Friedrich J, Apstein C S, Ingwall J S
Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Circulation. 1995 Dec 15;92(12):3527-38. doi: 10.1161/01.cir.92.12.3527.
The clinical course of a patient with a myocardial infarction (MI) depends largely on the ability of the noninfarcted region to remodel and compensate for the loss of the infarcted region. Previous studies have shown that the remaining viable myocardium remodels morphologically, functionally, and biochemically. The purpose of this study was to define the regional distribution of the biochemical remodeling that occurs after MI in rat hearts by use of a technique that could be applied noninvasively to human subjects.
Infarcts of the left ventricular apex and anterolateral wall were induced by occluding a coronary artery. Eight to 10 weeks after infarction, one-dimensional chemical shift imaging (CSI) was used to obtain 31P nuclear magnetic resonance (NMR) spectra of eight 2.5-mm-thick cross-sectional slices along the long axis (from base to apex) of isolated buffer-perfused rat hearts. Regional ATP and phosphocreatine (PCr) contents were compared in remodeled versus normal (sham) myocardium. Spin-echo 1H MR images identified the mass of each slice, allowing calculations of metabolite amount per unit myocardium in each slice. 1H MR images identify the hypertrophy of remodeled myocardium but do not discriminate between scar and viable tissue. In contrast, 31P CSI does distinguish viable tissue. Compared with shams, there was less 31P signal in the slices distal to the occlusion containing mainly scar tissue and increased signal intensity in slices proximal to the occlusion because of myocyte hypertrophy. The ATP signal intensity changed in direct proportion to the viable tissue mass in the slice, suggesting that the amount of ATP per unit mass in viable remodeled myocardium is the same as that of the shams. In contrast, the amount of PCr per unit mass in remodeled myocardium decreased. This decrease is uniform across the slices, correlates with infarct size, and parallels a similar decrease in tissue creatine content.
31P CSI of post-MI hearts shows that (1) PCr decreases uniformly (ie, independent of the distance from the scar) in the noninfarcted remodeled myocardium, and its amount inversely correlates with infarct size; and (2) the ATP signal provides a profile of viable myocardium and is a biochemical marker of morphological remodeling and hypertrophy that has occurred in noninfarcted regions. Thus, 31P CSI provides both a marker that tissue injury has occurred (decreased PCr) and a marker of the extent of remodeling in response to injury (ATP distribution) in a single set of noninvasive measurements.
心肌梗死（MI）患者的临床病程在很大程度上取决于未梗死区域重塑和代偿梗死区域损失的能力。先前的研究表明，剩余的存活心肌在形态、功能和生化方面会发生重塑。本研究的目的是通过一种可无创应用于人体受试者的技术，确定大鼠心脏心肌梗死后发生的生化重塑的区域分布。
通过阻断冠状动脉诱导左心室心尖和前侧壁梗死。梗死后8至10周，使用一维化学位移成像（CSI）获取沿离体缓冲灌注大鼠心脏长轴（从心底到心尖）的8个2.5毫米厚横截面切片的31P核磁共振（NMR）谱。比较重塑心肌与正常（假手术）心肌的区域ATP和磷酸肌酸（PCr）含量。自旋回波1H MR图像确定每个切片的质量，从而能够计算每个切片中每单位心肌的代谢物量。1H MR图像可识别重塑心肌的肥大，但无法区分瘢痕组织和存活组织。相比之下，31P CSI能够区分存活组织。与假手术组相比，主要包含瘢痕组织的闭塞远端切片中的31P信号较少，而由于心肌细胞肥大，闭塞近端切片中的信号强度增加。ATP信号强度与切片中的存活组织质量成正比变化，这表明存活的重塑心肌中每单位质量的ATP量与假手术组相同。相比之下，重塑心肌中每单位质量的PCr量减少。这种减少在各切片中是均匀的，与梗死面积相关，并且与组织肌酸含量的类似减少平行。
心肌梗死后心脏的31P CSI显示：（1）在未梗死的重塑心肌中，PCr均匀减少（即与距瘢痕的距离无关），其含量与梗死面积呈负相关；（2）ATP信号提供了存活心肌的概况，并且是未梗死区域发生的形态重塑和肥大的生化标志物。因此，31P CSI在一组无创测量中既提供了组织损伤发生的标志物（PCr减少），又提供了对损伤的重塑程度的标志物（ATP分布）。
