Maehashi N, Yokota Y, Takarada A, Seo T, Kubo M, Nakanishi O, Toh S, Usuki S, Fukuzaki H, Sugiyama T
First Department of Internal Medicine, Kobe University School of Medicine.
J Cardiol. 1987 Jun;17(2):273-84.
Relationships between segmental left ventricular wall motion abnormalities and myocardial fibrosis at autopsy were examined in 12 patients who died of dilated cardiomyopathy. In each case, wall motion abnormalities were assessed by two-dimensional echocardiograms for 11 segments, and semiquantitatively evaluated as normokinesis (N) to hypokinesis (H), severe hypokinesis (SH) or akinesis (A). From the necropsy specimens, the myocardial fibrosis ratio was histologically quantitated using a point-counting method in each segment corresponding to the echocardiographic segment. Wall motion abnormalities and the fibrosis ratio correlated significantly in a total of 132 segments of the 12 patients, but there were some discordances. The cases were then categorized in uniform and non-uniform groups based on the patterns of myocardial fibrosis. Wall motion abnormalities correlated much better with the fibrosis ratio in a total of 44 segments among four cases with non-uniform fibrosis, whereas no significant correlation was found in a total of 88 segments in eight cases with uniform fibrosis. The latter group had more severe segmental wall motion abnormalities in the interventricular septum than in the left ventricular free wall; and in the apical portion rather than in the basal portion, although no significant difference was observed in the fibrosis ratio among these regions. Patients with non-uniform fibrosis had higher incidences of chest pain and sudden deaths and a significantly larger left ventricular end-diastolic dimension on M-mode echocardiogram as compared to those with uniform fibrosis. Pathologically, in the former group, the heart was heavier, the mean left ventricular fibrosis ratio was significantly higher, and there was a greater incidence of infiltration of the myocardium by mononuclear cells, but there was no difference in the mean left ventricular wall thickness. These results suggest that myocardial fibrosis mainly contributes to the wall motion abnormalities in cases with non-uniform fibrosis which may be caused by chronic myocarditis, but not in cases with uniform fibrosis. In the latter group, other factors such as reduced contractility of the myocardial cells or lack of a compensatory mechanism for wall stress seem to play important roles in causing left ventricular wall motion abnormalities.
对12例死于扩张型心肌病的患者进行尸检，研究节段性左心室壁运动异常与心肌纤维化之间的关系。在每例患者中，通过二维超声心动图评估11个节段的壁运动异常，并半定量地评价为正常运动（N）至运动减弱（H）、严重运动减弱（SH）或运动消失（A）。从尸检标本中，采用点计数法对与超声心动图节段相对应的每个节段的心肌纤维化比例进行组织学定量。12例患者共132个节段的壁运动异常与纤维化比例显著相关，但也存在一些不一致的情况。然后根据心肌纤维化的模式将病例分为均匀组和非均匀组。在4例非均匀纤维化病例的总共44个节段中，壁运动异常与纤维化比例的相关性更好，而在8例均匀纤维化病例的总共88个节段中未发现显著相关性。后一组在室间隔的节段性壁运动异常比左心室游离壁更严重；在心尖部而非基部更严重，尽管这些区域的纤维化比例没有观察到显著差异。与均匀纤维化患者相比，非均匀纤维化患者胸痛和猝死的发生率更高，M型超声心动图上左心室舒张末期内径显著更大。病理上，在前一组中，心脏更重，平均左心室纤维化比例显著更高，单核细胞浸润心肌的发生率更高，但平均左心室壁厚度没有差异。这些结果表明，心肌纤维化主要导致非均匀纤维化病例的壁运动异常，非均匀纤维化可能由慢性心肌炎引起，而均匀纤维化病例则不然。在后一组中，其他因素如心肌细胞收缩力降低或壁应力缺乏代偿机制似乎在导致左心室壁运动异常中起重要作用。
