title: The quantification of dipyridamole induced changes in regional deformation in normal, stunned or infarcted myocardium as measured by strain and strain rate: an experimental study.
abstract: Strain rate imaging (SRI) during dobutamine stress-echocardiography (DSE) has been shown to differentiate between ischemic substrates based on the segmental response. Dipyridamole stress echo (DIPSE) is currently used as an alternative to DSE in detecting coronary artery disease. The aim of this study was: (a) to determine the normal response in peak-systolic myocardial strain (S) and strain-rate (SR) during DIPSE and (b) to compare the S and SR responses of DSE and DIPSE in the same chronically ischemic/infarcted segments in the setting of single vessel disease.
  
  
  METHODS
  The deformation response to DIPSE was studied in 7 normal pigs and in an additional 18 pigs, with a spectrum of ischemic substrates. S and SR data were extracted from a posterior wall "at risk" segment at baseline and during both DSE and DIPSE. The animals were divided into different ischemic substrate (stunning, non-transmural and transmural infarction), based on the DSE response as previously suggested.
  
  
  RESULTS
  In normal myocardium, dipyridamole induced no changes in regional systolic deformation neither during nor after the infusion. Furthermore there was no detectable response in S and SR in segments with either a non-transmural or a transmural infarction. However, in myocardial segments with a DSE "stunning response", both end systolic S and peak-systolic SR tended to "normalize" at peak dipyridamole dose.
  
  
  CONCLUSIONS
  These results suggest that dipyridamole does not induce changes in regional deformation in normal or (partially) infarcted myocardium. Only in stunned myocardium (in the setting of single-vessel disease), dipyridamole tends to normalize deformation.
authors.affiliation: Department of Cardiology, KULeuven, Leuven, Belgium.
authors.forename: Maciej
authors.initials: M
authors.lastname: Marciniak
authors.forename: Piet
authors.initials: P
authors.lastname: Claus
authors.forename: Witold
authors.initials: W
authors.lastname: Streb
authors.forename: Anna
authors.initials: A
authors.lastname: Marciniak
authors.forename: Petra
authors.initials: P
authors.lastname: Boettler
authors.forename: Myles
authors.initials: M
authors.lastname: McLaughlin
authors.forename: Jan
authors.initials: J
authors.lastname: D'hooge
authors.forename: Frank
authors.initials: F
authors.lastname: Rademakers
authors.forename: Bart
authors.initials: B
authors.lastname: Bijnens
authors.forename: George R
authors.initials: GR
authors.lastname: Sutherland
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology; D004176:Dipyridamole; D004195:Disease Models, Animal; D004280:Dobutamine; D025401:Echocardiography, Stress / Q000379:methods*; D005260:Female; D006439:Hemodynamics; D008297:Male; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology; D017682:Myocardial Stunning / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology; D012016:Reference Values; D012107:Research Design; D034421:Sus scrofa; D013997:Time Factors; D014665:Vasodilator Agents
chemical_list: D002316:Cardiotonic Agents; D014665:Vasodilator Agents; D004280:Dobutamine; D004176:Dipyridamole