title: Coronary patency and its relation to contractile reserve in hibernating myocardium.
abstract: OBJECTIVE
  Recent clinical studies suggest that contractile reserve may occur in a minority of viable, chronically dysfunctional segments with reduced resting flow (hibernating myocardium). We hypothesized that epicardial artery patency might predict which segments have critically reduced subendocardial flow reserve and limited contractile reserve.
  
  
  METHODS
  Pigs were chronically instrumented with a fixed stenosis on the left anterior descending coronary artery (LAD) to produce hibernating myocardium. At least 3 months later, flow at rest and during adenosine vasodilation (microspheres), ventricular function and contractile reserve (contrast ventriculography), and (18)F-2-deoxyglucose (FDG) deposition (ex vivo tissue counting) were quantified.
  
  
  RESULTS
  Hibernating myocardium (regional dysfunction with reduced resting perfusion) was present in animals with an occluded (n=40) or patent (n=19) LAD. Viability was confirmed by histology and FDG deposition. In collateral-dependent hibernating myocardium, subendocardial flow did not increase above baseline levels during epinephrine or adenosine stimulation, consistent with exhausted subendocardial flow reserve at rest. This was associated with limited contractile reserve and regionally increased FDG deposition. In contrast, subendocardial flow reserve was present in hibernating myocardium distal to a patent artery. Contractile reserve during epinephrine infusion in this group was significantly greater than in animals with an occluded artery.
  
  
  CONCLUSIONS
  The physiology and metabolism of hibernating myocardium was dependent upon stenosis severity and its effects on subendocardial flow reserve. In collateral-dependent hibernating myocardium, contractile reserve was limited in the setting of exhausted subendocardial flow reserve, thus supporting the hypothesis that metabolic imaging may be preferable for determining viability distal to a complete occlusion.
authors.affiliation: Veterans Affairs Western New York Health Care System, The University at Buffalo, 14214, USA. jaf7@buffalo.edu
authors.forename: James A
authors.initials: JA
authors.lastname: Fallavollita
authors.forename: Michael
authors.initials: M
authors.lastname: Logue
authors.forename: John M
authors.initials: JM
authors.lastname: Canty
mesh_terms: D000241:Adenosine; D000818:Animals; D003097:Collateral Circulation; D003331:Coronary Vessels / Q000473:pathology*; D004699:Endocardium / Q000473:pathology; D004837:Epinephrine; D019788:Fluorodeoxyglucose F18 / Q000378:metabolism; D023421:Models, Animal; D009200:Myocardial Contraction; D017682:Myocardial Stunning / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism; D010496:Pericardium / Q000473:pathology; D015635:Radionuclide Ventriculography; D013268:Stimulation, Chemical; D013552:Swine; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D019788:Fluorodeoxyglucose F18; D000241:Adenosine; D004837:Epinephrine