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Visfatin and 25-Hydroxy Vitamin D3 Levels Affect Coronary Collateral Circulation Development in Patients with Chronic Coronary Total Occlusion

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Research Article | DOI: https://doi.org/10.31579/2692-9759/183

Visfatin and 25-Hydroxy Vitamin D3 Levels Affect Coronary Collateral Circulation Development in Patients with Chronic Coronary Total Occlusion

  • Xiaoling Ji 1*
  • Shuqi Jin 2
  • Yuxia Wang 1
  • Yumiao Chen 1
  • Jing Zhang 1

1Department of Cardiology, China Aerospace Science and Industry Corporation 731 Hospital, Beijing, 100074, China.

2Department of Cardiology, Shenzhen Bao'an Disteict Songgang People's Hospital, Shenzhen 518105, China.

*Corresponding Author: Xiaoling Ji Department of Cardiology, China Aerospace Science and Industry Corporation 731 Hospital, Beijing, 100074, China.

Citation: Xiaoling Ji, Shuqi Jin, Yuxia Wang, Yumiao Chen, Jing Zhang, (2026), Visfatin and 25-Hydroxy Vitamin D3 Levels Affect Coronary Collateral Circulation Development in Patients with Chronic Coronary Total Occlusion, Cardiology Research and Reports, 8(1); DOI:10.31579/2692-9759/183

Copyright: © 2026, Xiaoling Ji. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Received: 19 December 2025 | Accepted: 31 December 2025 | Published: 05 January 2026

Keywords: 25-hydroxyvitamin D3; coronary collateral circulation; chronic total occlusion

Abstract

Background:

CCC plays a vital role in the myocardial blood supply, especially for ischaemic myocardium. Evidence suggests that the visfatin and 25-(OH)D3 levels are related to the degree and incidence of vascular stenosis associated with coronary artery disease. However, few studies have evaluated the effect of visfatin and 25-(OH)D3 on CCC development in CTO patients. This study aimed to evaluate the relationship between the serum visfatin level and 25-hydroxy vitamin D3 [25-(OH)D3] and coronary collateral circulation (CCC) in patients with chronic total occlusion (CTO).

Methods:

A total of 189 patients with CTO confirmed by coronary angiography were included. CCC was graded from 0 to 3 according to the Rentrop-Cohen classification. Patients with grade 0 or 1 collateral development were included in the poor CCC group (n=82), whereas patients with grade 2 or 3 collateral development were included in the good CCC group (n=107). The serum visfatin and 25-(OH)D3 levels were measured by ELISA.

Results:

The visfatin level was significantly higher in the poor CCC group than in the good CCC group, and the 25-(OH)D3 level was significantly lower in the poor CCC group than in the good CCC group (P≤0.001).

Correlation analysis showed that the Rentrop grade was negatively correlated with the visfatin level (r=-0.692, P≤0.001) but positively correlated with the 25-(OH)D3 level (r=0.635, P≤0.001). Logistic regression analysis showed that the visfatin and 25-(OH)D3 levels were independent risk factors for CCC (OR=1.597, 95% CI: 1.3-1.961, P≤0.001 and OR=0.566, 95% CI: 0.444-0.722, P≤0.001, respectively). The visfatin and 25-(OH)D3 levels can effectively predict the CCC status.

Conclusion: The serum visfatin and 25-(OH)D3 levels are related to CCC development and are independent predictors of poor CCC.

1.Introduction

Coronary collateral circulation (CCC) is crucial and is related to the prognosis of patients with coronary artery disease (CAD). Well-developed coronary collaterals can restore blood flow to ischaemic areas of the myocardium and protect myocardial tissue at risk [1]. Studies have shown that well-developed collateral circulation can limit the area of myocardial infarction, reduce arrhythmia, protect cardiac function, reduce mortality, and ultimately improve the cardiovascular prognosis [2-4]. Currently, there is no noninvasive technology to evaluate collateral function [2,5]. Therefore, the identification of circulating biomarkers to assess the advantages and disadvantages of CCC and exploration of its internal mechanism have important clinical significance.

Visfatin is an adipocyte factor that is produced in large quantities in visceral adipose tissue [6] and is additionally expressed within the heart, liver, muscle, placenta, lung，kidney and bone marrow[7].It has also been reported that visfatin plays a direct role in arterial remodeling[8].Therefore, the connection between visfatin and CCC has become an area of interest, but research in this area is still lacking.

Vitamin D is a steroid hormone produced by irradiating the skin with ultraviolet rays of the sun.It performs biological functions by binding to vitamin D receptors (VDRs) that are widely present in human tissues. VDRs have been confirmed on the surface of cardiomyocytes,smooth muscle cell, and sendothelial cells,and control the proliferation and differentiation of these cells[9,10].

Current studies have shown that vitamin D in an independent manner to promote human umbilical vein endothelial cells (HUVECs) proliferation and migration [11].Additionally, increases in the number of myeloid cells (MCs) [12] and regulation of the VEGF [13] signal transduction pathway affect arteriogenesis and angiogenesis. Although evidence exists to support a positive regulatory role of vitamin D in both arteriogenesis and angiogenesis, few reports have examined its relationship with CCC in patients with chronic total occlusion (CTO).

In this study, we explored the relationship among the serum visfatin level, serum 25-(OH)D3 level and CCC status in CTO patients.

2. Methods

2.1 Patient population

189 cases of coronary angiography confirmed that at least one coronary artery with 100% diameter stenosis was collected in the Department of Cardiology from November 2018 to February 2019[100 men and 89 women; mean age: 62±8 years].Patients were divided into a good CCC group (n= 107, Rentrop grade 2 or 3) and a poor CCC group (n=82, Rentrop grade 0 or 1) according to the Rentrop-Cohen classification of CCC on coronary angiography.

The exclusion criteria included recent acute coronary syndrome (<3 months), coronary artery bypass operation, heart failure, cardiomyopathy, valvular heart disease, previous revascularization history, peripheral vascular disease, chronic obstructive pulmonary disease, chronic kidney or liver disease, previous diagnosis of malignancy, concomitant inflammatory disease, metabolic disease related to vitamin D, and the use of medications containing vitamin D preparations within the previous 3 months. Coronary heart disease risk factors such as hypertension, diabetes, hyperlipidaemia, body mass index (BMI) and smoking history were recorded for all patients.

The study was approved by the hospital ethics committee, and informed consent of each patient was obtained.

2.2 Coronary angiography

Coronary angiography was performed using the Judkins method through radial artery puncture. CCC was graded according to the Rentrop-Cohen classification, as follows [14]: grade 0, no obvious collateral vessels (opaque area, no contrast medium filling in the distal infarction); grade 1, collateral perfusion of the coronary artery that did not reach the coronary artery of the pericardium; grade 2, partial perfusion of the subepithelial segment by CCC; and grade 3, perfusion of the coronary epicardial segment by CCC.

2.3 Biochemical measurements

Fasting venous blood was drawn from the enrolled patients on the day of coronary angiography. Routine laboratory parameters, including the troponin I (TnI), creatinine, total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and calcium levels, were immediately determined. The blood samples collected for 25-(OH)D3 and visfatin measurements were snap frozen and stored at -70°C until analysis. The serum concentrations of 25-(OH)D3 and visfatin were measured by the ELISA method with a Roche 601 (BISL kit, UK).

2.4 Statistical analysis

Statistical analysis was performed using the SPSS 23.0 statistical package (IBM Corporation, New York, NY, USA).

Continuous variables are expressed as the mean ± SD or median and 25th and 75th percentiles [(M (P25, P75)], categorical variables are expressed as percentages, and the chi-square test was used to assess the rational distribution hypothesis of continuous variables. Differences between two groups of normally distributed continuous variables were compared with a T-test, and differences between non-normally distributed continuous variables were assessed using the Mann-Whitney U test. Categorical data were compared with the chi-square test, and Spearman’s correlation coefficient was used to assess the correlations between the serum 25-(OH)D3 and visfatin levels and the Rentrop grade. Binary logistic regression analysis was used to determine independent predictors of poor CCC development. A P value of 0.05 or less was considered to indicate statistical significance.

3. Results

3.1 Baseline patient characteristics

The 189 patients included in the study were included in the good CCC group (good collaterals, 107 patients, Rentrop grade 2 or 3) or poor CCC group (poor collaterals, 82 patients, Rentrop grade 0 or 1). 

The baseline characteristics of patients with good CCC group and poor CCC group are shown in Table 1. Both groups were similar in age, gender, BMI, smoking history, hypertension, cholesterol and calcium levels (P>0.05). However, the proportion of patients with diabetes was higher in the poor CCC group than in the good CCC group (52.4% vs. 33.6%, P≤0.001). Furthermore, the LDL-C, TnI, and creatinine levels were obviously higher in the poor CCC group than in the good CCC group, as shown in Table 1 

Variable       good(n=107)Poor(n=82)P 
age （years） 63（56，68）                                       64（58，69） 0.078
Gender male n(%)                                                     55（51.4）45（54.9）0.064 
Hypertension n( %)                                                   57（53.3）54（65.9）0.082
Diabetes n（%）                                                         36（33.6）43（52.4）0.009     
Smoking n（%）                                                     55（51.4）45（54.9）0.635
BMI（kg/m2）                                                   26（25，29）26（26，29）0.204 
LDL-C (mmol/l)                                         1.5(0.65,3.02 )2.6(2.03,3.02) ≤0.001
TG(mmol/l)                                         2.2（1.7，2.6）2.03（1.58，2.08） 0.15
TC(mmol/l)                                         4.2（3.8，5.01）4.3（3.9，4.8）0.32
TNI(ng/ml )                                     0.08(0.05,0.16) 0.16(0.12,0.25)       ≤0.001
Creatinine(mg/l)                                           66（50，90）75（59，90） 0.034
25（OH）D3 (ng/ml)                                         32(29,35)   25(21,28)     ≦0.001
Calcium(mmol/l)                                 2.06（2.02，2.1）   2.06（2.03，2.1）0.182
Visfatin(ng/ml)                                   10.3(9.2,12.8)   17.4(14.2,21.13)     ≤0.001
Rentrop score (n)                                                                                
0 18 
1 64 
264  
343  

Table 1: Demographic properties and biochemical parameters of the good CCC group and the poor CCC group.

CCC, coronary collateral circulation; BMI, Body mass index；TnI:Troponin I;TC , Total cholesterol; TG, triglycerides; LDL-c, low-density lipoprotein cholesterol.

3.2 Serum visfatin and 25-(OH)D3 levels in each patient group

The serum visfatin level was significantly higher in the poor CCC group than in the good CCC group (P≤0.001). The serum 25-(OH)D3 level was significantly lower in the poor CCC group than in the good CCC group (P≤0.001), as shown in Figure 1-2.

3.3 Relationship among the serum visfatin and 25-(OH)D3 levels and the Rentrop grade

Spearman correlation analysis showed a significant negative correlation between the visfatin level and the Rentrop grade (r=-0.692, P≤0.001) (Figure 3). A significant positive correlation was observed between the 25-(OH)D3 level and the Rentrop grade (r=0.689, P≤0.001) (Figure 4). Furthermore, an L-shaped relationship was observed between the 25-(OH)D3 and visfatin levels (Figure 5).

3.4 Binary logistic regression analysis:

Binary logistic regression was performed between CCC development and 25-(OH) D3, visfatin, LDL-C and other factors. CCC development was used as the dependent variable, and all univariate analyses with P values less than 

0.1 were included in the logistic regression equation as independent variables. Stepwise regression was used for multivariate analysis. The serum 25-(OH)D3, visfatin, and LDL-C levels and diabetes were independent risk factors for poor CCC development (Figure 6).

Discussion

The present study revealed the following findings. (1) The visfatin level was significantly higher in CTO patients in the poor CCC group than in those in the good CCC group, and a positive correlation was observed between a high visfatin level and poorly developed CCC. A high visfatin level was an independent predictor of poor CCC in patients with CTO. (2) The 25-(OH)D3 level was significantly lower in CTO patients in the poor CCC group than in patients in the good CCC group. A low serum 25-(OH)D3 level was positively correlated with poorly developed CCC in CTO patients. It is worth noting that a low serum 25-(OH)D3 level was an independent predictor of poorly developed CCC in CTO patients. (3) An L-shaped relationship was observed between the serum 25-(OH)D3 and visfatin levels. (4) A high LDL-C level and a history of diabetes also contributed to poor CCC development in CTO patients.

Coronary collateral growth is thought to develop by the expansion of a pre-existing collateral network and the formation of new blood vessels [15,16]. Recent studies have found that the main factor affecting the development of coronary collateral vessels is the pressure gradient between segments located at the proximal and distal ends of the occlusion [17,18]. VEGF, EPCs, FGF, transforming growth factors (TGF-β), and nitric oxide (NO)-activated biological substances also play significant roles in both angiogenesis and arteriogenesis [19].

Visfatin is a known proinflammatory cytokine that plays an important role in many chronic inflammatory diseases, including atherosclerosis and cardiovascular diseases.As a cytokine, visfatin can regulate the expression of key regulators of vascular remodelling, such as vascular endothelial growth factor (VEGF) [20], fibroblast growth factor 2 (FGF-2) [21] and matrix metalloproteinases (MMPs) [22].Recent studies shows that visfatin promotes angiogenesis through a VEGF-dependent mechanism in endothelial progenitor cells (EPCs) [23].Auguet et al. found that visfatin was highly expressed in unstable carotid plaques and coronary atherosclerotic plaques of lipomacrophages[24].In addition, it has recently been reported that extracellular visfatin is directly involved in vascular remodeling[8].However,the relationship between visfatin and coronary collateral circulation is still unclear.

This study reports, for the first time, the relationship between visfatin and CCC in CTO patents. The visfatin level was significantly higher in CTO patients in the poor CCC group than in patients in the good CCC group, which may be related to the following mechanisms: (1) Visfatin induces LOX-1 expression in vascular endothelial cells, which causes inflammation, leads to endothelial cell damage and dysfunction, and promotes the vicious cycle of atherosclerosis [25]. (2) Visfatin activates ERK 1/2 and NF-κB, resulting in increased inducible nitric oxide synthase (iNOS) production [26]. iNOS is a proinflammatory enzyme that can cause an imbalance in NO production, induce endothelial dysfunction, and ultimately lead to impaired angiogenesis. Therefore, the inflammatory effect of visfatin promotes endothelial dysfunction, which may result in poor CCC development. Visfatin also has a two-way regulatory effect in metabolic diseases. Further research is needed to understand the impact of visfatin in different situations and clinical conditions related to cardiovascular disease.

Recent studies have shown that vitamin D can regulate the growth of endothelial cells and smooth muscle[27].Even vitamin D deficiency is positively correlated with the degree of coronary vascular stenosis [28]. Vitamin D is also closely related to the degree of vascular endothelial dysfunction in patients with coronary heart disease [29]. However, the relationship between vitamin D and collateral circulation and the underlying mechanism are largely unclear.

In our study, the 25-(OH)D3 level was significantly higher in the good CCC group than in the poor CCC group. This is consistent with the research results reported by Dogan Y [30]. The following points may provide a reasonable explanation for the poor CCC development caused by vitamin D deficiency: (1) vitamin D promotes the adhesion of white blood cells, increases VEGF-A expression, and promotes the growth and migration of vascular smooth muscle cells [31,32]; therefore, vitamin D deficiency can lead to impaired CCC development; (2) vitamin D activates and induces NO production, mediates the VEGF signalling pathway, and stimulates the growth of coronary collaterals [33,34], leading to poor CCC development. Cianciolo et al. [35] confirmed that VDRs are also present on circulating EPCs. Vitamin D deficiency can not only reduce the number of circulating EPCs but also decrease their ability to proliferate and form blood vessels, leading to impaired CCC development.

Our study is also the first to show an L-shaped relationship between 25(OH)D3 and visfatin. In the absence of 25(OH)D3, when the visfatin level was less than 30 nmol/L, a negative correlation was observed between 25(OH)D3 and visfatin. However, when the 25(OH)D3 level was greater than 30 nmol/L, the visfatin level did not continue to decrease with increasing 25(OH)D3; in contrast, the level remained constant. This phenomenon may suggest that supplementation with vitamin D to the normal range will not lead to further declines in endolipids in patients with vitamin D deficiency. This may also provide another possible explanation for the recent results reported by Heike et al. [36], indicating an absence of cardiovascular benefits from vitamin supplementation (it is worth noting that in the intervention and control groups, the plasma 25(OH)D3 levels at baseline and 12 months after the intervention were higher than 50 nmol/L).

Our study found that the serum LDL-C level was significantly higher in the poor CCC group than in the good CCC group. Moreover, the 25-(OH)D3 level was negatively correlated with the LDL-C level, which is similar to the results reported by Song et al. [37].

High levels of LDL-C are a definite risk factor for coronary arteries, which can induce endothelial cell dysfunction and impair the growth of coronary collateral vessels[38,39].

In our study, the frequency of diabetes was significantly higher in the poor CCC group (52.4%) than in the good CCC group (33.6%), and diabetic patients had lower vitamin D levels than nondiabetic patients. Nisanci et al. [40] also found insufficient opening of the collateral circulation in diabetic patients by measuring the coronary wedge pressure. Studies have found that due to the severely impaired function of vascular endothelial cells in diabetic patients, the abilities of these cells for proliferation, adhesion, integration and eventually angiogenesis are significantly reduced [41].

In conclusion, visfatin and vitamin D seem to play important roles in the regulation of key mechanisms involved in CCC development.

Seasonal changes in vitamin D levels and sun exposure may affect the results of the study, so we recruited patients from November to February to minimize inter-individual variability. In addition, physical exercise is also one of the factors that affect the level of vitamin D and the development of collateral circulation. Although the patients we selected indicated that they did not participate in regular physical exercise, this could not completely eliminate the impact on the results of the study. This is the shortcoming of this study.

Conclusion

Our study shows that CTO patients with poor CCC development have lower serum 25-(OH)D3 and higher serum visfatin levels than CTO patients with good CCC development. Low serum 25-(OH)D3 and high serum visfatin levels are independent predictors of poor collateral circulation in CTO patients.

 

Data Availability

The analyzed data sets generated during the study are available from the corresponding author on reasonable request. 

Ethics approval and consent to participate 

The ethics committee of China Aerospace Science and Industry Corporation 731 Hospital approved the present study, and all participants provided their written, informed consent. 

Conflicts of interest

The authors declare that there is no conflict of interest regarding the publication of this paper.

Acknowledgements

Part of the data was presented as a peer exchange, at the 29th Great Wall International Congress of Cardiology.

Funding 

This study was supported by the Science Foundation of AMHT (2018-LCYL-009) and the Medical and health research project of China aerospace science and industry corporation LTD (KYLX-56).

Authors' contributions 

X.-L. Ji wrote the manuscript. X.-L. Ji designs and performs experiments, analyzes data, interprets data. X.-L. Ji and S.-Q. Jin drafts experiments. Y.-X. Wang,Y.-M. Chen and J.-Zhang were responsible for ELISA and recorded date. All authors approved the manuscript. 

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Dear Editorial Team, Clinical Medical Reviews and Reports. My experience with the journal was highly positive. The peer-review process was rigorous, constructive, and completed in a timely manner. The reviewers provided valuable comments that helped improve the quality and clarity of our manuscript. The editorial office was professional, responsive, and supportive throughout all stages of the publication process. Communication was clear and efficient, and any questions were addressed promptly. Overall, I found the journal to maintain high scientific standards and an excellent publication workflow. I would be pleased to consider submitting future work to this journal. Best wishes from, Elena Popa.

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Dr Elena Popa

It was my pleasure to submit my testimonial concerning the Reviewer Board of our Scientific Journal “Brain and Neurological Disorders”. The Reviewers focused on some modifications and their contribution was helpful. The ladies of our Editorial Office were also supported my efforts. It was my honor to have such a co-operation and I am looking forward for more collaboration.

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Dr Nikolaos Andreas Chrysanthakopoulos

Dear Grace Pierce, Editorial Coordinator of Journal of Clinical Research and Reports, Thank you for the speedy and efficient peer review process. I appreciate the fact that your peer reviewers do not take months to respond like with some other journals. I would also like to thank the editorial office for responding quickly to my questions. It is an excellent journal. I plan to submit more manuscripts in the future. Best wishes from, Robert W. McGee

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Robert W McGee

Dear Grace Pierce, Editorial Coordinator of Journal of Clinical Research and Reports, Working with you and your team on our recent publication in JCRR has been a truly wonderful and enjoyable experience. The responses were prompt, and the reviewers were patient, constructive, and highly professional. One reviewer in particular gave me the feeling that a professor was carefully reading and commenting on my coursework, which was deeply touching. The entire process was straightforward and hassle‑free, with no tedious online forms to complete. I highly recommend this journal. Best wishes from, DR Aibing Rao, Head of R&D

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Aibing Rao

I Appreciate the Opportunity to Share my Experience with the Journal of Clinical Research and Reports. The peer review process was timely and constructive, and the feedback provided helped improve the quality of our manuscript. The editorial office was professional, responsive, and supportive throughout the process, ensuring smooth communication and efficient handling of the submission. Overall, it was a positive experience collaborating with your team.

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Kashani Mehdi

Dear Mercy Grace, Editorial Coordinator of Obstetrics Gynecology and Reproductive Sciences, We would like to express our gratitude for your help at all stages of publishing and editing the article. The editors of the magazine answer all the necessary questions and help at every stage. We will definitely continue to cooperate and publish other works in the Obstetrics Gynecology and Reproductive Sciences! Best wishes from, Alla Konstantinovna Politova,

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Alla Konstantinovna Politova