title: Effects of tadalafil on myocardial blood flow in patients with coronary artery disease.
abstract: OBJECTIVE
  Erectile dysfunction and coronary artery disease share similar risk factors. Although phosphodiesterase-5 inhibitors used to treat erectile dysfunction do not adversely affect hemodynamic parameters in patients with coronary artery disease, their effects on myocardial blood flow are unknown.
  
  
  METHODS
  In a randomized, double-blind, crossover study we examined the effects of tadalafil, 20 mg, compared with placebo on myocardial blood flow in patients with stable coronary artery disease (n=7, 52-73 years old). After tadalafil or placebo, myocardial blood flow was measured with positron emission tomography (nine-segment model) at rest, during maximal coronary hyperemia with adenosine, and during increased myocardial work with dobutamine. Abnormal flow was defined as myocardial blood flow <75% of maximum perfusion during adenosine plus placebo (46 normal/17 abnormal segments dentified).
  
  
  RESULTS
  Compared with placebo, tadalafil had no significant effect on global myocardial blood flow at rest, during adenosine infusion, or during dobutamine infusion. Similarly, in normal and abnormal segments, tadalafil versus placebo had no significant effect on resting myocardial blood flow or on adenosine-induced increases in myocardial blood flow. In normal segments, myocardial blood flow with dobutamine plus tadalafil was greater than that with dobutamine plus placebo (1.79+/-0.56 versus 1.56+/-0.37 ml/g per min, P<0.01), and in abnormal segments, there was a trend for tadalafil compared with placebo to increase myocardial blood flow during dobutamine infusion (1.46+/-0.44 versus 1.36+/-0.36 ml/g per min, P=0.7).
  
  
  CONCLUSIONS
  Tadalafil had no significant effect on global myocardial blood flow at rest, during adenosine infusion, or during dobutamine infusion. Compared with placebo, tadalafil significantly augmented myocardial blood flow during increased workload in normal regions, with a trend toward improving myocardial blood flow in poorly perfused regions.
authors.affiliation: Department of Medicine, Division of Cardiology, College of Physicians and Surgeons of Columbia University, New York, New York 10003, USA.
authors.forename: Jonathan W
authors.initials: JW
authors.lastname: Weinsaft
authors.forename: Kathleen
authors.initials: K
authors.lastname: Hickey
authors.forename: Sabahat
authors.initials: S
authors.lastname: Bokhari
authors.forename: Arsalan
authors.initials: A
authors.lastname: Shahzad
authors.forename: Alun
authors.initials: A
authors.lastname: Bedding
authors.forename: Timothy M
authors.initials: TM
authors.lastname: Costigan
authors.forename: Margaret R
authors.initials: MR
authors.lastname: Warner
authors.forename: Jeffrey T
authors.initials: JT
authors.lastname: Emmick
authors.forename: Steven R
authors.initials: SR
authors.lastname: Bergmann
mesh_terms: D000241:Adenosine / Q000008:administration & dosage; D000368:Aged; D002243:Carbolines / Q000494:pharmacology*; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology; D018592:Cross-Over Studies; D004280:Dobutamine / Q000008:administration & dosage; D004311:Double-Blind Method; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D011877:Radionuclide Imaging; D000068581:Tadalafil
chemical_list: D002243:Carbolines; D010726:Phosphodiesterase Inhibitors; D004280:Dobutamine; D000068581:Tadalafil; D000241:Adenosine