title: [Decrease ApoB/ApoA-1 ratio and cardiovascular risk improvement: a tadalafil pleiotropic effect? Preliminary study on healthy volunteers].
abstract: OBJECTIVE
  Recognition of erectile dysfunction (ED) as an early sign of systemic cardiovascular disease offers an opportunity for prevention. Cardiac risk assessment may deserve measurement of Apolipoprotein B/Apolipoprotein A-1 ratio. An elevated ApoB/ApoA-1 ratio is a risk factor for future coronary artery disease. ApoA-1 production, which is recognized as a cardioprotective lipid fraction, is down regulated by NFkappaB activation in vitro. Because inhibition of phosphodiesterases (PDEs) 5, 6 and 9 negatively attenuates NFkappaB translocation/activation, tadalafil, a selective PDE 5 inhibitor used for treatment of ED could present some interesting pleiotropic effects. The objective of this open study is to test the hypothesis that tadalafil treatment could decrease serum ApoB/ApoA-1 ratio.
  
  
  METHODS
  Ten healthy men without any complain of ED or known cardiovascular risk factors were administered tadalafil 10mg intake on alternate days for 4 weeks. Lipid profile with total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, ApoA-1 and ApoB, was assessed at baseline (T0), after 2weeks (T1), at the end of the treatment period (T2) and after 2weeks of wash-out follow-up (T3).
  
  
  RESULTS
  ApoB/ApoA-1 ratio was significantly decreased during treatment (mean+/-SEM, T0: 0.80+/-0.11, T1: 0.64+/-0.06, T2: 0.65+/-0.06; p<0.05) and remained lower after wash-out (T3: 0.67+/-0.05; p=0.08). Serum ApoA-1 (mg/dl) increased but not significantly during the treatment period (15.2+/-8.8, 16.5+/-7.9, 16.9+/-6, 15.3+/-7, p=0.26) and ApoB (mg/dl) significantly decreased (11.7+/-10.8, 10.3+/-8.4, 10.6+/-9.9, 10.2+/-8.6, p=0.03). HDL and LDL cholesterol were unchanged.
  
  
  CONCLUSIONS
  This preliminary study showed the interest of PDE 5 inhibitors to decrease the cardiac risk factor ApoB/ApoA-1 ratio. Randomised controlled studies with longer follow-up are needed to confirm those results.
authors.affiliation: Laboratoire de médecine expérimentale, unité 222, CHU Charleroi, université Libre de Bruxelles, Montigny-le-Tilleul, Belgique. thierry.roumeguere@ulb.ac.be
authors.forename: T
authors.initials: T
authors.lastname: Roumeguère
authors.forename: K
authors.initials: K
authors.lastname: Zouaoui Boudjeltia
authors.forename: C
authors.initials: C
authors.lastname: Hauzeur
authors.forename: A
authors.initials: A
authors.lastname: Ramal
authors.forename: C
authors.initials: C
authors.lastname: Schulman
authors.forename: M
authors.initials: M
authors.lastname: Vanhaeverbeek
authors.forename: J
authors.initials: J
authors.lastname: Ducobu
authors.forename: E
authors.initials: E
authors.lastname: Wespes
mesh_terms: D000328:Adult; D016632:Apolipoprotein A-I / Q000097:blood*; D001055:Apolipoproteins B / Q000097:blood*; D002243:Carbolines / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000097:blood* / Q000517:prevention & control*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use*; D012307:Risk Factors; D000068581:Tadalafil
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D002243:Carbolines; D010726:Phosphodiesterase Inhibitors; D000068581:Tadalafil