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The Relationship between Vitamin D and Coronary Artery Ectasia in Subjects with a Normal C-Reactive Protein Level
Goksel Cagirci1, Selcuk Kucukseymen1, Isa Oner Yuksel1
1Department of Cardiology, Antalya Education and Research Hospital, Antalya, Turkey.
Insights
Low vitamin D levels are associated with coronary artery ectasia (CAE) in patients without inflammation. This study suggests vitamin D may play a non-inflammatory role in the development of CAE, a type of coronary artery disease.
Area of Science:
- Cardiology
- Endocrinology
- Nutritional Science
Background:
- Vitamin D is linked to inflammation, but its role in coronary artery disease (CAD) is not fully understood.
- Coronary artery ectasia (CAE), a form of CAD, is increasingly common.
- This study investigates the relationship between vitamin D and CAE independent of inflammatory processes.
Purpose of the Study:
- To examine the association between 25-OH vitamin D levels and coronary artery ectasia (CAE).
- To determine if vitamin D plays a role in CAE pathophysiology outside of inflammation.
- To compare vitamin D and parathyroid hormone (PTH) levels in CAE patients versus controls.
Main Methods:
- A case-control study involving 201 patients with isolated CAE and 197 healthy controls.
- Participants underwent biochemical tests, inflammatory marker assessments, and 25-OH vitamin D level measurements.
- Statistical comparisons were made for clinical characteristics, inflammatory markers, PTH, and vitamin D levels.
Main Results:
- No significant differences in basic clinical characteristics or inflammatory markers were found between groups.
- CAE patients had significantly higher parathyroid hormone (PTH) levels (41.8±15.1 pg/mL) compared to controls (19.1±5.81 pg/mL; p<0.001).
- CAE patients exhibited significantly lower 25-OH vitamin D levels (14.5±6.3 ng/mL) than controls (24.6±9.3 ng/mL; p<0.001).
Conclusions:
- An association exists between vitamin D deficiency and CAE in the absence of inflammatory processes.
- Vitamin D may contribute to CAE pathophysiology as a non-inflammatory factor.
- Findings support further research into vitamin D's role in cardiovascular health and disease.
Background And Objectives:
Vitamin D is generally known to be closely related to inflammation. The effects of vitamin D on coronary artery disease (CAD) are not fully explained. Nowadays, coronary artery ectasia (CAE) cases are common and are regarded as being a kind of CAD. We aimed to investigate, in a case-control study, the relationship between vitamin D and CAE without an associated inflammatory process.
Subjects And Methods:
This study population included 201 patients (CAE group, 121 males; mean age, 61.2±6.4 years) with isolated CAE; and 197 healthy individuals (control group, 119 males; mean age, 62.4±5.8 years), comprising the control group, who had normal coronary arteries. These participants concurrently underwent routine biochemical tests, tests for inflammatory markers, and tests for 25-OH vitamin D in whole-blood draws. These parameters were compared.
Results:
There are no statistical significance differences among the groups for basic clinical characteristics (p>0.05). Inflammatory markers were recorded and compared to exclude any inflammatory process. All of them were similar, and no statistical significance difference was found. The average parathyroid hormone (PTH) level of patients was higher than the average PTH level in controls (41.8±15.1 pg/mL vs. 19.1±5.81 pg/mL; p<0.001). Also, the average 25-OH vitamin D level of patients was lower than the average 25-OH vitamin D level of controls (14.5±6.3 ng/mL vs. 24.6±9.3 ng/mL; p<0.001). In receiver operating characteristic curve analysis, the observed cut-off value for vitamin D between the control group and patients was 10.8 and 85.6% sensitivity and 75.2% specificity (area under the curve: 0.854, 95% confidence interval: 0.678-0.863).
Conclusion:
We found that there is an association between vitamin D and CAE in patients who had no inflammatory processes. Our study may provide evidence for the role of vitamin D as a non-inflammatory factor in the pathophysiology of CAE.