title: Reconstituted HDL in acute coronary syndromes.
abstract: OBJECTIVE
  The strong inverse relationship between plasma high-density lipoprotein (HDL)-cholesterol and atherosclerotic cardiovascular disease provides the epidemiological basis that HDL is atheroprotective. Since HDL enhances cholesterol efflux and exhibits potent antiinflammatory properties, the aim of the present study was to investigate whether infusion of reconstituted HDL (rHDL) impacts on vascular function, a well-established surrogate of atherosclerotic vascular disease, as well as markers of inflammation and oxidative stress in patients with acute coronary syndromes (ACS).
  
  
  METHODS
  Twenty-nine patients with ACS were randomized to double-blind treatment with rHDL or albumin. Endothelium-dependent and independent vasodilatation to intraarterial acetylcholine and sodium nitroprusside were measured by forearm venous occlusion plethysmography. In addition, oxidized LDL and high-sensitivity C-reactive protein were determined as markers of oxidative stress and vascular inflammation.
  
  
  RESULTS
  rHDL infusion increased plasma HDL (P < 0.0001) and decreased LDL (P < 0.0001). Oxidized LDL (P= 0.11), high-sensitivity C-reactive protein (P= 0.12) and the response to endothelium-dependent and -independent vasodilatators remained unchanged after rHDL compared to albumin infusion (14.9 ± 9.2 versus 14.5 ± 12.4, P= 0.93 and 12.8 ± 7.1 versus 13.2 ± 9.6, P= 0.27, respectively).
  
  
  CONCLUSIONS
  An increase of HDL and a reduction of LDL notwithstanding, human rHDL did not improve vascular function in patients with ACS thus further challenging the clinical benefit of interventions, which rapidly raise HDL in ACS, particularly with the infusion of reconstituted HDL.
authors.affiliation: Cardiovascular Center, Cardiology, University Hospital, Zurich, Switzerland.
authors.forename: Rémy
authors.initials: R
authors.lastname: Chenevard
authors.forename: David
authors.initials: D
authors.lastname: Hürlimann
authors.forename: Lukas
authors.initials: L
authors.lastname: Spieker
authors.forename: Markus
authors.initials: M
authors.lastname: Béchir
authors.forename: Frank
authors.initials: F
authors.lastname: Enseleit
authors.forename: Matthias
authors.initials: M
authors.lastname: Hermann
authors.forename: Andreas J
authors.initials: AJ
authors.lastname: Flammer
authors.forename: Isabella
authors.initials: I
authors.lastname: Sudano
authors.forename: Roberto
authors.initials: R
authors.lastname: Corti
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Lüscher
authors.forename: Georg
authors.initials: G
authors.lastname: Noll
authors.forename: Frank
authors.initials: F
authors.lastname: Ruschitzka
mesh_terms: D000109:Acetylcholine; D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000503:physiopathology; D000368:Aged; D015415:Biomarkers; D004311:Double-Blind Method; D004562:Electrocardiography; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D004791:Enzyme Inhibitors; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D008075:Lipoproteins, HDL / Q000009:adverse effects / Q000097:blood / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside; D018384:Oxidative Stress / Q000502:physiology; D010991:Plethysmography; D014657:Vasculitis / Q000175:diagnosis; D014665:Vasodilator Agents; D019323:omega-N-Methylarginine
chemical_list: D015415:Biomarkers; D004791:Enzyme Inhibitors; D005343:Fibrinolytic Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D008075:Lipoproteins, HDL; D014665:Vasodilator Agents; D009599:Nitroprusside; D019323:omega-N-Methylarginine; D000109:Acetylcholine