title: Global alteration in perfusion response to increasing oxygen consumption in patients with single-vessel coronary artery disease.
abstract: BACKGROUND
  Recent evidence suggests that, in coronary artery disease (CAD), myocardial blood flow (MBF) regulation is abnormal in regions supplied by apparently normal coronary arteries. However, the relation between this alteration and MBF response to increasing metabolic demand has not been fully elucidated.
  
  
  RESULTS
  MBF was assessed at baseline, during atrial pacing tachycardia, and after dipyridamole (0.56 mg/kg IV over 4 minutes) in 9 normal subjects and in 24 patients with ischemia on effort, no myocardial infarction, and isolated left anterior descending (n = 19) or left circumflex (n = 5) coronary artery stenosis (> or = 50% diameter narrowing). Perfusion of both poststenotic (S) and normally supplied (N) areas was measured off therapy by positron emission tomography and [13N]ammonia. Normal subjects and CAD patients showed similar rate-pressure products at baseline, during pacing, and after dipyridamole. In CAD patients, MBF was lower in S than in N territories at rest (0.68 +/- 0.14 versus 0.74 +/- 0.18 mL.min-1.g-1, respectively, P < .05), during pacing (0.92 +/- 0.29 versus 1.16 +/- 0.40 mL.min-1.g-1, respectively, P < .01), and after dipyridamole (1.18 +/- 0.34 versus 1.77 +/- 0.71 mL.min-1.g-1, respectively, P < .01). However, normal subjects showed significantly higher values of MBF both at rest (0.92 +/- 0.13 mL.min-1.g-1, P < .05 versus both S and N areas), during pacing tachycardia (1.95 +/- 0.64 mL.min-1.g-1, P < .01 versus both S and N areas), and after dipyridamole (3.59 +/- 0.71 mL.min-1.g-1, P < .01 versus both S and N areas). The percent change in flow was strictly correlated with the corresponding change in rate-pressure product in normal subjects (r = .85, P < .01) but not in either S (r = .04, P = NS) or N regions (r = .08, P = NS) of CAD patients.
  
  
  CONCLUSIONS
  Besides epicardial stenosis, further factors may affect flow response to increasing metabolic demand and coronary reserve in patients with CAD.
authors.affiliation: CNR Institute of Clinical Physiology, Pisa, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Sambuceti
authors.forename: P
authors.initials: P
authors.lastname: Marzullo
authors.forename: A
authors.initials: A
authors.lastname: Giorgetti
authors.forename: D
authors.initials: D
authors.lastname: Neglia
authors.forename: M
authors.initials: M
authors.lastname: Marzilli
authors.forename: P
authors.initials: P
authors.lastname: Salvadori
authors.forename: A
authors.initials: A
authors.lastname: L'Abbate
authors.forename: O
authors.initials: O
authors.lastname: Parodi
mesh_terms: D000328:Adult; D000368:Aged; D002304:Cardiac Pacing, Artificial; D017023:Coronary Angiography; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology*; D004176:Dipyridamole; D005260:Female; D006339:Heart Rate; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption
chemical_list: D004176:Dipyridamole