Lim Pascal, Pasquet Agnès, Gerber Bernhard, D'Hondt Anne Marie, Vancraeynest David, Guéret Pascal, Vanoverschelde Jean Louis J
Division of Cardiology, Cliniques Universitaires Saint-Luc, Brussels, Belgium.
J Am Soc Echocardiogr. 2008 May;21(5):452-7. doi: 10.1016/j.echo.2007.09.004. Epub 2007 Oct 29.
During acute myocardial ischemia, myocardial postsystolic shortening (PSS) is considered as a sign of viability. In chronic left ventricular (LV) ischemic dysfunction, the value of PSS is less well established. In this study, PSS was compared with transmural extent of necrosis and contractile reserve in patients with chronic LV ischemic dysfunction.
A total of 25 patients (20 men, mean age: 63 +/- 8 years) with LV dysfunction (mean ejection fraction: 32 +/- 10%, range: 14%-47%) and stable coronary artery disease underwent rest color Doppler myocardial imaging, low-dose dobutamine echocardiography, and late enhancement gadolinium-magnetic resonance imaging. Strain (epsilon) curves were computed in 16 segments from color Doppler myocardial imaging sequences and were compared with transmural extent of necrosis and with contractile reserve. End-systolic epsilon was defined as epsilon value at aortic valve closure, peak epsilon (epsilon-peak) as maximal epsilon value during cardiac cycle, and time to epsilon-peak as time interval between aortic valve closure and epsilon-peak. PSS was considered when epsilon-peak occurred after aortic valve closure.
Of 348 analyzable segments, 212 (61%) were graded as abnormal. In dysfunctional segments, PSS was more prevalent in transmural than in nontransmural infarcted segments (96% vs 50%, P < .001) and time to epsilon-peak was correlated to transmural extent of necrosis (r = 0.69, P < .0001). In nontransmurally infarcted segments, prevalence of PSS was similar in segments with or without contractile reserve (37% vs 45%, respectively).
In chronic LV dysfunction, PSS is not a specific marker of viability. These results suggest strongly that delayed myocardial shortening may be associated to scarred segments.
在急性心肌缺血期间,心肌收缩后缩短(PSS)被视为存活的标志。在慢性左心室(LV)缺血性功能障碍中,PSS的价值尚未完全明确。在本研究中,对慢性LV缺血性功能障碍患者的PSS与透壁坏死范围及收缩储备进行了比较。
共有25例(20例男性,平均年龄:63±8岁)左心室功能障碍(平均射血分数:32±10%,范围:14%-47%)且冠状动脉疾病稳定的患者接受了静息彩色多普勒心肌成像、小剂量多巴酚丁胺超声心动图检查以及延迟强化钆磁共振成像。从彩色多普勒心肌成像序列中计算16个节段的应变(ε)曲线,并与透壁坏死范围及收缩储备进行比较。收缩末期ε定义为主动脉瓣关闭时的ε值,峰值ε(ε-peak)为心动周期中的最大ε值,达到ε-peak的时间为主动脉瓣关闭与ε-peak之间的时间间隔。当ε-peak在主动脉瓣关闭后出现时考虑为PSS。
在348个可分析节段中,212个(61%)被评为异常。在功能障碍节段中,PSS在透壁梗死节段比非透壁梗死节段更常见(96%对50%,P<.001),且达到ε-peak的时间与透壁坏死范围相关(r = 0.69,P<.0001)。在非透壁梗死节段中,有或无收缩储备的节段中PSS的发生率相似(分别为37%对45%)。
在慢性左心室功能障碍中,PSS不是存活的特异性标志物。这些结果强烈提示延迟的心肌缩短可能与瘢痕节段有关。