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Vitamin D Status in Patients with Atrial Fibrillation and Heart Failure - Is there a Link? by Miglena Nikolova, Neshe Nazifova-Tasinova, Deyana Vankova, Daniela Gerova, Yoto Yotov, Atanas Atanasov, Milena Pasheva, Yoana Kiselova-Kaneva, Bistra Galunska

Background: The disturbed pleiotropic functions of vitamin D are related to numerous chronic non-skeletal diseases. The role of vitamin D insufficiency/deficiency in cardiovascular diseases (CVD) is controversial. Therefore, the aim was to study the vitamin D status in CVD patients and to reveal possible relationships with CVD risk factors.
Methods: This prospective study includes 93 individuals devided into two groups - patients with CVD (n = 49) and patients at risk for CVD (n = 44) served as controls. The CVD-patients were stratified into AF-group - with paroxysmal or persistent atrial fibrillation and HF-group - with heart failure with preserved ejection fraction, in sinus rhythm.
Vitamin D status was assessed by measurement of serum 25-hydroxy-vitamin D (25OHD) using liquid chromatography with mass detection. Gene expression of the regulatory enzyme of vitamin D metabolism, 1-alfa-hydroxylase (CYP27B1), was evaluated by two-step real-time qPCR. Coronary artery calcium scans were performed and coronary artery calcium score (CACS) was calculated. Routine biochemical parameters were extracted from the medical documentation.
Standard statistical methods (descriptive statistics, unpaired Student’s t-test, one-way ANOVA, simple and multiple linear regression analyses) were applied. Statistical significance was considered at p < 0.05.
Results: Serum 25OHD levels of the controls were higher than those of the CVD-patients (37.36 ± 15.10 ng/mL vs. 27.70 ± 11.80 ng/mL, p = 0.008). The vitamin D status worsened with the severity of CVD pathology: significant decrease of 25OHD levels was found in the AF-group (29.56 ± 11.76 ng/mL, p = 0.044) and HF-group (24.47 ± 11.61 ng/mL, p = 0.003) vs. controls (37.36 ± 15.10 ng/mL). Significant reduction in circulating vitamin D levels with the increase of CACS (p = 0.007) was also observed. Linear regression analysis revealed significant negative association for serum 25OHD with CACS for both the entire studied group (p = 0.008) and for CVD patients (p = 0.049). The gene expression of CYP27B1 was down regulated with both the severity of CVD pathology (p = 0.05) and coronary calcium accumulation (p = 0.08). Moreover, we found a significant positive relationship (p = 0.041) between serum 25OHD levels and CYP27B1 gene expression.
Conclusions: Vitamin D deficiency may be an independent cardiovascular risk factor associated with the severity of CVD pathology and increased coronary calcium deposition. The mechanism by which vitamin D itself can affect cardiovascular outcomes remains to be clarified.

DOI: 10.7754/Clin.Lab.2020.200902