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J Am Coll Cardiol Img, 2009; 2:1253-1261, doi:10.1016/j.jcmg.2009.07.008
© 2009 by the American College of Cardiology Foundation
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Assessment of Myocardial Ischemic Memory Using Persistence of Post-Systolic Thickening After Recovery From Ischemia

Toshihiko Asanuma, MD, PhD*, Ayumi Uranishi, MSc, Kasumi Masuda, PhD, Fuminobu Ishikura, MD, PhD, Shintaro Beppu, MD, PhD, Satoshi Nakatani, MD, PhD

Department of Functional Diagnostic Science, Division of Health Sciences, Osaka University Graduate School of Medicine, Suita, Osaka, Japan


Figure 1
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Figure 1 Study Protocols

Serial data from tissue strain echocardiography (TSE) were acquired in dogs with brief left anterior descending artery (LAD) occlusion followed by reperfusion in Protocol 1 and before, during, and after dobutamine administration in dogs with nonflow-limiting stenosis of the left circumflex artery (LCX) in Protocol 2. MCE = myocardial contrast echocardiography; TTC = 2,3,5-triphenyltetrazolium chloride.

 

Figure 2
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Figure 2 Tissue Strain Echocardiography

Tissue strain echocardiography at mid-systole and radial strain profiles analyzed within circular regions of interest in the anterior myocardium during mild ischemia (A and B) and severe ischemia (C and D) induced by occlusion of the left anterior descending artery. Orange or yellow indicates positive strain values. Blue indicates negative strain values. Note that blue is assigned to the anterior myocardium during severe ischemia as the result of systolic wall thinning. With the use of the strain profile, peak systolic strain ({varepsilon}-sys), post-systolic strain ({varepsilon}-post), and maximal strain ({varepsilon}-max) were measured, and post-systolic strain index was calculated (see the Data analysis section for details). AVC = aortic valve closure.

 

Figure 3
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Figure 3 Peak Systolic Strain in Protocol 1

Peak systolic strain in the risk area with 15 min (A) and 5 min (B) of occlusion. Peak systolic strain was significantly decreased at the end of occlusion compared with that at baseline in both occlusion groups. The decrease in the 15-min occlusion group did not completely recover to baseline levels even by 120 min after reperfusion, but the decrease in the 5-min occlusion group recovered immediately after reperfusion. *p < 0.05 vs. baseline.

 

Figure 4
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Figure 4 Post-Systolic Strain Index in Protocol 1

Shown is PSI in the risk area with 15 min (A) and 5 min (B) of occlusion. The PSI in the 5-min occlusion group recovered to baseline levels by 120 min after reperfusion, but the significant increase was prolonged until 30 min after reperfusion despite the rapid recovery of peak systolic strain. *p < 0.05 vs. baseline. PSI = post-systolic strain index.

 

Figure 5
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Figure 5 Strain Profiles in Protocol 1

Profiles of radial strain in the risk area with 15 min (A) and 5 min (B) of occlusion. Aortic valve closure is demonstrated as an orange line. Systolic wall thinning and post-systolic thickening (PST) were shown during occlusion in both groups of dogs. Complete recovery of peak systolic strain was not observed, and PST (arrows) was sustained until 120 min after reperfusion with 15 min of occlusion. Although peak systolic strain recovered immediately after reperfusion with 5 min of occlusion, PST was clearly apparent until 30 min after reperfusion.

 

Figure 6
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Figure 6 Post-Systolic Strain Index in Protocol 2

Shown is the PSI before, during, and after dobutamine infusion in dogs with nonflow-limiting stenosis. The PSI did not change during peak dobutamine stress in the normal area. However, that in the risk area was significantly increased and remained increased until 20 min after stopping dobutamine infusion. *p < 0.05 vs. baseline. Abbreviation as in Figure 4.

 




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