Schulz-Menger Jeanette, Gross Michael, Messroghli Daniel, Uhlich Frank, Dietz Rainer, Friedrich Matthias G
Franz Volhard Clinic at the Max Delbrück Center, Helios-Klinikum, Berlin-Buch, Medical Faculty of the Charité, Department Cardiology, Humboldt University of Berlin, Berlin, Germany.
J Am Coll Cardiol. 2003 Aug 6;42(3):513-8. doi: 10.1016/s0735-1097(03)00717-4.
Very early changes in myocardial tissue composition during acute myocardial infarction (AMI) are difficult to assess in vivo. Cardiovascular magnetic resonance (CMR) imaging provides techniques for visualizing tissue pathology.
The diagnostic role of CMR in very acute stages of myocardial infarction is uncertain. We investigated signal intensity changes beginning within 60 min after acute coronary occlusion in patients undergoing therapeutic septal artery embolization.
We investigated eight patients with hypertrophic obstructive cardiomyopathy undergoing interventional septal artery embolization by applying microparticles to reduce left ventricular outflow tract obstruction. In a clinical 1.5-tesla (T) CMR system, we visualized infarct-related myocardial signal by T(1)-weighted sequences before and 20 min after administration of contrast media (delayed enhancement) and edema-related signal by T(2)-weighted spin-echo sequences before and 58 +/- 14 min after the intervention as well as on days 1, 3, 7, 14, 28, 90, and 180 during follow-up.
Infarct-related changes as defined by contrast enhancement were observed as early as 1 h after the intervention and during six months of follow-up. In contrast, infarct-related myocardial edema, as visualized by high signal intensity in T(2)-weighted spin-echo sequences, was not consistently detectable 1 h after acute arterial occlusion; this was possible in all subsequent studies until day 28.
Contrast-enhanced magnetic resonance imaging detected infarct-related signal changes as early as 1 h after AMI in humans, whereas the sensitivity of edema-related signal changes was not sufficient during this very early stage.
急性心肌梗死(AMI)期间心肌组织成分的极早期变化难以在体内进行评估。心血管磁共振(CMR)成像提供了可视化组织病理学的技术。
CMR在心肌梗死极急性期的诊断作用尚不确定。我们研究了接受治疗性间隔动脉栓塞的患者在急性冠状动脉闭塞后60分钟内开始的信号强度变化。
我们研究了8例肥厚性梗阻性心肌病患者,他们接受了介入性间隔动脉栓塞,通过应用微粒来减轻左心室流出道梗阻。在临床1.5特斯拉(T)CMR系统中,我们在注射造影剂前和注射后20分钟通过T1加权序列观察梗死相关心肌信号(延迟强化),并在干预前和干预后58±14分钟以及随访期间的第1、3、7、14、28、90和180天通过T2加权自旋回波序列观察水肿相关信号。
干预后1小时及随访6个月期间观察到了由对比增强定义的梗死相关变化。相比之下,通过T2加权自旋回波序列中的高信号强度显示的梗死相关心肌水肿在急性动脉闭塞后1小时不能始终如一地检测到;在随后直到第28天的所有研究中均能检测到。
对比增强磁共振成像在人类AMI后1小时即可检测到梗死相关信号变化,而在此极早期阶段,水肿相关信号变化的敏感性不足。