Abstract
BackgroundLipoprotein(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.ObjectiveThe 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.MethodsWe 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.ResultsIn 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.ConclusionsIn 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.
Highlights
Despite major advances in vascular medicine including high-dose statin treatment, cardiovascular diseases remain the leading cause of death in the Western world.[1]
Lipoprotein(a) (Lp(a)) is a plasma lipoprotein that consists of a cholesterol-rich, low-density lipoprotein (LDL)-like particle and an additional protein apolipoprotein(a), which is covalently bound to the ApoB of the LDL-like particle.[2,3]
Accumulating evidence suggested a further division of CD16-positive cells into 2 subtypes of cells, which was officially acknowledged in a consensus article under the auspices of the Nomenclature Committee of the International Union of Immunological Societies proposing the following classification: CD1411CD162, CD1411CD161, and CD141CD1611.13
Summary
Despite major advances in vascular medicine including high-dose statin treatment, cardiovascular diseases remain the leading cause of death in the Western world.[1] Lipoprotein(a) (Lp(a)) is a plasma lipoprotein that consists of a cholesterol-rich, low-density lipoprotein (LDL)-like particle and an additional protein apolipoprotein(a), which is covalently bound to the ApoB of the LDL-like particle.[2,3] Today it is established as an independent risk factor for the development of stable ischemic disease and myocardial infarction.[2,3,4] Genetic studies suggest causality; mechanistic insights are scarce.[5,6] The European Atherosclerosis Society suggests to measure Lp(a) in all intermediate or high-risk patients and advises a desirable level of less than 50 mg/dL (,80th percentile).[2]. 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
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