Inflammation
Elevated Lp(a) shifts monocytes toward a more inflammatory subset, a study of 90 patients with stable coronary disease (J Clin Lipidol 2015)
Original title: Monocyte subset distribution in patients with stable atherosclerosis and elevated levels of lipoprotein(a)
This study examined whether elevated Lp(a) and oxidized phospholipids on apoB-100 (OxPL/apoB) relate to monocyte subset distribution in 90 patients with stable coronary artery disease, using flow cytometry to identify classical, intermediate, and nonclassical monocytes. Patients with Lp(a) above 50 mg/dL had a higher proportion of intermediate monocytes (7.0% vs 5.2%, P=.026), while classical (82.6% vs 82.0%, P=.73) and nonclassical monocytes (10.5 vs 12.8, P=.10) did not differ significantly, an association independent of clinical risk factors, statin treatment, and inflammatory markers. OxPL/apoB was also higher in patients with elevated Lp(a) and correlated with intermediate monocytes but not classical or nonclassical subsets. The findings provide a potential link between elevated Lp(a) and a proatherogenic shift in monocyte subset distribution in stable atherosclerotic disease.
Original abstract
Background: Lipoprotein(a) (Lp(a)) is a proatherogenic plasma lipoprotein currently established as an independent risk factor for the development of atherosclerotic disease and as a predictor for acute thrombotic complications. In addition, Lp(a) is the major carrier of proinflammatory oxidized phospholipids (OxPL). Today, atherosclerosis is considered to be an inflammatory disease of the vessel wall in which monocytes and monocyte-derived macrophages are crucially involved. Circulating monocytes can be divided according to their surface expression pattern of CD14 and CD16 into at least 3 subsets with distinct inflammatory and atherogenic potential.
Objective: The aim of this study was to examine whether elevated levels of Lp(a) and OxPL on apolipoprotein B-100-containing lipoproteins (OxPL/apoB) are associated with changes in monocyte subset distribution.
Methods: We included 90 patients with stable coronary artery disease. Lp(a) and OxPL/apoB were measured, and monocyte subsets were identified as classical monocytes (CMs; CD14++CD16-), intermediate monocytes (IMs; CD14++CD16+), and nonclassical monocytes (NCMs; CD14+CD16++) by flow cytometry.
Results: In patients with elevated levels of Lp(a) (>50 mg/dL), monocyte subset distribution was skewed toward an increase in the proportion of IM (7.0 ± 3.8% vs 5.2 ± 3.0%; P = .026), whereas CM (82.6 ± 6.5% vs 82.0 ± 6.8%; P = .73) and NCM (10.5 ± 5.3 vs 12.8 ± 6.0; P = .10) were not significantly different. This association was independent of clinical risk factors, choice of statin treatment regime, and inflammatory markers. In addition, OxPL/apoB was higher in patients with elevated Lp(a) and correlated with IM but not CM and NCM.
Conclusions: In conclusion, we provide a potential link between elevated levels of Lp(a) and a proatherogenic distribution of monocyte subtypes in patients with stable atherosclerotic disease.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.