title: Postocclusion hyperemia provides a better estimate of coronary reserve than intracoronary adenosine in patients with coronary artery stenosis.
abstract: OBJECTIVE
  The aim of this study was to compare the ability of intracoronary adenosine (ADE) and postocclusion hyperemia (PH) to cause maximal hyperemia in humans.
  
  
  BACKGROUND
  The current clinical standard for induction of maximal coronary hyperemia is intracoronary ADE. However, animal studies have shown that maximal hyperemia was not achieved by ADE and that PH yielded a higher hyperemic response.
  
  
  METHODS
  In 10 stable patients with coronary artery stenosis > or = 80%, basal and peak coronary blood flow velocity (intracoronary Doppler) were measured before and after coronary angioplasty (PTCA), both after an intracoronary bolus of 60 mcg ADE, and after 30-second occlusion of the coronary artery by a balloon angioplasty catheter. Coronary reserve was estimated through coronary flow reserve (CFR = peak-to-resting coronary blood flow velocity), and coronary resistance reserve (CRR = [resting aortic pressure/resting coronary flow velocity]/[aortic pressure at peak velocity/peak coronary flow velocity]).
  
  
  RESULTS
  Before PTCA, ADE and PH result in comparable CFR (1.79 +/- 0.65 vs. 1.95 +/- 0.52, respectively; p = 0.0846), but CRR was higher with PH (1.75 +/- 0.52 vs. 2.14 +/- 0.81, respectively; p = 0.0125). After PTCA, CFR and CRR were significantly lower with ADE than with PH (CFR = 2.53 +/- 0.58 vs. 3.31 +/- 0.67, respectively; p = 0.0001, and CRR = 2.58 +/- 0.49 vs. 3.46 +/- 0.79; p = 0.0004, respectively). Lastly, the higher the coronary reserve, the greater the differences between ADE and PH values.
  
  
  CONCLUSIONS
  Because intracoronary 60 mcg ADE elicits a lower hyperemic response than PH, intracoronary ADE represents a potential source of error in coronary reserve measurements, and may result in an underestimation of the physiological significance of a coronary artery stenosis.
authors.affiliation: Service de Physiologie et d'Explorations Fonctionnelles, CHU Jean Verdier, Assistance Publique-Hôpitaux de Paris, Université Paris 13, Bondy, France. alain.nitenberg@jvr.aphp.fr
authors.forename: Alain
authors.initials: A
authors.lastname: Nitenberg
authors.forename: Eric
authors.initials: E
authors.lastname: Durand
authors.forename: Bertrand
authors.initials: B
authors.lastname: Delatour
authors.forename: Wissem
authors.initials: W
authors.lastname: Sdiri
authors.forename: Saliha
authors.initials: S
authors.lastname: Raha
authors.forename: Antoine
authors.initials: A
authors.lastname: Lafont
mesh_terms: D000241:Adenosine; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D001011:Aorta; D001794:Blood Pressure; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000175:diagnosis* / Q000503:physiopathology* / Q000628:therapy; D006339:Heart Rate; D006801:Humans; D006940:Hyperemia / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D014655:Vascular Resistance; D014665:Vasodilator Agents