Retrospective analysis of dogs and cats with a mixed form of pulmonary hypertension and suspected pulmonary capillary hemangiomatosis in comparison to animals with predomination of precapillary pulmonary hypertension

Abstract

Background: Pulmonary capillary hemangiomatosis (PCH) is an idiopathic disease with the anomalous proliferation of a small capillary-like vessel in the pulmonary tissue, which can lead to a severe form of PH. There are only several cases of PCH described in veterinary literature: 27 cases in dogs and 2 cases in cats. In veterinary medicine, PH is mostly recognized as a consequence of left heart failure as a progression of the postcapillary PH to the precapillary form. PCH is mostly described as a primary disease, but resistant postcapillary PH with the high possibility of pulmonary edema raises speculation that PCH could be a secondary malformation to the left heart disease.

Aim: Discover the features associated with the shift between left- and right-sided heart disease in the context of PH development.

Methods: Retrospective analysis of materials from cats and dogs with histological markers of PCH (sPCH) versus those with right heart failure (RHF).

Results: Animals with histological and immunohistochemistry markers of PCH had a previous history of disease with left heart volume overload. There were no differences between the groups in radiography and gross pathology. Histologically, pulmonary fibrosis and arteriopathy could be found in RHF; in sPCH-a duplication of capillaries in alveolar septa and bizarre proliferation in surrounding structures.

Conclusion: PCH could be a secondary pattern of vascular remodeling due to volume overload.

Keywords: Pulmonary hypertension; canine; feline; pulmonary capillary hemangiomatosis.

Fig. 1.. Lateral thoracic radiographs of 2 dogs. Left one—RHF group, right -sPCH. Both presented with unstructured interstitial and local alveolar patterns.

Fig. 2.. Gross lungs pathology. Left one—sPCH, presented with numerous and patchy distributed blood-stained foci and zones with fibrous thickening of pleura. Right—RHF group, nodules and loci of white pale tissue on the surface diffusely distributed into the lobe tissue.

Fig. 3.. RHF group. Left top—aggressive lung remodeling, resembling organizing diffuse alveolar damage with collapse and fusion of the alveoli and loss of typical structure. Right top—tunica media and adventitia proliferation around pulmonary vessel. Left bottom—partial occlusion of pulmonary vessel. Right bottom—plexiform vasculopathy with lumen obstruction and revascularization, presented with onion-like structure. Stained with H&E.

Fig. 4.. sPCH group. Left (dog)—portions of alveolar septae with duplicated capillaries and capillaries proliferation into arterial walls. Right (cat)—less prominent septal alteration, significant arterial walls capillary proliferation. Stained with H&E.

Fig. 5.. sPCH group. Net-like capillaries organization in alveolar septa (cat).

Fig. 6.. RHF group. Immunohistochemistry. Left top right top, left bottom—factor von Willebrand active expression on endothelial surface in pulmonary vessels. Right bottom—absence of reaction on CD31 marker of endothelial cells.

Fig. 7.. sPCH group. Immunohistochemistry. Left—active expression of CD31 marker in numerous endothelial cells in alveolar septae. Right—almost absent of factor von Willebrand expression in cells.

Fig. 8.. Schematic representation of volume overload heart failure development.