首页> 外文期刊>Japanese heart journal >Fetal Cardiac Failure Resulting from Endocardial Fibroelastosis
【24h】

Fetal Cardiac Failure Resulting from Endocardial Fibroelastosis

机译:心内膜纤维弹性增生导致胎儿心脏衰竭

获取原文
       

摘要

An autopsy was performed on a female stillborn infant with generalized edema associated with ascites. On gross examination of the heart the pulmonary trunk was atretic from its origin of the heart to the bifurcation. The ductus arteriosus was abnormally wide. The right ventricle was hypoplastic and its endocardium was diffusely thickened. The inner surface of right ventricle appeared pale, obscuring the identification of trabeculae carneae and papillary muscles. At the posterior wall there was an extremely thin lesion where no apparent cardiac muscle was contained. The tricuspid orifice was stenotic and the valve was hypoplastic. The right atrium was markedly enlarged and its wall was thickened. The foramen ovale had patency of the valvular competent type. Atrial septal defect (ASD) was not present. The left ventricle was remarkably dilated with markedly thick wall. Ventricular septal defect (VSD) was present immediately beneath the right coronary cusp of the aortic valve.Light microscopic examination of the right ventricle revealed a marked increase of collagen and elastic fibers with extensive deposits of calcium not only in the endocardium but also in the deep portion of myocardium. Fibroelastosis appeared particularly prominent in the subendocardial layer. The muscle fibers surrounded by these penetrating fibers and deposits of calcium showed degeneration. The entire myocardial layer of the specific area in the right ventricle where the wall was paperthin was fully replaced by fibers and calcium. Inflammatory cell infiltration was found only at some places of the pericardium. The left ventricular wall also showed fibroelastosis, although the degree of involvement was much less as compared to that seen in the right ventricle. There were no significant pathological changes in both atria.
机译:对死于腹水的全身性水肿的死胎婴儿进行尸检。从心脏的总体检查来看,肺干从心脏起源到分叉处都是闭锁的。动脉导管异常宽。右心室发育不良,其心内膜弥漫性增厚。右心室的内表面发白,遮盖了小梁肌和乳头肌。在后壁有一个非常薄的病变,其中没有明显的心肌。三尖瓣口狭窄,瓣膜发育不良。右心房明显扩大,其壁增厚。卵圆孔通畅的瓣膜胜任型。不存在房间隔缺损(ASD)。左心室明显扩张,壁明显增厚。室间隔缺损(VSD)出现在主动脉瓣右冠状动脉的正下方。光学显微镜检查右心室显示胶原和弹性纤维明显增加,不仅在心内膜而且在深层中都有大量钙沉积心肌部分。纤维弹性增生在心内膜下层特别明显。这些穿透性纤维和钙沉积物所包围的肌肉纤维表现出变性。壁厚薄的右心室特定区域的整个心肌层被纤维和钙完全替代。仅在心包的某些部位发现炎性细胞浸润。左心室壁也显示纤维弹性增生,尽管其受累程度远小于右心室。两个心房均无明显病理改变。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号