title: Contractile versus microvascular reserve for the determination of the extent of myocardial salvage after reperfusion. The effect of residual coronary stenosis.
abstract: BACKGROUND
  We hypothesized that microvascular reserve is a better indicator of the extent of viable myocardium postinfarction than contractile reserve, especially in the presence of a residual stenosis of the infarct-related artery.
  
  
  RESULTS
  Fifteen dogs with various infarct sizes were studied after reperfusion. Contractile reserve, studied by use of dobutamine echocardiography, and microvascular reserve, studied by use of myocardial contrast echocardiography, were measured both before and after creation of a stenosis. In the absence of a stenosis, the relation between infarct size, expressed as percent of risk area, and wall thickening improved with increasing doses of dobutamine (r = .41, .71, and .90 for 5, 10, and 15 micrograms.kg-1.min-1, respectively; P < .01 for dobutamine 15 micrograms.kg-1.min-1). In the presence of a stenosis, however, the relation was poor for all doses of dobutamine (r = .22, .57, and .32 for 5, 10, and 15 micrograms.kg-1.min-1, respectively; P < .01 for 15 micrograms.kg-1.min-1 dobutamine in the absence of a stenosis). There was a fair correlation between infarct size and perfusion defect size on myocardial contrast echocardiography after reperfusion (r = .82), with the defect size underestimating infarct size by approximately 20%. This relationship improved (P < .01) during infusions of both adenosine (r = .99) and dobutamine (r = .94) in the absence of a stenosis. The correlations between infarct size and perfusion defect on myocardial contrast echocardiography also remained good in the presence of a stenosis (r = .95 and .81 for adenosine and dobutamine, respectively; P = NS compared with stenosis).
  
  
  CONCLUSIONS
  Microvascular reserve is superior to contractile reserve for definition of the spatial topography of necrosis and hence the extent of viable myocardium within the infarct bed after reperfusion, particularly when a residual stenosis is present in the infarct-related artery.
authors.affiliation: Cardiovascular Division, University of Virginia, Charlottesville 22908, USA.
authors.forename: J
authors.initials: J
authors.lastname: Sklenar
authors.forename: G
authors.initials: G
authors.lastname: Camarano
authors.forename: N C
authors.initials: NC
authors.lastname: Goodman
authors.forename: S
authors.initials: S
authors.lastname: Ismail
authors.forename: A R
authors.initials: AR
authors.lastname: Jayaweera
authors.forename: S
authors.initials: S
authors.lastname: Kaul
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology; D002317:Cardiovascular Agents / Q000494:pharmacology; D003287:Contrast Media; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D004280:Dobutamine / Q000494:pharmacology; D004285:Dogs; D004452:Echocardiography; D008833:Microcirculation; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D016879:Salvage Therapy
chemical_list: D002316:Cardiotonic Agents; D002317:Cardiovascular Agents; D003287:Contrast Media; D004280:Dobutamine; D000241:Adenosine