title: The partition coefficient of Gd-DTPA reflects maintained tissue viability in a canine model of chronic significant coronary stenosis.
abstract: OBJECTIVE
  The underlying assumption in delayed enhancement or constant infusion techniques to detect infarcted myocardium is that the partition coefficient (lambda) of Gd-DTPA only increases in permanently damaged tissue. This assumption is supported in canine models of stunned and infarcted myocardium but has not been adequately tested in models of chronic, reversibly damaged tissue.
  
  
  METHODS
  A significant coronary stenosis was maintained for 3 (n = 9) or 10 (n = 4) weeks in a canine model. Myocardial perfusion was assessed using radioactively labeled microspheres, and Doppler flow was used to monitor the effect on flow caused by the stenosis formation. Function and in vivo lambda were assessed using magnetic resonance imaging (MRI) and a constant infusion of Gd-DTPA. 201Tl and 111In-DTPA were used to assess ex vivo myocardial viability and lambda, respectively.
  
  
  RESULTS
  Baseline Doppler-measured blood flow through the left anterior descending coronary artery was reduced by 72.4 +/- 1.6% (SEM) during the stenosis formation. However, shortly after creation of the stenosis and at sacrifice, regional myocardial blood flow at rest was not decreased in the Region at Risk (RAR) despite the persistence of the stenosis. Perfusion reserve in this model, measured using adenosine stress, was significantly reduced. The in vivo lambda values in the RAR and remote tissue ranged between 0.32-0.45 mL/g and 0.31-0.42 mL/g, respectively. 201Tl uptake was maintained in all tissue, confirming the maintenance of tissue viability. Global function was unchanged while regional function was significantly depressed at 10 days but returned to baseline values by day 21.
  
  
  CONCLUSIONS
  This study is consistent with the hypothesis that lambda is not increased in reversibly dysfunctional myocardium.
authors.affiliation: Department of Nuclear Medicine, Imaging Program, Lawson Health Research Institute, University of Western Ontario, London, Ontario, Canada. klekx@lri.sjhc.london.on.ca
authors.forename: Katie S
authors.initials: KS
authors.lastname: Lekx
authors.forename: Frank S
authors.initials: FS
authors.lastname: Prato
authors.forename: Jane
authors.initials: J
authors.lastname: Sykes
authors.forename: Gerald
authors.initials: G
authors.lastname: Wisenberg
mesh_terms: D000318:Adrenergic beta-Agonists / Q000008:administration & dosage; D000818:Animals; D002908:Chronic Disease; D003287:Contrast Media / Q000378:metabolism; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000502:physiology; D023921:Coronary Stenosis / Q000175:diagnosis* / Q000503:physiopathology; D004195:Disease Models, Animal; D004280:Dobutamine / Q000008:administration & dosage; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D025401:Echocardiography, Stress; D005260:Female; D005500:Follow-Up Studies; D019786:Gadolinium DTPA / Q000378:metabolism; D007089:Image Enhancement; D018810:Magnetic Resonance Angiography; D008955:Models, Cardiovascular; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D013318:Stroke Volume / Q000502:physiology
chemical_list: D000318:Adrenergic beta-Agonists; D003287:Contrast Media; D004280:Dobutamine; D019786:Gadolinium DTPA