This study revealed a significant relationship
between 25(OH)D levels and the severity of CAD
in obese patients. Our findings suggest that lower
25(OH)D levels are associated with increased
coronary lesion complexity and severity. Furthermore,
25(OH)D levels were an independent predictor of
SYNTAX scores in obese patients.
Previous studies have shown an inverse relationship
between serum 25(OH)D levels and obesity.[5-8]
Several hypotheses have been proposed to explain
how obesity leads to Vitamin D deficiency. The most
likely mechanism is believed to be the volumetric
distribution of Vitamin D. Since adipose tissue acts
as a reservoir for Vitamin D, obese patients tend
to have lower serum concentrations compared to
lean individuals, even when their overall 25(OH)D
levels are similar.[9,10] Additionally, obese individuals
tend to respond less effectively to Vitamin D
supplements.[11] Another possible mechanism is the
impairment of 25-hydroxylation caused by hepatic
steatosis, a condition commonly observed in obese
individuals. This impairment leads to a reduction in
the conversion of Vitamin D into its active form.[9]
Other hypotheses include poor dietary habits, reduced
sun exposure, and variations in gene expression that
affect Vitamin D metabolism.[9]
Our results also align with observational studies
identifying a link between serum 25(OH)D levels
and CAD.[12,13] A comprehensive meta-analysis of
prospective studies involving over 18,000 participants
demonstrated that the serum 25(OH)D level was inversely associated with the risk of cardiovascular
events and cardiovascular mortality.[14] Verdoia et
al.[4] demonstrated that lower 25(OH)D levels were
associated with the severity of CAD. Similarly, a
study involving 348 patients undergoing coronary
angiography found that lower serum 25(OH)D levels
were independently associated with higher SYNTAX
scores, indicating more severe coronary lesions.[15]
Notably, our findings extend these observations
specifically to obese patients, confirming that low
25(OH)D levels are associated with increased coronary
lesion complexity and severity.
Vitamin D appears to play a protective role in
atherosclerosis through multiple mechanisms. It
prevents endothelial dysfunction by increasing nitric
oxide production, reducing oxidative stress, and
inhibiting inflammatory cytokines and adhesion
molecules.[16] Vitamin D also regulates vascular
tone and angiogenesis.[16] In vascular smooth
muscle cells, it has antiproliferative effects and
impacts processes such as cell migration and
fibrosis.[16] Another potential mechanism by which
Vitamin D might influence myocardial infarction
risk is through its effect on vascular calcification,
as evidenced by the negative relationship between
levels of 1,25-dihydroxyvitamin D and vascular
calcification.[17] Vitamin D modulates immune
responses by shifting the balance from proatherogenic
T helper 1 cells to antiatherogenic T helper
2 profiles.[16] It also influences atherosclerosis by
improving systemic conditions that contribute to
it, such as insulin sensitivity, beta cell function,
and lipid profiles.[16] Furthermore, it suppresses the
renin-angiotensin-aldosterone system.[16]
Obesity is associated with a chronic, low-level
inflammatory state that affects several metabolic
and vascular pathways, such as insulin resistance,
endothelial function, and lipid metabolism, all of which
are also influenced by Vitamin D.[18] Additionally,
obesity has been linked to increased inflammation
in epicardial adipose tissue, which significantly
correlates with the pathogenesis of CAD.[19] In obese
individuals, low 25(OH)D levels can worsen these
conditions, leading to increased atherosclerosis and
higher cardiovascular risk. This is primarily assumed
to be because low 25(OH)D levels fail to counteract
oxidative stress.[20] However, it is unclear whether
these factors are impaired simultaneously or whether
there is a causal relationship.
There were some limitations to this study. First,
as a cross-sectional study, the causal relationship
between 25(OH)D levels and the severity of coronary
artery stenosis could not be established. Second,
25(OH)D levels were measured only once within six
months before angiography, which might not reflect
seasonal or lifestyle changes. Third, the number of
patients in the study was relatively low.
In conclusion, this study demonstrates a
significant association between low serum 25(OH)D
levels and higher SYNTAX scores, indicating more
severe CAD in obese individuals. Additionally, in
obese patients, Vitamin D levels were an independent
predictor of SYNTAX scores.
Data Sharing Statement: The data that support the
findings of this study are available from the corresponding
author upon reasonable request.
Author Contributions: Conceptualization,
investigation, writing-original draft, review, and editing:
B.C.; Data curation, investigation, methodology, review and
editing: B.A.Y.; Methodology, formal analysis, supervision,
writing-review and editing: M.C.
Conflict of Interest: The authors declared no conflicts
of interest with respect to the authorship and/or publication
of this article.
Funding: The authors received no financial support for
the research and/or authorship of this article.
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