title: Evaluation of patterns of perfusion and metabolism in dobutamine-responsive myocardium.
abstract: OBJECTIVE
  We investigated the patterns of perfusion and metabolism in dysfunctional myocardium whose contractility improved with dobutamine.
  
  
  BACKGROUND
  Clinical studies have suggested that dobutamine echocardiography can identify hibernating myocardium, but laboratory studies suggest that reduced perfusion limits the response to dobutamine.
  
  
  METHODS
  Twenty-five patients with coronary disease and ventricular dysfunction underwent low (5 and 10 micrograms/kg body weight per min) and high dose (maximum of 50 micrograms/kg per min) dobutamine echocardiography and positron emission tomography (PET) using nitrogen-13 (N-13) ammonia and fluorine-18 fluorodeoxyglucose (FDG) for imaging of perfusion and metabolism. Wall motion and tracer uptake were scored in 16 left ventricular segments.
  
  
  RESULTS
  Perfusion and metabolism were normal in 56.4%, mildly reduced in 29.1% and mismatched (reduced perfusion, preserved FDG uptake) in 14.5% of dysfunctional segments viable on PET. Wall motion improved with dobutamine in 89 dysfunctional segments (62 at low dose, 27 only at peak dose), and 86 of these (97%) were viable on PET. Improvement in wall motion with dobutamine was more common in segments with normal perfusion and metabolism (56.5%) than in those with mildly reduced tracer uptake (28.5%, p < 0.001) and those with mismatch (32%, p = 0.03). All the segments with a biphasic response were supplied by vessels with > or = 70% stenosis, and 88% had normal perfusion and metabolism.
  
  
  CONCLUSIONS
  The majority of viable segments with rest dysfunction had normal perfusion and metabolism, suggesting that myocardial stunning was common. Improvement of wall motion at low and high doses of dobutamine was highly correlated with myocardial viability on PET and was more common in myocardium with normal perfusion. A biphasic response to dobutamine identified segments with normal perfusion and metabolism supplied by severely diseased vessels.
authors.affiliation: Department of Medicine, Indiana University School of Medicine, Indianapolis, USA.
authors.forename: S
authors.initials: S
authors.lastname: Sawada
authors.forename: G
authors.initials: G
authors.lastname: Elsner
authors.forename: D S
authors.initials: DS
authors.lastname: Segar
authors.forename: M
authors.initials: M
authors.lastname: O'Shaughnessy
authors.forename: S
authors.initials: S
authors.lastname: Khouri
authors.forename: J
authors.initials: J
authors.lastname: Foltz
authors.forename: P D
authors.initials: PD
authors.lastname: Bourdillon
authors.forename: J R
authors.initials: JR
authors.lastname: Bates
authors.forename: N
authors.initials: N
authors.lastname: Fineberg
authors.forename: T
authors.initials: T
authors.lastname: Ryan
authors.forename: G D
authors.initials: GD
authors.lastname: Hutchins
authors.forename: H
authors.initials: H
authors.lastname: Feigenbaum
mesh_terms: D000641:Ammonia; D017023:Coronary Angiography; D003847:Deoxyglucose / Q000031:analogs & derivatives; D004280:Dobutamine; D004452:Echocardiography / Q000379:methods*; D005069:Evaluation Studies as Topic; D005260:Female; D005462:Fluorine Radioisotopes; D019788:Fluorodeoxyglucose F18; D006321:Heart / Q000000981:diagnostic imaging; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D017682:Myocardial Stunning / Q000175:diagnosis* / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D009590:Nitrogen Radioisotopes; D014055:Tomography, Emission-Computed
chemical_list: D005462:Fluorine Radioisotopes; D009590:Nitrogen Radioisotopes; D019788:Fluorodeoxyglucose F18; D004280:Dobutamine; D000641:Ammonia; D003847:Deoxyglucose