title: Dipyridamole-induced increased glucose uptake in patients with single-vessel coronary artery disease assessed with PET.
abstract: BACKGROUND
  The aim of this study was to determine the relationship between vasodilatation-induced ischemia and poststress glucose uptake. Coronary vasodilators may induce myocardial ischemia due to coronary steal through collateral circulation or transmural blood flow redistribution with diminished subendocardial perfusion. Myocardial ischemia can be demonstrated by increased glucose uptake as previously shown in patients with exercise-induced ischemia.
  
  
  RESULTS
  We studied 11 patients with single-vessel disease and no history of myocardial infarction. Five patients had no collateral circulation, and 6 had angiographic evidence of collateral vessels. We measured myocardial blood flow (MBF) and glucose uptake at baseline and after the administration of dipyridamole (0.56 mg/kg) with positron emission tomography, using O-15 water and fluorine 18 deoxyglucose (FDG) as perfusion and glucose tracers. MBF at baseline was 0.82 +/- 0.13 mL/g/min in normal areas and 0.80 +/- 0.15 mL/g/min in areas supplied by stenotic arteries. MBF during dipyridamole was 2.05 +/- 0.66 and 1.19 +/- 0.66 mL/g/min in normal areas and areas with stenotic arteries, respectively (P < or = .001). FDG uptake at baseline was 1.36 +/- 0.55 in normal areas and 1.57 +/- 0.62 in areas supplied by stenotic arteries. FDG uptake after dipyridamole infusion was 1.79 +/- 1.1 and 4.04 +/- 0.84 in normal areas and areas with stenotic arteries, respectively (P < or =.001). MBF and FDG uptake were not different between patients with collateral circulation and those without collateral circulation.
  
  
  CONCLUSIONS
  Increased myocardial glucose uptake was consistently observed after dipyridamole administration in those areas with diminished coronary vasodilatory capacity. The similar MBF and FDG findings in patients with and without collateral circulation may indicate that transmural blood flow redistribution appears to be a possible mechanism of dipyridamole-induced myocardial ischemia.
authors.affiliation: Divisions of Nuclear Medicine and Cardiology, Hospital of the University of Pennsylvania, Philadelphia 19104, USA. araujo@rad.upenn.edu
authors.forename: L I
authors.initials: LI
authors.lastname: Araujo
authors.forename: E O
authors.initials: EO
authors.lastname: McFalls
authors.forename: A A
authors.initials: AA
authors.lastname: Lammertsma
authors.forename: T
authors.initials: T
authors.lastname: Jones
authors.forename: A
authors.initials: A
authors.lastname: Maseri
mesh_terms: D001786:Blood Glucose / Q000187:drug effects* / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003327:Coronary Disease / Q000139:chemically induced* / Q000000981:diagnostic imaging / Q000378:metabolism*; D003331:Coronary Vessels / Q000502:physiology; D004176:Dipyridamole / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009206:Myocardium / Q000378:metabolism; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D014055:Tomography, Emission-Computed; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D001786:Blood Glucose; D014665:Vasodilator Agents; D004176:Dipyridamole