivariable logistic regression to identify independent determinants of vitamin D deficiency. • Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. • A p-value <0.05 was considered statistically significant. Data Collection Data were collected using a structured predesigned case record form. Information regarding socio-demographic characteristics, cardiovascular risk factors, lifestyle variables, anthropometric measurements, clinical history, laboratory investigations, serum vitamin D levels, and coronary artery disease characteristics was recorded systematically. The collected data were verified for completeness and accuracy before statistical analysis.

Table 1. Overall demographic, clinical and biochemical characteristics of patients with coronary artery disease (N=200)

*Statistically significant at p<0.05.

Table 1 presents the overall demographic, clinical, lifestyle and biochemical characteristics of 200 patients with coronary artery disease. The mean age of the participants was 59.3 ± 10.8 years, with a 95% confidence interval of 57.79–60.81 years. A slightly higher proportion of patients were aged 60 years or above, accounting for 103 (51.5%) participants, while 97 (48.5%) were younger than 60 years; however, the age-group distribution was not statistically significant (p=0.671). Males constituted the majority of the study population, with 117 (58.5%) participants, compared with 83 (41.5%) females, and the difference was statistically significant (p=0.016). Most patients resided in urban areas, 129 (64.5%), whereas 71 (35.5%) were from rural areas, showing a statistically significant urban predominance (p<0.001).

The mean body mass index was 26.8 ± 4.1 kg/m². Obesity was present in 87 (43.5%) patients and absent in 113 (56.5%), although this distribution did not reach statistical significance (p=0.066). Diabetes mellitus was present in 103 (51.5%) patients, while 97 (48.5%) were non-diabetic, with no significant difference between the two categories (p=0.671). Hypertension was observed in 129 (64.5%) patients and was significantly more common than absence of hypertension (p<0.001). Dyslipidaemia was present in 109 (54.5%) patients, but its distribution was not statistically significant (p=0.203).

Current smoking was reported by 62 (31.0%) patients, whereas 138 (69.0%) were non-smokers, with a statistically significant predominance of non-smokers (p<0.001). A sedentary lifestyle was reported by 118 (59.0%) participants and was significantly more common than an active lifestyle (p=0.011). Low sunlight exposure was present in 104 (52.0%) patients, while 96 (48.0%) had adequate sunlight exposure, with no significant difference between the groups (p=0.572). Acute coronary syndrome was the presenting diagnosis in 109 (54.5%) patients, whereas 91 (45.5%) had chronic coronary syndrome; this difference was not statistically significant (p=0.203).

The mean serum 25-hydroxyvitamin D level was 18.4 ± 8.2 ng/mL, indicating an overall low vitamin D status in the study population. The mean fasting blood glucose level was 128.7 ± 42.6 mg/dL, while the mean total cholesterol and LDL cholesterol levels were 184.6 ± 43.8 mg/dL and 112.8 ± 36.7 mg/dL, respectively. All continuous biochemical parameters showed statistically significant one-sample test results with p<0.001.

Table 2. Prevalence and distribution of vitamin D status among patients with coronary artery disease (N=200)

The prevalence of vitamin D deficiency among patients with coronary artery disease was 65.5% (95% CI: 58.7–71.7%).

*Statistically significant at p<0.05.

Table 2 shows the prevalence and distribution of vitamin D status among patients with coronary artery disease. Of the 200 patients, 131 (65.5%) had vitamin D deficiency, defined as serum 25-hydroxyvitamin D levels below 20 ng/mL. The estimated prevalence of vitamin D deficiency was therefore 65.5%, with a 95% confidence interval of 58.7–71.7%. A further 47 (23.5%) patients had vitamin D insufficiency, with serum levels between 20 and 29.9 ng/mL, while only 22 (11.0%) had sufficient vitamin D levels of 30 ng/mL or above. The distribution of deficient, insufficient and sufficient vitamin D status was statistically significant (χ²=91.81, p<0.001).

When deficiency was further classified according to severity, 38 (19.0%) patients had severe vitamin D deficiency with serum levels below 10 ng/mL, while 93 (46.5%) had moderate deficiency with levels between 10 and 19.9 ng/mL. The remaining 69 (34.5%) patients were classified as non-deficient. This distribution was also statistically significant (χ²=76.88, p<0.001), demonstrating that moderate vitamin D deficiency was the most frequent category.

The overall mean serum 25-hydroxyvitamin D level was 18.4 ± 8.2 ng/mL. Among vitamin D-deficient patients, the mean level was 12.7 ± 4.1 ng/mL, with a 95% confidence interval of 11.99–13.41 ng/mL. In comparison, the mean serum vitamin D level among non-deficient patients was 29.2 ± 7.1 ng/mL, with a 95% confidence interval of 27.50–30.90 ng/mL. These findings indicate a high burden of vitamin D deficiency among patients with coronary artery disease.

Table 3. Association of vitamin D deficiency with demographic, lifestyle and clinical characteristics among patients with coronary artery disease (N=200)

Continuous-variable comparison

*Statistically significant at p<0.05.

Table 3 demonstrates the association between vitamin D deficiency and demographic, lifestyle and clinical characteristics among patients with coronary artery disease. Vitamin D deficiency was significantly more common among patients aged 60 years or above. Of the deficient patients, 76 (58.0%) were aged 60 years or older, compared with 24 (34.8%) in the non-deficient group. Patients aged 60 years or above had 2.59 times higher odds of vitamin D deficiency than younger patients (OR=2.59, 95% CI: 1.42–4.74; p=0.002). Female patients also had significantly higher odds of deficiency than males (OR=1.86, 95% CI: 1.01–3.43; p=0.045). Urban residence was not significantly associated with vitamin D deficiency (p=0.275).

Obesity showed a strong association with vitamin D deficiency. Obesity was present in 69 (52.7%) deficient patients compared with 18 (26.1%) non-deficient patients. Obese patients had over three times higher odds of deficiency than non-obese patients (OR=3.15, 95% CI: 1.67–5.96; p<0.001). Diabetes mellitus was also significantly associated with deficiency, with diabetic patients having 2.59 times higher odds of vitamin D deficiency (95% CI: 1.42–4.73; p=0.002). Hypertension was more common among deficient patients and was associated with 1.86 times higher odds of deficiency (95% CI: 1.02–3.39; p=0.043). Dyslipidaemia, however, did not show a statistically significant association (p=0.169).

Current smoking was reported by 47 (35.9%) deficient patients compared with 15 (21.7%) non-deficient patients. Smokers had approximately twice the odds of vitamin D deficiency compared with non-smokers (OR=2.01, 95% CI: 1.03–3.95; p=0.040). A sedentary lifestyle was strongly associated with deficiency, with sedentary patients having 2.92 times higher odds than physically active patients (95% CI: 1.60–5.34; p<0.001). Low sunlight exposure showed the strongest unadjusted association. It was present in 84 (64.1%) deficient patients compared with only 20 (29.0%) non-deficient patients. Patients with low sunlight exposure had 4.38 times higher odds of deficiency than those with adequate exposure (95% CI: 2.33–8.23; p<0.001).

Vitamin D deficiency was also significantly associated with acute coronary syndrome and multivessel coronary artery disease. Patients with acute coronary syndrome had nearly twice the odds of deficiency compared with those with chronic coronary syndrome (OR=1.98, 95% CI: 1.09–3.57; p=0.023). Similarly, patients with multivessel coronary disease had 1.96 times higher odds of deficiency than those without multivessel involvement (95% CI: 1.08–3.55; p=0.026). Statin therapy was not significantly associated with vitamin D status (p=0.356).

In the continuous-variable comparison, vitamin D-deficient patients were significantly older than non-deficient patients, with mean ages of 61.2 ± 10.3 years and 55.7 ± 10.9 years, respectively. The mean age difference was 5.50 years (95% CI: 2.43–8.57; p<0.001). Deficient patients also had a significantly higher mean body mass index than non-deficient patients, 27.8 ± 4.0 kg/m² versus 24.9 ± 3.6 kg/m², with a mean difference of 2.90 kg/m² (p<0.001).

As expected, the mean serum 25-hydroxyvitamin D level was significantly lower among deficient patients than among non-deficient patients, 12.7 ± 4.1 ng/mL versus 29.2 ± 7.1 ng/mL, with a mean difference of −16.50 ng/mL (p<0.001). Deficient patients also had significantly higher fasting blood glucose levels, with a mean difference of 25.80 mg/dL (p<0.001), and higher LDL cholesterol levels, with a mean difference of 11.90 mg/dL (p=0.029).

Table 4. Multivariable logistic regression analysis of independent determinants of vitamin D deficiency among patients with coronary artery disease (N=200)

Dependent variable: Vitamin D deficiency: yes=1 and no=0.

Model χ²: 58.72; df: 10; p<0.001.

Nagelkerke R²: 0.36.

Hosmer–Lemeshow test: χ²=6.27, df=8, p=0.617.

Overall classification accuracy: 75.5%.

Table 4 presents the multivariable logistic regression analysis used to identify the independent determinants of vitamin D deficiency among patients with coronary artery disease. After simultaneous adjustment for demographic, lifestyle and clinical variables, age of 60 years or above remained a significant independent determinant. Older patients had approximately twice the adjusted odds of vitamin D deficiency compared with younger patients (adjusted OR=2.08, 95% CI: 1.13–3.83; p=0.018).

Obesity was independently associated with vitamin D deficiency. Obese patients had 2.49 times higher adjusted odds of deficiency than non-obese patients (95% CI: 1.28–4.84; p=0.007). Diabetes mellitus also remained a significant predictor, with diabetic patients having nearly twice the odds of deficiency compared with non-diabetic patients (adjusted OR=1.99, 95% CI: 1.08–3.66; p=0.026).

A sedentary lifestyle was another significant independent determinant. Patients reporting a sedentary lifestyle had 2.16 times higher adjusted odds of vitamin D deficiency than physically active patients (95% CI: 1.13–4.12; p=0.020). Low sunlight exposure emerged as the strongest independent determinant in the model. Patients with low sunlight exposure had 3.29 times higher adjusted odds of vitamin D deficiency than those with adequate sunlight exposure (95% CI: 1.72–6.29; p<0.001).

Female sex, hypertension, current smoking and acute coronary syndrome were associated with increased adjusted odds of vitamin D deficiency, but these associations were not statistically significant. Multivessel coronary artery disease showed a borderline association with deficiency (adjusted OR=1.73, 95% CI: 0.94–3.19; p=0.076), suggesting a possible relationship that did not achieve statistical significance after adjustment.

The overall logistic regression model was statistically significant (model χ²=58.72, df=10, p<0.001), indicating that the included variables collectively contributed to predicting vitamin D deficiency. The Nagelkerke R² value of 0.36 suggested that approximately 36% of the variation in vitamin D deficiency was explained by the model. The non-significant Hosmer–Lemeshow test result (χ²=6.27, p=0.617) indicated good model calibration and an acceptable fit to the observed data. The model correctly classified 75.5% of the patients. Overall, age ≥60 years, obesity, diabetes mellitus, sedentary lifestyle and low sunlight exposure were identified as significant independent determinants of vitamin D deficiency among patients with coronary artery disease.

The present cross-sectional study evaluated the prevalence and determinants of vitamin D deficiency among 200 patients with coronary artery disease. The principal findings were that 65.5% of patients had serum 25-hydroxyvitamin D levels below 20 ng/mL, while only 11.0% had sufficient levels. Older age, obesity, diabetes mellitus, sedentary lifestyle and low sunlight exposure were identified as independent determinants of deficiency. Vitamin D deficiency was also associated on unadjusted analysis with female sex, hypertension, smoking, acute coronary syndrome and multivessel coronary artery disease. These findings support the high frequency of hypovitaminosis D in patients with established CAD, although the cross-sectional nature of the study does not establish a causal relationship.

Demographic, clinical and biochemical characteristics

The mean age of the patients in the present study was 59.3±10.8 years, and 51.5% were aged 60 years or above. Males constituted 58.5% of the study population. This age and sex distribution reflects the usual demographic profile of patients presenting with established coronary artery disease. Dhibar et al. (2016)^[1], in an Indian angiography-based study involving 315 patients, also observed that CAD predominantly affected middle-aged and older adults and that men formed a substantial proportion of the study population. Similarly, Alsancak et al. (2015)^[2] studied 746 patients undergoing coronary angiography and reported a patient population characterized by older age and a high burden of conventional cardiovascular risk factors.

The present study demonstrated a high prevalence of established cardiovascular risk factors, including hypertension in 64.5%, dyslipidaemia in 54.5%, diabetes mellitus in 51.5%, obesity in 43.5% and current smoking in 31.0% of patients. The mean BMI was 26.8±4.1 kg/m², indicating that the average patient was overweight. These findings are consistent with Dhibar et al. (2016)^[1], who noted that vitamin D deficiency and CAD frequently coexist with diabetes, hypertension, increased BMI and dyslipidaemia. Bakthavatchalam et al. (2023)^[3] also reported significant relationships between low vitamin D status and conventional CAD risk factors, particularly hypertension, diabetes and obesity.

A sedentary lifestyle was recorded in 59.0% of patients, and 52.0% reported low sunlight exposure. These lifestyle factors may contribute both to cardiovascular risk and to reduced cutaneous synthesis of vitamin D. Limited outdoor activity may therefore represent an important common pathway linking physical inactivity, obesity and low vitamin D concentrations. Cosentino et al. (2021)^[4] highlighted that vitamin D status is influenced by age, adiposity, physical activity, latitude, season, dietary intake and sunlight exposure, all of which may confound its observed relationship with cardiovascular disease.

The mean serum 25(OH)D level in the present study was 18.4±8.2 ng/mL. This was comparable to the value reported by Alsancak et al. (2015)^[2], who found a mean serum vitamin D concentration of 15.54±7.46 ng/mL among patients undergoing coronary angiography. In their study, vitamin D-deficient patients had a mean level of 12.6±3.3 ng/mL, closely resembling the mean of 12.7±4.1 ng/mL observed among deficient patients in the present study.

The mean fasting blood glucose was 128.7±42.6 mg/dL, while mean total cholesterol and LDL cholesterol were 184.6±43.8 mg/dL and 112.8±36.7 mg/dL, respectively. These values demonstrate the clustering of metabolic and lipid abnormalities among patients with CAD. Heidari et al. (2015)^[5] reported that vitamin D deficiency was particularly common among patients with type 2 diabetes and that assessment of 25(OH)D could add information to cardiovascular risk evaluation in diabetic individuals. However, lipid and glycaemic abnormalities may act as mediators or confounders rather than being direct consequences of low vitamin D status.

Prevalence of vitamin D deficiency

In the present study, vitamin D deficiency was found in 131 (65.5%) patients, insufficiency in 47 (23.5%) and sufficiency in only 22 (11.0%). Thus, 89.0% of patients had either deficient or insufficient vitamin D levels. Among the deficient patients, 19.0% had severe deficiency below 10 ng/mL and 46.5% had moderate deficiency between 10 and 19.9 ng/mL. This distribution indicates that vitamin D inadequacy was highly prevalent among patients with coronary artery disease.

The prevalence found in the present study was lower than that reported by Alsancak et al. (2015)^[2], in which 602 of 746 patients, or approximately 80.7%, had vitamin D levels below 20 ng/mL. The difference may be related to variations in geography, season of blood collection, clothing, diet, assay technique and characteristics of the angiography population.

Patil et al. (2017)^[6], in a Maharashtra-based study of patients with acute coronary syndrome, reported vitamin D deficiency in 46% and insufficiency in 33% of patients. Although their deficiency prevalence was lower than the 65.5% observed in the present study, the combined burden of deficient and insufficient vitamin D status was similarly high. Their study also found that only a minority of ACS patients had adequate vitamin D concentrations.

Knežević Praveček et al. (2017)^[7] demonstrated that patients with acute coronary syndrome had significantly lower mean 25(OH)D levels than controls, 35.19 nmol/L versus 58.08 nmol/L. Their findings support the present observation that vitamin D inadequacy is common among patients presenting with coronary disease. However, they did not establish a significant association between vitamin D levels and major cardiovascular events during three years of follow-up.

Dhibar et al. (2016)^[1] similarly reported a high prevalence of vitamin D deficiency among patients undergoing coronary angiography and found a significant association between deficient vitamin D status and the presence of CAD. In contrast, Ho et al. (2015)^[8], in a study of 1,131 individuals evaluated using coronary calcium scoring and computed tomographic angiography, found vitamin D deficiency in only 11.7% and insufficiency in 26.1%. They did not observe an association between vitamin D levels, coronary calcium scores or severe obstructive stenosis. This discrepancy highlights the influence of population selection and baseline vitamin D status on study findings.

Association with demographic factors

Patients aged 60 years or above had significantly higher odds of vitamin D deficiency in the present study, with a crude OR of 2.59 and an adjusted OR of 2.08. The deficient group was also significantly older than the non-deficient group, with mean ages of 61.2 and 55.7 years, respectively. Age-related decline in skin synthesis, reduced outdoor activity, dietary inadequacy and comorbid conditions may explain this association. Cosentino et al. (2021)^[4] similarly described advancing age as an important determinant of reduced vitamin D status and cardiovascular vulnerability.

Female sex was significantly associated with deficiency on univariate analysis, but it did not remain significant after adjustment. Verdoia et al. (2015)^[9] reported that the association between lower vitamin D levels and CAD prevalence and severity appeared more evident among women than men. In their study, lower vitamin D tertiles were associated with increased CAD prevalence and severity among female patients. The loss of significance for female sex in the present multivariable model suggests that the initial association may have been partly explained by age, obesity, sunlight exposure or physical inactivity.

Urban residence was not significantly associated with deficiency in the present study. Although urban populations may have reduced sunlight exposure because of indoor occupations, pollution and limited outdoor activity, residence alone may not adequately measure actual ultraviolet exposure, dietary practices or socioeconomic status.

Association with obesity, diabetes and hypertension

Obesity was one of the strongest determinants of vitamin D deficiency. Obese patients had a crude OR of 3.15 and an adjusted OR of 2.49. The mean BMI was also significantly higher among deficient patients than among non-deficient patients, 27.8±4.0 versus 24.9±3.6 kg/m². Vitamin D is fat-soluble, and greater adipose tissue volume may reduce its circulating bioavailability through volumetric dilution or sequestration. Obesity may also be associated with reduced outdoor physical activity and poorer dietary patterns.

Diabetes mellitus was present in 59.5% of deficient patients compared with 36.2% of non-deficient patients. It remained an independent determinant, with an adjusted OR of 1.99. Gondim et al. (2016)^[10] found that vitamin D deficiency among patients with type 2 diabetes was associated with more severe acute coronary syndrome and more extensive coronary lesions. Knežević Praveček et al. (2017)^[7] also reported that the lowest vitamin D concentrations were observed among diabetic patients with ACS. These findings agree with the present observation of higher fasting blood glucose and a greater prevalence of diabetes in the vitamin D-deficient group.

Hypertension was significantly associated with deficiency during bivariate analysis, but it did not remain significant after multivariable adjustment. This suggests that its relationship with vitamin D deficiency may have been confounded by age, obesity, diabetes and physical inactivity. Nargesi et al. (2016)^[11] reported that vitamin D deficiency contributed to CHD risk, although the magnitude of the association was influenced by conventional cardiovascular risk factors. In the ARIC cohort, Michos et al. (2015)^[12] also found that the relationship between low 25(OH)D and incident coronary heart disease was attenuated after adjustment for potential mediators such as diabetes and hypertension.

Dyslipidaemia was not significantly associated with vitamin D deficiency in categorical analysis, although mean LDL cholesterol was significantly higher in deficient patients. This difference may reflect the greater sensitivity of continuous-variable analysis. However, evidence regarding vitamin D and lipid metabolism remains inconsistent. Vitamin D supplementation trials have generally not demonstrated consistent improvements in total cholesterol or LDL cholesterol, indicating that low vitamin D may be a marker of an adverse metabolic profile rather than a direct cause of dyslipidaemia.

Association with lifestyle factors

Current smoking was associated with vitamin D deficiency on unadjusted analysis, with smokers having approximately twice the odds of deficiency. However, the association became non-significant after adjustment. Smoking may correlate with poor diet, reduced physical activity, socioeconomic disadvantage and more severe cardiovascular risk, which could explain the unadjusted relationship.

A sedentary lifestyle remained independently associated with vitamin D deficiency, with an adjusted OR of 2.16. Sedentary patients may spend less time outdoors and consequently receive less ultraviolet B exposure. Physical inactivity also promotes obesity, insulin resistance and adverse metabolic profiles, all of which were associated with deficiency in the present study.

Low sunlight exposure was the strongest independent determinant. Patients with inadequate sunlight exposure had a crude OR of 4.38 and an adjusted OR of 3.29. This finding is biologically plausible because cutaneous synthesis following ultraviolet B exposure is the principal natural source of vitamin D. The strength of this association indicates that sunlight-related behaviours should be assessed when evaluating vitamin D status among CAD patients. Nevertheless, variables such as season, duration and timing of exposure, skin pigmentation, clothing and sunscreen use should be measured more objectively in future studies.

Association with coronary disease presentation and severity

Vitamin D deficiency was significantly associated with acute coronary syndrome in unadjusted analysis. Patients with ACS had nearly twice the odds of deficiency compared with those with chronic coronary syndrome. Knežević Praveček et al. (2017)^[7] found significantly lower vitamin D concentrations among ACS patients than controls, while Ismail et al. (2021)^[13] reported abnormalities of vitamin D and its metabolites among patients with ACS undergoing coronary angiography. These findings support an association between low vitamin D status and acute coronary presentations, although acute illness itself may alter circulating vitamin D concentrations.

Multivessel coronary artery disease was associated with deficiency on bivariate analysis, with a crude OR of 1.96, but the association became borderline after adjustment (adjusted OR=1.73, p=0.076). Dziedzic et al. (2019)^[13] reported that lower vitamin D concentrations were associated with greater coronary atherosclerosis severity and a higher incidence of acute coronary syndrome among non-diabetic cardiac patients. Gondim et al. (2016)^[10] similarly found that deficiency predicted more extensive coronary lesions among diabetic ACS patients.

However, not all studies have demonstrated an association with angiographic severity. Alsancak et al. (2015)^[2] found no significant difference in Gensini scores between vitamin D-deficient and non-deficient groups. Ho et al. (2015)^[8] also found no relationship between vitamin D status and severe obstructive stenosis or coronary calcium. These contrasting findings indicate that vitamin D deficiency may coexist with CAD risk factors without necessarily having an independent linear relationship with anatomical disease severity.

Independent determinants and model interpretation

The multivariable analysis showed that age ≥60 years, obesity, diabetes mellitus, sedentary lifestyle and low sunlight exposure were independent determinants of vitamin D deficiency. The logistic model was statistically significant and explained approximately 36% of the variance, with an overall classification accuracy of 75.5%. The non-significant Hosmer–Lemeshow test indicated acceptable calibration.

The attenuation of female sex, hypertension, smoking, ACS and multivessel disease after adjustment emphasizes the importance of controlling for overlapping demographic, metabolic and behavioural factors. The findings suggest that vitamin D deficiency in CAD is multifactorial and is strongly influenced by age, adiposity, glucose metabolism and reduced outdoor activity.

Vitamin D deficiency was highly prevalent among patients with coronary artery disease, affecting 65.5% of the study population, while only 11.0% had sufficient vitamin D levels. Older age, obesity, diabetes mellitus, sedentary lifestyle and low sunlight exposure were identified as significant independent determinants of vitamin D deficiency. Low sunlight exposure was the strongest predictor, followed by obesity and sedentary behaviour. Vitamin D-deficient patients also had significantly higher age, body mass index, fasting blood glucose and LDL cholesterol levels than non-deficient patients. Although deficiency was associated with acute coronary syndrome and multivessel coronary artery disease on univariate analysis, these associations did not remain independently significant after adjustment for confounding factors. The findings indicate that vitamin D deficiency is common among patients with CAD and is closely related to adverse demographic, metabolic and lifestyle characteristics. Screening for vitamin D deficiency may be considered in high-risk CAD patients, particularly older, obese, diabetic and physically inactive individuals with inadequate sunlight exposure. However, prospective studies are required to determine whether correction of vitamin D deficiency can improve cardiovascular outcomes. LIMITATIONS OF THE STUDY The present study had several limitations. First, the cross-sectional design allowed assessment of associations but could not establish a temporal or causal relationship between vitamin D deficiency and coronary artery disease. Second, the study was conducted at a single tertiary care hospital, which may limit the generalizability of the findings to the wider community or to patients treated in primary and secondary healthcare settings. Third, the sample included only patients with established CAD and did not include a healthy control group for direct comparison of vitamin D status. Serum vitamin D was measured at a single time point, and possible seasonal variations in vitamin D concentration were not fully evaluated. Sunlight exposure, physical activity and dietary vitamin D intake were based mainly on patient-reported information and were therefore susceptible to recall and reporting bias. Factors such as skin pigmentation, clothing practices, sunscreen use, duration and timing of sunlight exposure, dietary supplementation and socioeconomic status were not assessed objectively. Although multivariable logistic regression was used to adjust for several potential confounders, residual confounding from unmeasured factors could not be excluded. The severity of coronary artery disease was not uniformly quantified using a standardized angiographic scoring system such as the Gensini or SYNTAX score. Furthermore, inflammatory markers, parathyroid hormone, serum phosphorus and other components of vitamin D metabolism were not evaluated. The study also did not assess follow-up cardiovascular events, mortality or the effect of vitamin D supplementation. Larger multicentric prospective studies with repeated vitamin D measurements and long-term follow-up are therefore recommended.

1. Dhibar DP, Sharma YP, Bhadada SK, Sachdeva N, Sahu KK. Association of vitamin D deficiency with coronary artery disease. J Clin Diagn Res. 2016;10(9).
2. Alsancak Y, Cengel A, Akyel A, Ozkan S, Sezenoz B, Unlu S, et al. Relationship between serum vitamin D levels and angiographic severity and extent of coronary artery disease. Eur J Clin Invest. 2015;45(9):940-8.
3. Bakthavatchalam R, Kumar S, Kumar A, Sinha N. Association of vitamin D with risk factors for coronary artery disease. J Clin Med Res. 2023;15:1-7.
4. Cosentino N, Campodonico J, Milazzo V, De Metrio M, Brambilla M, Camera M, et al. Vitamin D and cardiovascular disease: current evidence and future perspectives. Nutrients. 2021;13(10):3603.
5. Heidari B, Nargesi AA, Hafezi-Nejad N, Sheikhbahaei S, Pajouhi A, Nakhjavani M, et al. Assessment of serum 25-hydroxy vitamin D improves coronary heart disease risk stratification in patients with type 2 diabetes. Am Heart J. 2015;170(3):573-9.
6. Patil S, Prajapati P, Gandhi S, Kadam N, Bhat P. Prevalence of vitamin D deficiency in acute coronary syndrome in a tertiary care hospital, Maharashtra, India. J Evol Med Dent Sci. 2017;6(4):282-5.
7. Knežević Praveček M, Vuković-Arar Ž, Miškić B, Hadžibegović I. Vitamin D deficiency in acute coronary syndrome: clinically relevant or incidental finding? Cent Eur J Public Health. 2017;25(3):185-90.
8. Ho JS, Cannaday JJ, Barlow CE, Willis B, Haskell WL, FitzGerald SJ. Low 25-OH vitamin D levels are not associated with coronary artery calcium or obstructive stenoses. Coron Artery Dis. 2015;26(6):521-5.
9. Verdoia M, Schaffer A, Barbieri L, Di Giovine G, Marino P, Suryapranata H, et al. Impact of gender difference on vitamin D status and its relationship with the extent of coronary artery disease. Nutr Metab Cardiovasc Dis. 2015;25(5):464-70.
10. Gondim F, Caribé A, Vasconcelos KF, Segundo AD, Bandeira F. Vitamin D deficiency is associated with severity of acute coronary syndrome in patients with type 2 diabetes and high rates of multivessel lesions. BMC Cardiovasc Disord. 2016;16:207.
11. Nargesi AA, Heidari B, Esteghamati S, Hafezi-Nejad N, Sheikhbahaei S, Pajouhi A, et al. Contribution of vitamin D deficiency to the risk of coronary heart disease in subjects with essential hypertension. Atherosclerosis. 2016;244:165-71.
12. Michos ED, Misialek JR, Selvin E, Folsom AR, Pankow JS, Post WS, et al. 25-Hydroxyvitamin D levels, vitamin D binding protein gene polymorphisms and incident coronary heart disease among whites and blacks: the ARIC study. Atherosclerosis. 2015;241(1):12-7.
13. Dziedzic EA, Gąsior JS, Pawłowski M, Wodejko-Kucharska B, Saniewski T, Marcisz A, et al. Vitamin D level is associated with severity of coronary artery atherosclerosis and incidence of acute coronary syndromes in non-diabetic cardiac patients. Arch Med Sci. 2019;15(2):359-68.