Expression of Monocytes Subsets in Patients Diagnosed With Coronary Artery Atherosclerosis and Their Impact on Disease Severity

Introduction Many studies have supported inflammation as a mediator of lipoprotein (a) (Lp(a)) induced increase in cardiovascular disease risk, as it has pro-inflammatory effects on endothelial cells and monocytes. Aim This study aims to correlate Lp(a) level with different monocyte subsets in coronary atherosclerotic patients with different severity. Method The study included 60 patients with a mean age of 53.1 ± 10.5 diagnosed as coronary atherosclerotic patients by coronary angiography. Lp levels were measured using enzyme-linked immunosorbent assay (ELISA), while blood counts and monocyte subsets were analyzed by flow cytometry, and 30 apparently healthy individuals were included as the control group. Results Patients showed significantly higher median monocytic %, Lp(a), and higher C-reactive protein (CRP) values than the control group. Patients were subdivided into two groups: normal Lp(a) < 6.2 mg/dL (n = 24) and hyperlipoproteinemia(a) (hyper Lp(a)) ≥ 6.2 mg/dL (n = 36). Patients with hyper Lp(a) had higher non-classical monocytes (31.5% vs. 20%). Coronary atherosclerosis severity was associated with higher Lp(a) levels as well as non-classical monocytes; patients with mild atherosclerosis showed the highest classical and intermediate subset levels. While for a non-classical subset, patients with severe atherosclerosis showed the highest median level. A significant moderate positive correlation between Lp(a) and monocyte counts, as well as monocyte-lymphocyte (M/L) index and non-classical monocytes, was found. Conclusions Hyper Lp(a) and increased count of non-classical monocytes are significantly increased with disease progression (triple-vessel coronary disease risk). These results suggest that the expansion of non-classical monocytes is a cardiovascular disease (CVD) risk and predictor for disease severity. Strategies targeting inflammatory monocytes may slow CVD progression.