Association of plasma apolipoprotein CIII, high sensitivity C-reactive protein and tumor necrosis factor-α contributes to the clinical features of coronary heart disease in Li and Han ethnic groups in China

Abstract

BackgroundApolipoprotein CIII (apoCIII) is an independent risk for coronary heart disease (CHD). In this study, we investigated the associations among plasma apoCIII, hs-CRP and TNF-α levels and their roles in the clinical features of CHD in the Li and Han ethnic groups in China.MethodsA cohort of 474 participants was recruited (238 atherosclerotic patients and 236 healthy controls) from the Li and Han ethnic groups. Blood samples were obtained to evaluate apoCIII, TNF-α, hs-CRP and lipid profiles. Chi-squared, t-tests, and Kruskal–Wallis or Wilcoxon–Mann–Whitney tests, Pearson or Spearman correlation tests and multiple unconditional logistic regression were employed to analyze lipid profiles and variations in plasma apoCIII, TNF-α, hs-CRP in subgroups of CHD and their contributions to CHD using SPSS version 20.0 software.ResultsCompared to healthy participants, unfavorable lipid profiles were identified in CHD patients with enhanced systolic pressure, diastolic pressure, fasting blood sugar (FBS), TG, TC, LDL-C, apoB, Lp(a) (P < 0.05, TC and Lp(a); P < 0.01, FBS, TG, LDL-C, apoB); and lower HDL-C and apoAI (P < 0.05). Plasma apoCIII, TNF-α and hs-CRP levels were higher in CHD individuals (16.77 ± 5.98 mg/dL vs. 10.91 ± 4.97 mg/dL; 17.23 ± 6.34 pg/mL vs. 9.49 ± 3.88 pg/mL; 9.55 ± 7.32 mg/L vs. 2.14 ± 1.56 mg/L; P < 0.01 vs. healthy participants). Identical patterns were obtained in the Li and Han groups (16.46 ± 6.08 mg/dL vs. 11.72 ± 5.16 mg/dL; 15.71 ± 5.52 pg/mL vs. 9.74 ± 4.31 pg/mL; 8.21 ± 7.09 mg/L vs. 2.15 ± 1.51 mg/L in Li people; 17.05 ± 5.90 mg/dL vs. 10.07 ± 4.63 mg/dL; 18.59 ± 6.73 pg/mL vs. 9.23 ± 3.38 pg/mL; 10.75 ± 7.44 mg/L vs. 2.12 ± 1.63 mg/L in Han people; P < 0.01). Paired comparisons of subgroups with stable angina, unstable angina, and acute myocardial infarction (AMI) revealed significant variation in plasma levels of apoCIII, TNF-α and hs-CRP (P < 0.01), but not among subgroups with mild, moderate and severe stenosis (P > 0.05). Plasma apoCIII, TNF-α and hs-CRP contributed to the development of CHD (OR = 2.554, 7.252, 6.035, P < 0.01) with paired correlations in CHD patients (apoCIII vs. TNF-α, r = 0.425; apoCIII vs. hs-CRP, r = 0.319; TNF-α vs. hs-CRP, r = 0.400, P < 0.01).ConclusionsAssociation among plasma apoCIII, hs-CRP and TNF-α interacts with unfavorable lipid profiles to contribute to the clinical features of CHD with stable angina, unstable angina, and AMI in the Li and Han ethnic groups in China.

Toll‐Like Receptors/TNF‐α Pathway Crosstalk and Impact on Different Sites of Recurrent Myocardial Infarction in Elderly Patients

“…Tumor necrosis factor- α (TNF- α ) was mainly produced by monocytes and macrophages. TNF- α was a pleiotropic inflammatory cytokine that promoted the proinflammatory response in coronary atherosclerosis and was also risk factor for coronary artery disease, and circulating TNF- α levels were related to increased risks of stable angina pectoris, unstable angina, and recurrent myocardial infarction [ 9 – 11 ]. TNF- α elicited inflammatory response via two receptors termed soluble TNF- α receptor-1 and 2 (sTNFR-1 and sTNFR-2).…”

Predictive Value of the HEART Score Combined with Hypersensitive C-Reactive Protein for 30 d Adverse Cardiovascular Events in Patients with Acute Chest Pain

“…Under normal circumstances, the concentration of hs-CRP in plasma was in a stable state for a long period. After tissue damage in patients, hs-CRP concentration could rise rapidly and be detected in blood within 6–8 h and reached the peak at 24–48 h. [ 25 ]. Caselli C et al concluded that hs-CRP, as a marker of inflammation, is able to monitor the severity of disease and has high predictive accuracy for the development of coronary artery disease in patients with chronic chest pain [ 26 ].…”

Trace Element, Immune and Opioid Biomarkers of Unstable Angina, Increased Atherogenicity and Insulin Resistance: Results of Machine Learning

“…Hyperglycemia, hyperinsulinemia and IR can all cause disorders in lipid metabolism, oxidative stress toxicity and vascular endothelial damage, ultimately leading to the aggravation of coronary ATS [97]. As such, hyperlipidemia may contribute to the development of UA [98] while interactions between immune-inflammatory and atherogenic pathways may further contribute to UA [99]. However, in our study, IL-6 was not significantly increased in UA vs. ATS without UA, although our results agree with previous data, which reported that IL-6 (and TNF-α and CRP) levels are higher in UA patients than in healthy controls [100,101].…”