title: Monocyte subset distribution in patients with stable atherosclerosis and elevated levels of lipoprotein(a).
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.
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria.
authors.forename: Konstantin A
authors.initials: KA
authors.lastname: Krychtiuk
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
authors.forename: Stefan P
authors.initials: SP
authors.lastname: Kastl
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
authors.forename: Sebastian L
authors.initials: SL
authors.lastname: Hofbauer
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
authors.forename: Anna
authors.initials: A
authors.lastname: Wonnerth
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
authors.forename: Georg
authors.initials: G
authors.lastname: Goliasch
authors.affiliation: Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
authors.forename: Maria
authors.initials: M
authors.lastname: Ozsvar-Kozma
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
authors.forename: Katharina M
authors.initials: KM
authors.lastname: Katsaros
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
authors.forename: Gerald
authors.initials: G
authors.lastname: Maurer
authors.affiliation: Ludwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria; 3rd Medical Department, Wilhelminenhospital, Vienna, Austria.
authors.forename: Kurt
authors.initials: K
authors.lastname: Huber
authors.affiliation: Krankenanstalten Dr. Dostal, Vienna, Austria.
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Dostal
authors.affiliation: Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
authors.forename: Christoph J
authors.initials: CJ
authors.lastname: Binder
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
authors.forename: Stefan
authors.initials: S
authors.lastname: Pfaffenberger
authors.affiliation: Krankenanstalten Dr. Dostal, Vienna, Austria; 2nd Department of Internal Medicine, Faculty of Medicine, Comenius University, Bratislava, Slovakia.
authors.forename: Stanislav
authors.initials: S
authors.lastname: Oravec
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria; Core Facilities, Medical University of Vienna, Vienna, Austria.
authors.forename: Johann
authors.initials: J
authors.lastname: Wojta
authors.affiliation: Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria. Electronic address: walter.speidl@meduniwien.ac.at.
authors.forename: Walter S
authors.initials: WS
authors.lastname: Speidl
mesh_terms: D000368:Aged; D053299:Apolipoprotein B-100 / Q000097:blood; D050197:Atherosclerosis / Q000097:blood* / Q000473:pathology; D019070:Cell Lineage; D003324:Coronary Artery Disease / Q000097:blood* / Q000473:pathology; D005260:Female; D058851:GPI-Linked Proteins / Q000097:blood; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000097:blood; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism* / Q000473:pathology; D010084:Oxidation-Reduction; D010743:Phospholipids / Q000097:blood; D017452:Receptors, IgG / Q000097:blood; D012307:Risk Factors
chemical_list: D053299:Apolipoprotein B-100; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D017270:Lipoprotein(a); D010743:Phospholipids; D017452:Receptors, IgG
keywords: Atherosclerosis; Coronary artery disease; Lipoprotein(a); Monocyte subsets; Oxidized phospholipids