Abstract 12842: Regional Relaxation Abnormality Does Not Precede Regional Contraction Abnormality in the Ischemic Myocardium Immediately After Coronary Occlusion
Background: Although it has been reported that diastolic dysfunction precedes systolic dysfunction in the whole ventricle in the ischemic cascade, it is unclear whether the relaxation abnormality precedes the contraction abnormality in the region of ischemic insult. We investigated the beat-by-beat change of contraction and relaxation parameters after coronary occlusion.
Methods: In 13 open-chest dogs, left ventricular short-axis images were continuously acquired with high frame rate speckle tracking echocardiography (109.3 fps, GE Vivid E9) along with hemodynamic data before and after left circumflex coronary artery occlusion (20 consecutive heartbeats after occlusion). Circumferential strain and strain rate were analyzed in the ischemic and non-ischemic regions. Peak systolic strain (εs), end-systolic strain (εes), and contraction duration as regional contraction parameters and the first positive peak of the strain rate (SRfirst positive peak) as a regional relaxation parameter were measured.
Results: Negative dP/dt began to decrease and tau began to prolong after the 15th beat of occlusion. In the ischemic region, εes and contraction duration significantly decreased after the 15th beat, and εs significantly decreased at the 20th beat. However, SRfirst positive peak did not decrease during 20 consecutive heartbeats but rather significantly increased after the 15th beat (0.51 ± 0.10 vs. 1.34 ± 0.15 /s, p<0.05). Because the contraction duration was prolonged in the non-ischemic region after the 15th beat, dyssynchrony during the isovolumic relaxation period became remarkable (figure, arrowheads).
Conclusions: In the ischemic myocardium immediately after coronary occlusion, the regional relaxation parameter did not become abnormal before the contraction parameter became abnormal. The deterioration of diastolic parameters for the whole ventricle (negative dP/dt and tau) seemed to be due to dyssynchrony during the isovolumic relaxation period.
Author Disclosures: E. Iwagami: None. T. Asanuma: None. K. Masuda: None. D. Sakurai: None. T. Kamimukai: None. S. Nakatani: None.
- © 2015 by American Heart Association, Inc.