Pathological Structural Alterations of Serous Cell Cilia in the Parietal Pericardium of Patients With Heart Failure Induced by Dilated Cardiomyopathy.

BACKGROUND

This study aimed to examine pathological surface structural changes in serous cells of the pericardial parietal layer in patients with heart failure due to dilated cardiomyopathy.

METHODS

Pericardial tissues from five patients with dilated cardiomyopathy-induced heart failure (case group) and two heart donors (control group) were analyzed using histological methods, scanning electron microscopy (SEM), transmission electron microscopy (TEM), and immunofluorescence.

RESULTS

In both groups, mesothelial cells in the parietal pericardium were classified as flat, oval, or short columnar, typically forming a single layer, occasionally multiple layers. Most cells exhibited a brush-like border on the surface facing the pericardial cavity. A layer of flattened fibroblasts was observed beneath the basement membrane. Polygonal cells extended protrusions to contact adjacent cells. Mesothelial cells were further divided into ciliated and non-ciliated types. Most cells displayed numerous typical cilia on their surface, whereas non-ciliated cells extended processes that spanned one or more cells to connect with distant cells. TEM revealed that most ciliated mesothelial cells had uniformly arranged cilia, with visible microtubules in some. Tight junctions, intermediate junctions, and desmosomes were present along the lateral surfaces of mesothelial cells, and the basement membrane appeared uniform. Compared with normal pericardial mesothelium, mesothelial cells from patients exhibited increased numbers of cilia, ciliary edema, microtubule dissolution within cilia, and elevated expression of β-tubulin.

CONCLUSIONS

Abundant cilia are present on the surface of mesothelial cells in the parietal pericardium of both healthy individuals and patients. Heart failure induced by dilated cardiomyopathy can severely damage the morphology and ultrastructure of mesothelial cilia, leading to reduced ciliary motility and impaired secretion and absorption, thereby disrupting pericardial fluid production and reflux.