Objectives The aim of the study is to 1. observe the changes of circulating visfatin levels in patients with coronary heart disease (CHD), 2. and investigate the relationship between visfatin levels and the severity of CHD and coronary artery stenosis.
Methods Participants and study design a total of 102 subjects were recruited from the first afflicted hospital of the university of South China, who underwent the coronary angiography (CAG) during 2010 to 2012.
Based on CAG, the subjects were divided into following groups: non-CHD of 35 cases and CHD group of 67 cases. According to clinical presentation, ECG and the serological markers, CHD group was further classified into 2 subgroups: 28 cases of stable angina pectoris (SAP) group and 39 cases of acute myocardial infarction (AMI) group.
According to the coronary artery lesion, all subjects can be divided into 4 groups: non-CHD group (35 cases), CHD single-vessel lesion group (26 cases), CHD double-vessel lesions group (20 cases), and CHD triple-vessel lesions group (21 cases). The quantitative assessment of the severity of coronary artery lesion was made in line with Gensini scores. The severity of coronary artery stenosis was assessed by the number of coronary artery lesion and the sum of the Gensini scores.
According to the median level of visfatin (M = 0.27 ng/mL), subjects can be divided into 2 groups: visfatin of A group is <0.27 ng/mL, visfatin of B group is ≥ 0.27 ng/mL.
Assessments of plasma visfatin and serological index.The visfatin levels were determined by ELISA. HT, WT, BP, BMI were mesured. The levels of CK, CK-MB, cTnT, ESR, hs-CRP, TG, TC, LDL-C, HDL-C, and FPG were also detected.
Statistical analysis Gensini score was calculated and the correlation between visfatin, serological markers and severity of coronary artery disease were analysed. The SPSS18.0 software was used for data analysis.
There was statistically difference in visfatin levels between CHD group and non-CHD group [(0.41 ± 0.28) ng/ml vs. (0.20 ± 0.21) ng/ml (P < 0.05)].
The visfatin levels in AMI group were higher compared with SAP group [(0.47 ± 0.25) ng/mL vs. (0.33 ± 0.30) ng/mL, (P < 0.05)] and non-CHD group [(0.47 ± 0.25) ng/mL vs. (0.20 ± 0.21) ng/mL, (P < 0.05)]; the visfatin levels in SAP were higher than non-CHD group[(0.33 ± 0.30) ng/ml vs. (0.20 ± 0.21) ng/ml, (P < 0.05)].
The risk rate of suffering from AMI for patients with visfatin ≥ 0.27 ng/mL is 6.83 times as much as that for patients with visfatin < 0.27 ng/mL.
The visfatin levels in CHD triple-vessel lesions group were higher than non-CHD group [(0.46 ± 0.30) vs.(0.20 ± 0.21) ng/ml, (P < 0.05)] and CHD single-vessel lesion group [(0.46 ± 0.30) vs. (0.30 ± 0.22) ng/ml, (P < 0.05)]; the visfatin levels were higher in double-vessel lesions group than non-CHD group [(0.43 ± 0.29) vs. (0.20 ± 0.21) ng/ml, (P <0.05)].
The visfatin levels were positively correlated with TG (r = 0.391, P < 0.05), TC(r = 0.386, P < 0.05), hs-CRP (r = 0.611, P < 0.05), the number of coronary artery lesion (r = 0.417, P < 0.05) and the Gensini scores (r = 0.482, P < 0.05); negatively correlated with HDL-C (r = -0.404, P < 0.05). Multiple stepwise regression analysis revealed hs-CRP and Gensini scores may be independent factors of visfatin (F = 15.905, P < 0.01).
The visfatin levels are closely related with CHD.
The visfatin levels may predict the severity of CHD.
The visfatin levels exist positive correlation with the risk of AMI event occurence.
hs-CRP and Gensini scores may be independent factors of visfatin.