Abstract 15109: Afterload Is a Determinant of Persistence of Myocardial Ischemic Memory Assessed by Post-Systolic Thickening
Background Post-systolic thickening (PST), which is defined as myocardial contraction after aortic valve closure, is a sensitive marker of ischemia and remains even after restoration of perfusion (myocardial ischemic memory). However, determinants of persistence of ischemic memory assessed by PST are still unclear. Because myocardial deformation is affected by afterload, we hypothesized that the duration of PST detected after relief from brief ischemia could be prolonged with afterload augmentation.
Methods Left circumflex artery was occluded for 2 minutes followed by 60-minute reperfusion in 11 dogs. In 7 of the 11 dogs, phenylephrine (PE) was infused throughout coronary occlusion and reperfusion to mildly increase afterload (1.0 μg/kg/min). For speckle tracking analysis, short-axis images were acquired at baseline, during occlusion, and after reperfusion using Vivid 7 (GE). Peak systolic radial strain (εS) and strain rate (SRS) were analyzed in the risk and normal areas. Post-systolic index (PSI) and peak positive strain rate during isovolumic relaxation (SRIVR) were also measured as parameters of PST.
Results Left ventricular systolic pressure increased about 27±5 mmHg during PE infusion. In the risk area, εS and SRS decreased during occlusion and recovered immediately after reperfusion regardless of PE. PSI and SRIVR increased during occlusion and recovered to the baseline level about 30 min after reperfusion without PE. However, it sustained to be elevated even 60 min after reperfusion with PE (Figure). PSI and SRIVR at 60min after reperfusion with PE were significantly higher compared to the baseline levels (PSI: 0.10±0.09 vs. 0.24±0.17, p<0.05; SRIVR: 0.47±0.30 vs. 0.94±0.49 /s, p<0.05)
Conclusion The duration of PST detected after relief from brief ischemia was prolonged with afterload augmentation. Afterload seems to be a determinant of persistence of myocardial ischemic memory assessed by post-systolic thickening.
- © 2011 by American Heart Association, Inc.