Peak strain (_PEAK) was defined as the highest strain value obtained for the transverse direction throughout the cardiac cycle. Time to peak strain (T) was defined as the interval from the onset of the Q-wave to _PEAK throughout the cardiac cycle. Strain values at both aortic valve closure (AVC) (A) and at one-third of diastole duration (1/3 DD) (B) were measured. Strain imaging (SI) diastolic index was calculated as: (A – B)/A x 100%. ECG = electrocardiogram.

Comparisons of peak strain (_PEAK) values at baseline, 20 and 50 s after coronary occlusion, and 2 min, 30 min, and 24 h after reperfusion in both proximal and distal at-risk segments and the remote nonischemic segment. Coronary occlusion induced a marked reduction in the systolic strain in both proximal and distal at-risk segments. Upon reperfusion, systolic deformation parameters retuned to near-normal pre-occlusion values. All values are mean ± SD. *p < 0.01, **p < 0.0001.

Comparisons of strain imaging diastolic index (SI-DI) values at baseline, 20 s after coronary occlusion, and 2 min, 30 min, and 24 h after reperfusion in both proximal and distal at-risk segments and the remote nonischemic segment. SI-DI values significantly decreased 20 s after coronary occlusion compared with those at baseline. Mean index was recovered but depressed 24 h after reperfusion. All values are mean ± SD. *p < 0.01, **p < 0.0001.

Two-dimensional (2D) speckle-tracking images in the apical long axis view (top) and transverse strain curves in mid-anteroseptal (orange curve), apical-anterior (green curve), and mid-inferolateral (purple curve) segments (bottom) obtained from a 65-year-old male patient with 90% coronary stenosis in segment 6 of the left anterior descending artery at baseline and 20 and 50 s after coronary occlusion (A) and 2 min, 30 min, and 24 h after coronary reperfusion (B). (A, top) The color bar of strain is set as yellow according to the increasing strain value. At 20 s after coronary occlusion, a high strain level (yellow arrow) appeared in at-risk segments at one-third diastole duration (1/3 DD) due to delayed relaxation; at 50 s, a low strain level (white arrow) developed in the same segments at end-systole, indicating ischemia-induced systolic dysfunction. (A, bottom) During coronary occlusion, peak strain was significantly decreased and significantly delayed in at-risk segments, and the strain imaging diastolic index was significantly decreased. (B, top) At 2 and 30 min after coronary reperfusion, a high strain level (yellow arrow) appeared in at-risk segments at 1/3 DD due to post-ischemic delayed relaxation or diastolic stunning. After 24 h, a faded yellow area is still present. (B, bottom) Immediately after reperfusion, peak strain significantly increased in the at-risk segments, which showed diastolic tardorelaxation at 30 min. The strain imaging diastolic index improved but remained depressed 24 h after reperfusion in the distal at-risk segment. 2D = 2-dimensional; AA = apical-anterior; AS = mid-anteroseptal; AVC = aortic valve closure; ECG = electrocardiogram; IL = mid-inferolateral.