title: Treatment with beta-blockers is associated with lower levels of Lp-PLA2 and suPAR in carotid plaques.
abstract: OBJECTIVE
  To determine whether a long-term treatment with beta-blockers influences the inflammatory activity in carotid artery disease by reducing the carotid plaque levels of lipoprotein-associated phospholipase A2 (Lp-PLA2), its enzymatic products lysophosphatidylcholine (lysoPCs), and of soluble urokinase plasminogen activator receptor (suPAR).
  
  
  METHODS
  One hundred and thirty-four patients with significant symptomatic or asymptomatic carotid stenosis undergoing surgery were prospectively included and divided into two groups (Group A or B) based on the absence or presence of an on-going long-term oral treatment with beta-blockers. The harvested carotid plaques were analyzed for the levels of lysoPCs using mass spectrometry and Lp-PLA2 and suPAR by Enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  Plaques of patients on long-term treatment with beta-blockers revealed lower levels of Lp-PLA2 (Group A 0.752 ± 0.393 ug/g vs. Group B 0.644 ± 0.445 ug/g, P=.049) as well as suPAR (Group A 0.044 ± 0.024 μg/g vs. Group B 0.036 ± 0.025 μg/g, P=.028). Levels of Lp-PLA2 and suPAR were positively correlated (r=.637, P<.0001). Lp-PLA2 and suPAR levels were also correlated (P<.0001) with the three lysoPC species tested (lysoPC 16:0, lysoPC 18:0. lysoPC 18:1). All the above-mentioned findings were confirmed after correction for age, gender, hypertension, coronary artery disease, and statin usage.
  
  
  CONCLUSIONS
  The reduced levels of Lp-PLA2 and suPAR in human carotid plaques of subjects on long-term treatment with beta-blockers suggest their possible protective role in plaque inflammation. Our findings support an even more selective Lp-PLA2 and suPAR inhibition as a possible strategy for the prevention of cardiovascular disease.
authors.affiliation: Vascular Center Malmö-Lund, Skåne University Hospital, Malmö, Sweden. Electronic address: giuseppe.asciutto@med.lu.se.
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Asciutto
authors.forename: Andreas
authors.initials: A
authors.lastname: Edsfeldt
authors.forename: Nuno V
authors.initials: NV
authors.lastname: Dias
authors.forename: Jan
authors.initials: J
authors.lastname: Nilsson
authors.forename: Cornelia
authors.initials: C
authors.lastname: Prehn
authors.forename: Jerzy
authors.initials: J
authors.lastname: Adamski
authors.forename: Isabel
authors.initials: I
authors.lastname: Gonçalves
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000284:Administration, Oral; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage*; D000368:Aged; D002339:Carotid Arteries / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology / Q000601:surgery; D016893:Carotid Stenosis / Q000201:enzymology* / Q000473:pathology / Q000601:surgery; D015536:Down-Regulation; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008244:Lysophosphatidylcholines / Q000032:analysis; D008297:Male; D013058:Mass Spectrometry; D008875:Middle Aged; D054467:Phospholipases A2 / Q000032:analysis*; D058226:Plaque, Atherosclerotic; D011446:Prospective Studies; D055293:Receptors, Urokinase Plasminogen Activator / Q000032:analysis*; D013997:Time Factors
chemical_list: D000319:Adrenergic beta-Antagonists; D008244:Lysophosphatidylcholines; C524898:PLAUR protein, human; D055293:Receptors, Urokinase Plasminogen Activator; D054467:Phospholipases A2; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; C526684:PLA2G7 protein, human
keywords: Beta-blockers; Carotid artery stenosis; Inflammation; Lp-PLA2; Treatment/Therapies; lysoPC; suPAR