Search

Sparse data assessed the association of apolipoprotein A1 (ApoA1) and high density lipoprotein cholesterol (HDL-C) with inflammation. We investigated this association in a hospital-based cross-sectional pilot study that included 7296 patients with coronary artery disease (CAD). In multivariate analysis, negative associations of ApoA1 and HDL-C with C-reactive protein (CRP), high sensitivity CRP (hsCRP), and tumor necrosis factor-α (TNF-α) were shown. The corresponding CRP, hsCRP, and TNF-α values were 5.28 (vs 11.70 mg/L), 4.50 (vs 11.50 mg/L), and 7.68 (vs 10.90 pg/mL) for ApoA1, and 7.13 (vs 10.60 mg/L), 6.27 (vs 9.19 mg/L), and 8.11 (vs 11.86 pg/mL) for HDL-C in the fourth quartiles compared with the first quartiles. ApoA1/HDL-C ratio was inversely associated with hsCRP and interleukin-6 (IL-6). No significant associations of ApoA1 and HDL-C with IL-6 and IL-8, and of ApoA1/HDL-C ratio with CRP, IL-8, and TNF-α were observed. In path analyses, there was no evidence of mediating effects of body mass index on the "ApoA1 and HDL-C-inflammation" relationship. Generally, our study of CAD patients identified graded and inverse associations of ApoA1, HDL-C, and ApoA1/HDL-C ratio with inflammatory marker (CRP, hsCRP, IL-6, IL-8, or TNF-α) levels. [ABSTRACT FROM AUTHOR]

This study determined the associations of apolipoprotein A1 (ApoA1), high-density lipoprotein cholesterol (HDL-C), and HDL-C/ApoA1 ratio with fasting blood glucose (FBG) and evaluated the mediating effects of high-sensitivity C-reactive protein (hsCRP) and body mass index (BMI). A cross-sectional study with 4805 coronary artery disease (CAD) patients was performed. In multivariable analyses, higher ApoA1, HDL-C, and HDL-C/ApoA1 ratio were associated with significantly lower FBG level (Q [quartile] 4 vs Q1: 5.67 vs 5.87 mmol/L for ApoA1; 5.64 vs 5.98 mmol/L for HDL-C; 5.63 vs 6.01 mmol/L for HDL-C/ApoA1 ratio). Moreover, inverse associations of ApoA1, HDL-C, and HDL-C/ApoA1 ratio with abnormal FBG (AFBG) were found with odd ratios (95% confidence interval) of .83 (.70–.98), .60 (.50–.71), and .53 (.45–.64) in Q4 compared with Q1. Path analyses indicated that “ApoA1 (or HDL-C)-FBG” associations were mediated by hsCRP and “HDL-C-FBG” association was mediated by BMI. Our data suggested that higher ApoA1, HDL-C, and HDL-C/ApoA1 ratio were favorably associated with a lower FBG level in CAD patients and these associations might be mediated by hsCRP or BMI. Collectively, higher concentrations of ApoA1, HDL-C, and HDL-C/ApoA1 ratio might decrease the risk of AFBG. [ABSTRACT FROM AUTHOR]