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J Am Coll Cardiol, 2001; 37:1141-1148
© 2001 by the American College of Cardiology Foundation
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Regional asynchrony during acute myocardial ischemia quantified by ultrasound strain rate imaging

Cristina Pislaru, MD*, Marek Belohlavek, MD, PhD{dagger}, Richard Y. Bae, MD{dagger}, Theodore P. Abraham, MD{dagger}, James F. Greenleaf, PhD* and James B. Seward, MD{dagger}

* Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota, USA
{dagger} Division of Cardiovascular Diseases Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota, USA



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Figure 1 Strain rate maps at baseline and during ischemia, and corresponding perfusion-stained specimen, in apical long-axis view. (A) Baseline strain rate imaging frame (left image) and the corresponding longitudinal M-mode strain rate map over one cardiac cycle (right image). Orange represents compression, blue expansion and green low motion. The two vertical straight lines approximate the time of the aortic valve closure and of the mitral valve opening (identified from gray-scale two-dimensional loops). The compression/expansion crossover is indicated by the solid black line as the color transition from orange to blue. The time from the electrocardiographic peak R-wave to the compression/expansion crossover (TCEC) is measured for each pixel line in the image. (B) Ischemic strain rate maps from the same view. A prolonged compression pattern (black arrows) can be observed in the apical and mid anteroseptal segments (supplied by the occluded left anterior descending coronary artery), while the rest of segments have normal compression/relaxation pattern. Note also the delayed onset of systolic compression (white arrows) in the same ischemic segments. (C) Computer reconstruction of the stained cardiac specimen at the same level in the heart. Myocardium at risk is represented by the white region (arrows), while the normally perfused myocardium is stained in red. The location of the apical postsystolic compression pattern in the strain-rate maps matches the location of the ischemic myocardium (Segments are abbreviated: bIL = basal inferolateral; mIL = mid inferolateral; aIL = apical inferolateral; aAS = apical anteroseptal; mAS = mid anteroseptal; bAS = basal anteroseptal).

 


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Figure 2 TCEC during ischemia in one animal: comparison with normal range and the extent of myocardium at risk. Ischemic TCEC from one animal during ischemia (black thick line) is plotted against the normal range of TCEC (mean ± SD, striped region) for unfolded left ventricle (LV) circumference (Y-axis). During left anterior descending coronary artery ischemia, prolonged TCEC occurs in both apical and midseptal segments, whereas in the rest of the segments TCEC did not exceed the normal range. The black bar on the right represents LV from the same apical view, reconstructed from the stained cardiac specimen: myocardium at risk corresponds to the unstained area (white zone), while normally perfused myocardium corresponds to the stained area (black zone). Note the good topographical match between the region with prolonged TCEC and the extent of myocardium at risk (bS = basal septal; mS = midseptal; aS = apical septal; aL = apical lateral; mL = mid lateral; bL = basal lateral).

 


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Figure 3 Range of TCEC (mean ± SD) at baseline and during ischemia, calculated from all animals. During ischemia, the mean TCEC values are shifted in ischemic regions (black-filled region, mean ± SD) from the normal range (striped region, mean ± SD) to a significantly discriminate higher range. Ischemic TCEC range in basal segments remained unchanged.

 


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Figure 4 The extent of myocardium at risk versus the extent of region with prolonged TCEC. (A) Plot of the extents of regions with prolonged TCEC measured from the longitudinal M-mode strain-rate maps, and of the myocardium at risk measured from the stained cardiac specimens. Line of identity and the 95% confidence limits are indicated as dashed lines. (B) Bland and Altman analysis of differences between the extent of myocardium at risk and extent of region with prolonged TCEC plotted against their mean. Horizontal dashed lines represent the limits of agreement between the two measurements (Abn.TCEC: abnormal TCEC; M.risk: myocardium at risk).

 


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Figure 5 Segmental TCEC during ischemia versus wall motion score and duration of occlusion. (A) Segmental TCEC per each wall motion score group. TCEC was significantly higher in hypo- and akinetic segments when compared with normally contracting segments (*p < 0.05). No significant difference in TCEC was found between akinetic and dyskinetic segments (p = NS). (B) Segmental TCEC in the ischemic segments shows no significant correlation with the duration of occlusion (p = NS).

 




 
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