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犬房室瓣心内膜炎三度房室传导阻滞的解剖学基础。

The anatomical basis of third-degree atrioventricular block in dogs with atrioventricular valve endocardiosis.

机构信息

Laboratory of Veterinary Clinical Oncology, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan.

Laboratory of Veterinary Clinical Oncology, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan.

出版信息

J Comp Pathol. 2023 Feb;201:63-69. doi: 10.1016/j.jcpa.2022.12.014. Epub 2023 Jan 28.

DOI:10.1016/j.jcpa.2022.12.014
PMID:36709730
Abstract

The cardiac conduction system was examined histologically in 13 canine cases of atrioventricular (AV) valve endocardiosis with third-degree AV block. In all cases, gross examination revealed marked thickening and distortion of the base of the central fibrous body (CFB) and varying degrees of endocardial thickening of the upper portion of the ventricular septum (VS) as well as marked thickening of the mitral and tricuspid valve leaflets due to myxomatous degeneration. Microscopically, the thickened and distorted CFB had encased or trapped, either partly or totally, the underlying penetrating and branching portions of the AV bundle. The myxomatous and/or fibrofatty tissue, which had proliferated at the base of the extensive CFB, protruded into or encroached on the AV bundle, causing severe (51-75%) to very severe (76% or more) reduction of the conduction fibres. The upper portions of the left and right bundle branches were involved in the endocardial thickening due to degenerative and fibrotic changes at the uppermost VS; however, both bundle branches were much less severely affected than the AV bundle, the degree of reduction of the conduction fibres ranging from mild (25% or less) to moderate (26-50%). These observations suggest that the sites most vulnerable to lesions in the AV conduction system are the penetrating and branching portions of the AV bundle, which would represent the anatomical basis for third-degree AV block in canine cases of AV valve endocardiosis.

摘要

在 13 例伴有三度房室传导阻滞的房室瓣心内膜炎的犬心脏传导系统中进行了组织学检查。所有病例大体检查均显示中央纤维体(CFB)基部明显增厚和变形,室间隔上部心内膜不同程度增厚,二尖瓣和三尖瓣叶因黏液样变性而明显增厚。显微镜下,增厚和变形的 CFB 部分或完全包裹或困住了房室束的穿透和分支部分。在广泛的 CFB 基部增殖的黏液样和/或纤维脂肪组织突入或侵犯房室束,导致传导纤维严重(51-75%)至非常严重(76%或以上)减少。左、右束支的上部由于最上部室间隔的退行性和纤维化改变而受累于心内膜增厚;然而,与房室束相比,这两个束支的受影响程度要小得多,传导纤维的减少程度从轻度(25%或以下)到中度(26-50%)不等。这些观察结果表明,房室传导系统中最易受损的部位是房室束的穿透和分支部分,这将成为犬房室瓣心内膜炎三度房室传导阻滞的解剖学基础。

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