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The aim of this study was to determine the levels of high-density lipoprotein 2 (HDL2), high-density lipoprotein 3 (HDL3), and monocyte chemoattractant protein (MCP-1) and their associations. We subsequently assessed the role of HDL particles and inflammatory factors in premature coronary artery disease (CAD) patients.
Based on an age threshold of 55 years for males and 65 years for females, 235 CAD patients diagnosed via coronary angiography were randomly assigned to the premature CAD group (n=107) and late-onset CAD group (n=128). Ninety-six healthy individuals with no history of CAD were selected as the control group. According to chest pain, ST segment changes, and cardiac marker levels of cardiac troponin T (cTnT), cardiac troponin I (cTnI) and creatine kinase-myocardial band (CK-MB), the premature CAD group was divided into 3 subgroups, which included the acute myocardial infarction group, unstable angina group, and stable angina group. The plasma HDL2 and HDL3 levels were determined via polyethylene glycol 20000 precipitation, whereas the MCP-1 level was determined via enzyme-linked immunosorbent assay (ELISA). Multiple linear regression was performed to analyze the associations between MCP-1 and HDL-C, HDL2, and HDL3. Logistic regression was used to assess the impact of clinical factors on premature CAD.
The HDL-C level (1.12±0.34 mmol/L) in the premature CAD group was significantly less and the MCP-1 level (median: 43pg/mL) was significantly greater than those of the late-onset CAD group (HDL-C, 1.20 mmol/L; MCP-1, 39 pg/mL) and the healthy control group (HDL-C, 1.36±0.41 mmol/L; MCP-1, 35.64 pg/mL) (p=<0.006; p < 0.0015). The findings via Logistic regression indicated that HDL2 may have a positive impact on premature CAD (OR: 0.051, 95%CI: 0.009-0.287, p=0.001) after adjustment for gender and age. Furthermore, the multiple linear regression results indicated that MCP-1 was negatively correlated with HDL2 (β=-0.609, p=0.024), whereas it was not correlated with HDL3 (β=-0.274, p=0.315) or HDL-C (β=-0.103, p=0.628) in the premature CAD group. Furthermore, MCP-1 was not associated with HDL-C (β=0.069, p=0.840), HDL2 (β=-0.146, p=0.134) or HDL3 (β=-0.096, p=0.608) in the stable angina subgroup.
The large-particle HDL2 level was decreased and the HDL maturation was arrested in premature CAD patients. HDL2 may be a more sensitive indicator of CAD. The MCP-1 level in premature CAD patients was increased, and the anti-inflammatory function of HDL may have been suppressed. The interaction between the inflammatory response and HDL2 may be a pivotal mechanism of premature CAD.