Association of Serum 25-Hydroxyvitamin D Levels With Acute Coronary Syndrome: A Case-Control Study.

BACKGROUND: Vitamin D deficiency has been proposed as a possible contributor to cardiovascular disease, but its relationship with acute coronary syndrome (ACS) remains uncertain. OBJECTIVE: This study assessed the association between serum 25-hydroxyvitamin D (25(OH)D) concentrations and ACS, including ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina (UA), among patients presenting to a tertiary care center. METHODS: This hospital-based case-control study was done at the medical wards and intensive care unit (ICU) of NKP Salve Institute of Medical Sciences & Research Center and Lata Mangeshkar Hospital, Nagpur, India, for two years from 01/2021 to 12/2022, and included 140 participants, comprising 70 patients with ACS and 70 age- and sex-matched controls without ACS. Demographic characteristics, clinical history, cardiovascular risk factors, and laboratory findings were recorded. Serum 25(OH)D concentrations were measured using a chemiluminescent immunoassay and categorized as severe deficiency (<10 ng/mL), mild-to-moderate deficiency (10.0-19.9 ng/mL), insufficiency (20.0-29.9 ng/mL), or sufficiency (≥30 ng/mL). Multivariable logistic regression analysis was performed to determine the association between vitamin D status and ACS after adjustment for age and sex. RESULTS: Vitamin D deficiency and insufficiency were more frequent among patients with ACS than among controls. Participants with serum 25(OH)D concentrations below 30 ng/mL had significantly higher odds of ACS than those with sufficient vitamin D levels (adjusted odds ratio: 3.28; 95% confidence interval: 1.49-7.21; p = 0.003). Severe and mild-to-moderate vitamin D deficiency were also more common among ACS cases. However, serum vitamin D status was not significantly associated with the angiographic extent of coronary artery disease. CONCLUSION: Lower serum 25(OH)D concentrations were significantly associated with ACS in this study population. However, the case-control design did not establish a causal or temporal relationship, and residual confounding could not be excluded. Larger prospective studies are required to clarify whether vitamin D deficiency independently contributes to ACS and whether its correction improves cardiovascular outcomes.