Background The pathological basis of coronary artery disease (CAD) is atherosclerosis which is associated with inflammation and dyslipidemia. However, the involvement of hypersensitive C-reactive protein (hs-CRP) in lipid metabolism and how it affects the pathogenesis of CAD is uncertain. Objective To explore whether the relationship between dyslipidemia and CAD is partly mediated by hs-CRP levels. Methods Three hundred fifteen pairs of randomly sexand age-matched CAD and non-CAD subjects collected from Zhongda Hospital Affiliated to Southeast University were involved in the final analysis. We gathered information about each subjects clinical history as well as their results of detected hs-CRP and lipid levels. Linear regression analysis was used to determine the association between dyslipidemia and hs-CRP levels in which univariate and multivariate logistic regression analyzes were performed to determine the relationship between hs-CRP levels and CAD as well as dyslipidemia and CAD. Mediation analysis was used to evaluate whether hs-CRP levels act as a mediator of the relationship between dyslipidemia and CAD. Results Dyslipidemia and hs-CRP levels were significantly associated with an increased risk of CAD, with β = 0.594 (P = 0.001) and β = 0.016 (P = 0.024), respectively, and there was a correlation between dyslipidemia and hs-CRP levels (β = 3.273, P = 0.004). Mediation analysis results revealed that the correlation between dyslipidemia and CAD was 8.27% mediated by hs-CRP levels with a direct effect of 0.621 and an indirect effect of 0.056. Conclusion Hs-CRP levels played a partial mediation role in the association between dyslipidemia and CAD.
Objective: The mechanism between smoking and coronary artery disease (CAD) remains unclear. It is likely that lipid (including triglycerides (TG), total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C)) have been functioning as one of the mediators between smoking and the CAD occurrence. The study aimed to investigate the mediating effect of lipid on the relationship between smoking and CAD risk. Methods: The case-control study included 2048 subjects. General linear regression analysis was used to corroborate the association between smoking and lipid levels. Univariate and multivariate logistic regression analysis were performed to reveal the relationship between smoking, lipid and the risk of CAD. Mediation analysis was used to investigate whether the association between smoking and CAD risk was mediated by lipid. Results: Smoking was found to be associated with the risk of CAD (odds ratio (OR) = 1.34, 95% confidence interval (CI): 1.05-1.71, P = 0.019). Regression analysis showed that TG, TC and HDL-C were associated with CAD (OR = 2.69, 95%CI: 2.12-3.40, P < 0.001; OR = 0.34, 95%CI: 0.29-0.43, P < 0.001; OR = 0.37, 95%CI: 0.30-0.47, P < 0.001). Moreover, the ratio of TG to HDL-C (TG/HDL-C) was also related to CAD (OR = 4.45, 95%CI: 3.52-5.64, P < 0.001). Mediation analysis showed that among the effects of smoking on CAD, 17.52% was mediated by lipid, in which HDL-C accounted for 11.16% and TG accounted for 6.36%. Further analysis showed that the effect was also partially mediated by TG/HDL-C, which was accounted for 28%. Conclusions: Lipid plays a partial mediation on the association between smoking and CAD risk. The study provides a clue on the mediation effect of lipids on the relationship between smoking and CAD risks, which is a novel insight to the progression of CAD.
Objective: In this study, Mendelian randomization method was used to determine whether there was a causal association between inflammatory cytokine IL-18 and cardiovascular disease risk. Methods: We performed a meta-analysis to evaluate the association between IL-18-137G/C and -607C/A polymorphisms and phenotype of IL-18 levels, and also the risks of CVD. All the literatures were searched before September 30, 2019. The logistic regression and linear regression were used to evaluate between IL-18 level and the risk of CVDs. Result: Twelve eligible articles of the association between IL-18-137G/C and CVD risks and 8 eligible literatures related to IL-18-607C/A and CVD risks; 2 qualified literatures of the association between IL-18 SNPs and IL-18 levels and 4 eligible literatures related to IL-18 levels and CVD risks. Data of 4 literatures on the correlation between IL-18 level and CVD were summarized. Compared with patients with CVD, the mean of IL-18 level in the normal group was significantly decreased by 50.844 pg/ml (P < 0.05). But the association between IL-18-137G/C, IL-18-607C/A and CVD were not significant (P > 0.05), and the association between IL-18-607C/A and IL-18 level was also not significant (P > 0.05), Mendelian randomization study was failed to prove the association between IL-18 level and CVD risk. Conclusion: This study does not support a causal association between IL-18 level and the risks of CVD.
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