title: Cardiovascular risk factors determine erectile and arterial function response to sildenafil.
abstract: BACKGROUND
  Erectile dysfunction is related to endothelial function. Cardiovascular risk factors determine endothelial function. Sildenafil is effective in treatment of erectile dysfunction but shows variable results. This study investigated the relationship of cardiovascular risk factors to acute and chronic responses to sildenafil.
  
  
  METHODS
  Cardiovascular risk factors and acute and chronic pulse wave responses to a single 50-mg dose of sildenafil were assessed in 45 patients with erectile dysfunction confirmed by low international index of erectile function (IIEF) score before and after chronic therapy with sildenafil.
  
  
  RESULTS
  On recruitment all patients showed evidence of erectile dysfunction with an IIEF score of 5 points (1 to 20 points). Chronic sildenafil therapy resulted in an increase of IIEF score of 13 points (range -1 to +24 points) and 24 patients (53%) achieved an IIEF score>or=21 points. Improvement in erectile function in response to sildenafil (rn=0.79; P<.001) was dependent on initial erectile function (P=.002) and baseline apolipoprotein B (P=.01). Vascular responses to acute treatment with sildenafil were assessed using pulse wave analysis. Acute changes in stiffness index induced by sildenafil (rn=0.65; P<.001) were related to apolipoprotein A-1 (P=.006), B (P=.02), and lipoprotein(a) (P=.008) concentrations, whereas reflection index (rn=0.69; P<.001) was related to pulse pressure (P<.001), albumin-to-creatinine ratio (P=.007), and lipoprotein(a) (P=.02).
  
  
  CONCLUSIONS
  The extent of acute and chronic effects of sildenafil on erectile function and pulse wave profiles is determined by metabolic cardiovascular risk factors. Improved cardiovascular risk factor control is likely to increase the efficacy of phosphodiesterase-5 inhibitor therapy in the treatment of erectile dysfunction.
authors.affiliation: Department of Cardiology, Cardiothoracic Centre, St. Thomas' Hospital, London, United Kingdom.
authors.forename: Hemant
authors.initials: H
authors.lastname: Solomon
authors.forename: Anthony S
authors.initials: AS
authors.lastname: Wierzbicki
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Lumb
authors.forename: Michelle
authors.initials: M
authors.lastname: Lambert-Hammill
authors.forename: Graham
authors.initials: G
authors.lastname: Jackson
mesh_terms: D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood / Q000187:drug effects; D001055:Apolipoproteins B / Q000097:blood / Q000187:drug effects; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000503:physiopathology*; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D007172:Erectile Dysfunction / Q000188:drug therapy* / Q000453:epidemiology / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use*; D010879:Piperazines / Q000627:therapeutic use*; D011687:Purines / Q000627:therapeutic use; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D000068677:Sildenafil Citrate; D013450:Sulfones / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000627:therapeutic use*
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D015415:Biomarkers; D017270:Lipoprotein(a); D010726:Phosphodiesterase Inhibitors; D010879:Piperazines; D011687:Purines; D013450:Sulfones; D014665:Vasodilator Agents; D000068677:Sildenafil Citrate