title: Quantitative relation between hemodynamic changes during intravenous adenosine infusion and the magnitude of coronary hyperemia: implications for myocardial perfusion imaging.
abstract: OBJECTIVE
  The goal of this study was to determine the relationship between changes in cardiac hemodynamics during intravenous adenosine (ADO) infusion, and myocardial blood flow (MBF).
  
  
  BACKGROUND
  The relationship between changes in MBF and the peripheral hemodynamic effects during peak adenosine infusion is unknown.
  
  
  METHODS
  We studied 348 (age 57 +/- 11 years; 106 females) without evidence of obstructive coronary artery disease by positron emission tomography (PET). Patients underwent [(13)N]ammonia PET imaging to measure MBF and coronary vascular resistance (CVR) at rest and during a standard 6-min ADO infusion. Changes in heart rate (HR) and mean arterial pressure (MAP) were measured at baseline and during peak hyperemia.
  
  
  RESULTS
  During ADO, HR increased (delta: 24 +/- 11 beats/min) and MAP decreased (delta: -2 +/- 10 mm Hg). Overall, delta HR correlated poorly with hyperemic MBF (R = 0.10, p = 0.06) and with CVR (R = 0.11, p = 0.04). Delta MAP also showed a weak correlation with hyperemic MBF (R = 0.04, p = 0.44) and with CVR (R = 0.11, p = 0.04). Patients in the lowest tertile for delta HR showed a 7% lower hyperemic MBF (1.84 +/- 0.6 ml/min/g vs. 1.98 +/- 0.6 ml/min/g, p = 0.022) and an 8% higher CVR (54 +/- 20 mm Hg/ml/min/g vs. 50 +/- 17 mm Hg/ml/min/g, p = 0.056) compared with those in the highest tertile. Patients in the lowest tertile for delta MAP (i.e., greatest decline) showed similar hyperemic MBF, and an 8% lower CVR compared with those in the highest tertile (p = NS for both). These small differences between tertiles remain, even after adjusting for differences in age, gender, smoking status, and lipid profile.
  
  
  CONCLUSIONS
  Changes in cardiac hemodynamics during intravenous ADO are generally poor predictors of changes in MBF and CVR during peak hyperemia, and, thus, they should not be used to assess the effectiveness of vasodilator stress in myocardial perfusion imaging.
authors.affiliation: Division of Nuclear Medicine, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Rakesh K
authors.initials: RK
authors.lastname: Mishra
authors.forename: Sharmila
authors.initials: S
authors.lastname: Dorbala
authors.forename: Giridhar
authors.initials: G
authors.lastname: Logsetty
authors.forename: Alita
authors.initials: A
authors.lastname: Hassan
authors.forename: Therese
authors.initials: T
authors.lastname: Heinonen
authors.forename: Heinrich R
authors.initials: HR
authors.lastname: Schelbert
authors.forename: Marcelo F
authors.initials: MF
authors.lastname: Di Carli
mesh_terms: D000241:Adenosine / Q000008:administration & dosage / Q000494:pharmacology*; D000293:Adolescent; D000328:Adult; D000368:Aged; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease; D003331:Coronary Vessels / Q000000981:diagnostic imaging*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006940:Hyperemia / Q000000981:diagnostic imaging; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D014665:Vasodilator Agents; D000241:Adenosine