Assessment of Myocardial Ischemic Memory Using Persistence of Post-Systolic Thickening After Recovery From Ischemia
Assessment of Myocardial Ischemic Memory Using Persistence of Post-Systolic Thickening After Recovery From Ischemia
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DOI：
10.1016/j.jcmg.2009.07.008
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发表时间：
2009-11-01
影响因子：
14
通讯作者：
Nakatani, Satoshi
中科院分区：
文献类型：
--
作者：
Asanuma, Toshihiko;Uranishi, Ayumi;Nakatani, Satoshi
目的探讨心肌短暂缺血恢复后收缩后增厚（PST）和收缩异常的时间过程。心肌缺血记忆成像是一种理想的成像方法，可以显示缺血引起的异常，即使在灌注恢复后也能持续，并且可以在事后识别缺血损伤。PST是心肌缺血的敏感标志，但这种异常增厚在短暂缺血缓解后是否仍然存在尚不清楚。方法对27只犬在2种不同的心肌缺血条件下的组织应变超声心动图数据进行采集，分别是短暂冠状动脉闭塞（15或5分钟）后再灌注（方案1）或在非血流限制性狭窄期间多巴酚丁胺应激（方案2）。对峰值收缩应变和收缩后应变指数（PSI）进行了分析。结果在方案1中，闭塞时危险区域的峰值收缩应变显著降低。即使在再灌注后120分钟，15分钟组的峰值收缩应变的下降也没有完全恢复到基线水平，而5分钟组的下降在再灌注后立即恢复。我们发现，封堵时PSI显著升高，但5min组PSI升高持续至再灌注后30min(-0.19 +/- 0.18[基线]vs. 0.19 +/- 0.14 [30 min], p < 0.05)，尽管收缩峰值应变恢复迅速。在方案2中，PSI升高持续到多巴酚丁胺输注结束后20分钟（-0.26 +/- 0.11[基线]vs -0.16 +/- 0.10[20分钟]，p < 0.05），尽管峰值收缩应变在多巴酚丁胺输注结束后5分钟恢复。结论缺血恢复后PST维持时间长于收缩应变异常峰值。评估PST对检测心肌缺血记忆可能有价值。[J]中华医学会心脏科杂志2009；2:1253- 1261)(C) 2009
OBJECTIVES We sought to investigate the time course of post-systolic thickening (PST) and systolic abnormality after recovery from brief myocardial ischemia.BACKGROUND Myocardial ischemic memory imaging, denoting the visualization of abnormalities provoked by ischemia and sustained even after restoration of perfusion, is desirable and allows after-the-fact recognition of ischemic insult. PST offers a sensitive marker of myocardial ischemia, but whether this abnormal thickening remains after relief from brief ischemia is unclear.METHODS Tissue strain echocardiographic data were acquired from 27 dogs under 2 different conditions of myocardial ischemia induced by either brief coronary occlusion (15 or 5 min) followed by reperfusion (Protocol 1) or by dobutamine stress during nonflow-limiting stenosis (Protocol 2). Peak systolic strain and post-systolic strain index (PSI), a parameter of PST, were analyzed.RESULTS In Protocol 1, peak systolic strain was significantly decreased in the risk area during occlusion. This decrease in peak systolic strain in the 15-min group did not completely recover to baseline levels even 120 min after reperfusion, whereas the decrease in the 5-min group recovered immediately after reperfusion. We found that PSI was significantly increased during occlusion, but increased PSI in the 5-min group remained until 30 min after reperfusion (-0.19 +/- 0.18 [baseline] vs. 0.19 +/- 0.14 [30 min], p < 0.05) despite the rapid recovery of peak systolic strain. In Protocol 2, increased PSI was sustained until 20 min after the end of dobutamine infusion (-0.26 +/- 0.11 [baseline] vs. -0.16 +/- 0.10 [20 min], p < 0.05), although peak systolic strain recovered by 5 min after the end of dobutamine infusion.CONCLUSIONS PST remained longer than abnormal peak systolic strain after recovery from ischemia. Assessment of PST may be valuable for detecting myocardial ischemic memory. (J Am Coll Cardiol Img 2009; 2: 1253-61) (C) 2009 by the American College of Cardiology Foundation