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在一只拳师犬中,致心律失常性右心室心肌病与左心室壁内层肌肉层的心脏纤维化同时出现。

Arrhythmogenic right ventricular cardiomyopathy coincided with the cardiac fibrosis in the inner muscle layer of the left ventricular wall in a boxer dog.

作者信息

Yamada Naoaki, Kitamori Takashi, Kitamori Fumiyo, Ishigami Kanako, Iwanaga Koji, Itou Taiki, Kobayashi Ryosuke, Kumabe Shino, Doi Takuya, Sato Junko, Wako Yumi, Tsuchitani Minoru

机构信息

Pathology Department, Kashima Laboratory, Nonclinical Research Center, LSI Medience Corporation, 14-1 Sunayama, Kamisu-shi, Ibaraki 314-0255, Japan.

出版信息

J Vet Med Sci. 2015 Oct;77(10):1299-303. doi: 10.1292/jvms.14-0513. Epub 2015 May 8.

DOI:10.1292/jvms.14-0513
PMID:25959955
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4638300/
Abstract

A 7-year-old female boxer dog died suddenly without any clinical signs. It was suspected that the dog had arrhythmogenic right ventricular cardiomyopathy (ARVC) due to ventricular premature complexes and ventricular tachycardia at 3 years of age. The final diagnosis of ARVC was confirmed by histological characteristics, such as loss of cardiocytes and fibrofatty replacement, occurring in the right and left ventricular walls. In the cardiocytes, non-lipid vacuoles were observed. Cardiac fibrosis and intimal thickening of the small arteries occurred without fatty replacement in the inner muscle layer including the papillary muscles of the left ventricular wall. This paper describes the pathomorphological details of an ARVC case with coincidental cardiac fibrosis in the inner muscle layer of the left ventricular wall.

摘要

一只7岁的雌性拳师犬突然死亡,生前无任何临床症状。该犬3岁时因室性早搏和室性心动过速被怀疑患有致心律失常性右室心肌病(ARVC)。通过组织学特征,如左右心室壁出现心肌细胞丢失和纤维脂肪替代,最终确诊为ARVC。在心肌细胞中观察到非脂质空泡。左心室壁包括乳头肌在内的内层肌肉出现心脏纤维化和小动脉内膜增厚,但无脂肪替代。本文描述了一例左心室壁内层肌肉合并心脏纤维化的ARVC病例的病理形态学细节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/802423d0f576/jvms-77-1299-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/79411e0ae8f3/jvms-77-1299-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/91c4ac59e3ca/jvms-77-1299-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/b48b1cca6241/jvms-77-1299-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/7327e618a6e9/jvms-77-1299-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/802423d0f576/jvms-77-1299-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/79411e0ae8f3/jvms-77-1299-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/91c4ac59e3ca/jvms-77-1299-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/b48b1cca6241/jvms-77-1299-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/7327e618a6e9/jvms-77-1299-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2727/4638300/802423d0f576/jvms-77-1299-g005.jpg

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本文引用的文献

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Electrophysiological abnormalities precede overt structural changes in arrhythmogenic right ventricular cardiomyopathy due to mutations in desmoplakin-A combined murine and human study.致心律失常性右室心肌病的心肌致密化不全相关基因突变导致电生理异常早于明显的结构改变:一项结合了鼠类和人类的研究。
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Acta Myol. 2017 Sep 1;36(3):135-150. eCollection 2017 Sep.
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