title: Comparison of dobutamine echocardiography and positron emission tomography in patients with chronic ischemic left ventricular dysfunction.
abstract: OBJECTIVE
  The aim of this study was to correlate dobutamine-induced contractile reserve as detected by echocardiography with findings on positron emission tomography in patients with chronic ischemic left ventricular dysfunction.
  
  
  BACKGROUND
  Contractile reserve induced by low dose dobutamine infusion has been proposed as a marker of myocardial viability.
  
  
  METHODS
  Sixty patients with stable coronary artery disease and left ventricular dysfunction (mean ejection fraction [+/- SD] 29 +/- 10%) underwent transthoracic echocardiography with dobutamine infusion (up to 10 micrograms/kg body weight per min) and positron emission tomography with nitrogen-13 ammonia and fluorine-18 (F-18) fluorodeoxyglucose as a perfusion and a metabolic tracer, respectively. Regional wall motion, perfusion and metabolism were analyzed semiquantitatively by using a 16-segment model. Segments with F-18 fluorodeoxyglucose uptake > 50% were considered viable on positron emission tomography.
  
  
  RESULTS
  After dobutamine infusion, hemodynamic variables changed significantly, and myocardial ischemia was evident in 17 patients. All 60 patients had dysfunctional myocardium considered viable on positron emission tomography (8 +/- 4 segments/patient), whereas 52 patients had dysfunctional myocardium with contractile enhancement by dobutamine echocardiography (4 +/- 2 segments/patient, p = 0.01). The extent of dysfunctional myocardium with contractile reserve appeared to correlate less closely with the total extent of viable dysfunctional myocardium identified by positron emission tomography than with the number of such segments associated with a pattern of perfusion-metabolism mismatch.
  
  
  CONCLUSIONS
  In patients with chronic ischemic left ventricular dysfunction, echocardiography can be used to identify enhancement in the contractile function of viable dysfunctional myocardium after infusion of low dose dobutamine. In this study, the presence and extent of such enhancement were relatively less than the values obtained from positron emission tomography.
authors.affiliation: Department of Cardiology, Austin and Repatriation Medical Center, Melbourne, Australia.
authors.forename: R K
authors.initials: RK
authors.lastname: Chan
authors.forename: K J
authors.initials: KJ
authors.lastname: Lee
authors.forename: P
authors.initials: P
authors.lastname: Calafiore
authors.forename: S U
authors.initials: SU
authors.lastname: Berlangieri
authors.forename: W J
authors.initials: WJ
authors.lastname: McKay
authors.forename: A M
authors.initials: AM
authors.lastname: Tonkin
mesh_terms: D003327:Coronary Disease / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology; D004280:Dobutamine / Q000494:pharmacology; D015150:Echocardiography, Doppler; D006439:Hemodynamics; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects; D014055:Tomography, Emission-Computed; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology
chemical_list: D004280:Dobutamine