title: Blood flow, flow reserve, and glucose utilization in viable and nonviable myocardium in patients with ischemic cardiomyopathy.
abstract: OBJECTIVE
  The aim of the study was to determine whether glucose uptake in viable myocardium of ischemic cardiomyopathy patients depends on rest myocardial blood flow (MBF) and the residual myocardial flow reserve (MFR).
  
  
  METHODS
  Thirty-six patients with ischemic cardiomyopathy (left ventricular ejection fraction 25 ± 10 %) were studied with (13)N-ammonia and (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET). Twenty age-matched normals served as controls. Regional MBF was determined at rest and during dipyridamole hyperemia and regional FDG extraction was estimated from regional FDG to (13)N-ammonia activity ratios.
  
  
  RESULTS
  Rest MBF was reduced in viable (0.42 ± 0.18 ml/min per g) and nonviable regions (0.32 ± 0.09 ml/min per g) relative to remote regions (0.68 ± 0.23 ml/min per g, p < 0.001) and to normals (0.63 ± 0.13 ml/min per g). Dipyridamole raised MBFs in controls, remote, viable, and nonviable regions. MBFs at rest (p < 0.05) and stress (p < 0.05) in viable regions were significantly higher than that in nonviable regions, while MFRs did not differ significantly (p > 0.05). Compared to MFR in remote myocardium, MFRs in viable regions were similar (1.39 ± 0.56 vs 1.70 ± 0.45, p > 0.05) but were significantly lower in nonviable regions (1.23 ± 0.43, p < 0.001). Moreover, the FDG and thus glucose extraction was higher in viable than in remote (1.40 ± 0.14 vs 0.90 ± 0.20, p < 0.001) and in nonviable regions (1.13 ± 0.21, p < 0.001). The extraction of FDG in viable regions was independent of rest MBF but correlated inversely with MFRs (r =-0.424, p < 0.05). No correlation between the FDG extraction and MFR was observed in nonviable regions.
  
  
  CONCLUSIONS
  As in the animal model, decreasing MFRs in viable myocardium are associated with increasing glucose extraction that likely reflects a metabolic adaptation of remodeling hibernating myocytes.
authors.affiliation: Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, University of California at Los Angeles, Los Angeles, CA 90095-6948, USA.
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Zhang
authors.forename: Thomas H
authors.initials: TH
authors.lastname: Schindler
authors.forename: John O
authors.initials: JO
authors.lastname: Prior
authors.forename: James
authors.initials: J
authors.lastname: Sayre
authors.forename: Magnus
authors.initials: M
authors.lastname: Dahlbom
authors.forename: Sung-Cheng
authors.initials: SC
authors.lastname: Huang
authors.forename: Heinrich R
authors.initials: HR
authors.lastname: Schelbert
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism*; D009202:Cardiomyopathies / Q000000981:diagnostic imaging* / Q000503:physiopathology; D016022:Case-Control Studies; D005260:Female; D019788:Fluorodeoxyglucose F18; D053805:Fractional Flow Reserve, Myocardial; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009590:Nitrogen Radioisotopes; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals; D012039:Regional Blood Flow
chemical_list: D001786:Blood Glucose; D009590:Nitrogen Radioisotopes; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18