Dilated cardiomyopathy (DCM) is among the most common cardiac diseases in dogs. Its pathogenesis is not fully understood, but myocardial remodeling and inflammation are suspected to be involved. The present study aimed to characterize the pathological processes in canine DCM, investigating morphological changes in association with the expression of relevant cytokines and remodeling markers. The myocardium of 17 dogs with DCM and 6 dogs without cardiac diseases was histologically evaluated, and selected cases were further examined by immunohistochemistry, morphometry, and reverse transcription quantitative PCR. In DCM, the myocardium exhibited subtle but statistically significant diffuse quantitative changes. These comprised increased interstitial collagen deposition and macrophage numbers, as well as an overall reduced proportion of contractile tissue. This was accompanied by a significant increase in myocardial transcription of intracellular adhesion molecule (ICAM) 1, inflammatory cytokines, and remodeling enzymes. Laser microdissection showed that cardiomyocytes transcribed most relevant markers including ICAM-1, tumor necrosis factor α, transforming growth factor β (TGF-β), matrix metalloproteinase 2 (MMP-2), tissue inhibitor of MMP (TIMP) 1 and TIMP-2. In addition, there were multifocal cell-rich lesions characterized by fibrosis, neovascularization, macrophage infiltration, and cardiomyocyte degeneration. In these, macrophages were often found to express ICAM-1, TGF-β, and vascular endothelial growth factor; the former two were also expressed by cardiomyocytes. These results characterize the diffuse myocardial remodeling processes that occur in DCM. The observed multifocal cell-rich lesions might result from reduced tissue perfusion. Macrophages and cardiomyocytes seem to actively contribute to the remodeling processes, which ultimately lead to cardiac dilation and dysfunction. The precise role of the involved cells and the factors initiating the remodeling process still needs to be identified.

中文翻译：

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犬扩张型心肌病：弥漫性重塑，局灶性病变以及巨噬细胞累及和新血管形成。

扩张型心肌病（DCM）是犬中最常见的心脏病。其发病机理尚未完全明了，但怀疑与心肌重塑和炎症有关。本研究旨在表征犬DCM中的病理过程，研究与相关细胞因子和重塑标记物表达相关的形态变化。对17只患有DCM的狗和6只没有心脏病的狗的心肌进行组织学评估，并通过免疫组织化学，形态计量学和逆转录定量PCR进一步对选定的病例进行检查。在DCM中，心肌表现出细微但统计上显着的弥散定量变化。这些包括增加的间质胶原沉积和巨噬细胞数量，以及收缩组织比例整体下降。这伴随着细胞内粘附分子（ICAM）1，炎症细胞因子和重塑酶的心肌转录显着增加。激光显微切割显示心肌细胞转录了最相关的标志物，包括ICAM-1，肿瘤坏死因子α，转化生长因子β（TGF-β），基质金属蛋白酶2（MMP-2），MMP组织抑制剂（TIMP）1和TIMP-2 。此外，还有多灶性富含细胞的病变，其特征在于纤维化，新血管形成，巨噬细胞浸润和心肌变性。其中，经常发现巨噬细胞表达ICAM-1，TGF-β和血管内皮生长因子。前两个也由心肌细胞表达。这些结果表征了DCM中发生的弥漫性心肌重塑过程。观察到的多灶细胞丰富病变可能是由于组织灌注减少所致。巨噬细胞和心肌细胞似乎积极地参与了重塑过程，最终导致心脏扩张和功能障碍。仍然需要确定参与细胞的确切作用以及引发重塑过程的因素。