Abstract 13030: Post-systolic Shortening and Early Systolic Lengthening in the Ischemic Segment are Affected by the Contractility in its Adjacent Segment
Background: Post-systolic shortening (PSS) and early systolic lengthening (ESL) are sensitive markers of acute myocardial ischemia and the magnitude of these deformation is considered proportional to the severity of ischemia. Theoretical and mathematical models have suggested these deformation is caused by the difference of contractility between the ischemic and its adjacent normal segments. However, it has not been fully confirmed in an in vivo model yet. The aim of the study was to investigate whether PSS and ESL are affected by the contractility of its adjacent segment in an animal model which underwent left anterior descending coronary artery (LAD) occlusion (ischemic segment) followed by left circumflex coronary artery (LCx) occlusion (adjacent segment).
Methods: In 6 open-chest dogs, left ventricular short-axis images with frame rate of over 90 fps (GE Vivid E9) and hemodynamics data were acquired at 3 conditions: (1) at baseline, (2) during LAD occlusion, and (3) during both LAD and LCx occlusion. Circumferential strain was analyzed in the LAD and LCx segments by speckle tracking software. End-systolic strain (εES) and the amplitude of PSS and ESL (εPSS and εESL) were measured.
Results: During LAD occlusion, εPSS and εESL in the LAD segment significantly increased compared with baseline (εPSS, 1.2 ± 1.1% vs. 9.5 ± 2.7%, p<0.05; εESL, 1.3 ± 1.0% vs. 8.5 ± 4.2%, p<0.05). During both LAD and LCx occlusion, εES in the LCx segment decreased, and both εPSS and εESL in the LAD segment significantly decreased compared with during LAD occlusion (εPSS, 9.5 ± 2.7% vs. 2.8 ± 1.3%, p<0.05; εESL, 8.5 ± 4.2% vs. 2.3 ± 1.9%, p<0.05) (figure).
Conclusions: PSS and ESL diminished with the decrease of contractility in its adjacent segment. This suggests PSS and ESL occur based on the interplay of contraction between ischemic and adjacent segments and do not always reflect the severity of ischemia.
Author Disclosures: D. Sakurai: None. T. Asanuma: None. K. Masuda: None. M. Oka: None. K. Kotani: None. K. Inoue: None. S. Nakatani: None.
- © 2014 by American Heart Association, Inc.