title: Assessment of myocardial ischemic memory using persistence of post-systolic thickening after recovery from ischemia.
abstract: OBJECTIVE
  We sought to investigate the time course of post-systolic thickening (PST) and systolic abnormality after recovery from brief myocardial ischemia.
  
  
  BACKGROUND
  Myocardial ischemic memory imaging, denoting the visualization of abnormalities provoked by ischemia and sustained even after restoration of perfusion, is desirable and allows after-the-fact recognition of ischemic insult. PST offers a sensitive marker of myocardial ischemia, but whether this abnormal thickening remains after relief from brief ischemia is unclear.
  
  
  METHODS
  Tissue strain echocardiographic data were acquired from 27 dogs under 2 different conditions of myocardial ischemia induced by either brief coronary occlusion (15 or 5 min) followed by reperfusion (Protocol 1) or by dobutamine stress during nonflow-limiting stenosis (Protocol 2). Peak systolic strain and post-systolic strain index (PSI), a parameter of PST, were analyzed.
  
  
  RESULTS
  In Protocol 1, peak systolic strain was significantly decreased in the risk area during occlusion. This decrease in peak systolic strain in the 15-min group did not completely recover to baseline levels even 120 min after reperfusion, whereas the decrease in the 5-min group recovered immediately after reperfusion. We found that PSI was significantly increased during occlusion, but increased PSI in the 5-min group remained until 30 min after reperfusion (-0.19 +/- 0.18 [baseline] vs. 0.19 +/- 0.14 [30 min], p < 0.05) despite the rapid recovery of peak systolic strain. In Protocol 2, increased PSI was sustained until 20 min after the end of dobutamine infusion (-0.26 +/- 0.11 [baseline] vs. -0.16 +/- 0.10 [20 min], p < 0.05), although peak systolic strain recovered by 5 min after the end of dobutamine infusion.
  
  
  CONCLUSIONS
  PST remained longer than abnormal peak systolic strain after recovery from ischemia. Assessment of PST may be valuable for detecting myocardial ischemic memory.
authors.affiliation: Department of Functional Diagnostic Science, Division of Health Sciences, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. toshi@sahs.med.osaka-u.ac.jp
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Asanuma
authors.forename: Ayumi
authors.initials: A
authors.lastname: Uranishi
authors.forename: Kasumi
authors.initials: K
authors.lastname: Masuda
authors.forename: Fuminobu
authors.initials: F
authors.lastname: Ishikura
authors.forename: Shintaro
authors.initials: S
authors.lastname: Beppu
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nakatani
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D004285:Dogs; D018618:Echocardiography, Doppler, Color; D006339:Heart Rate; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D015588:Observer Variation; D020127:Recovery of Function; D015203:Reproducibility of Results; D013599:Systole; D013997:Time Factors