Introduction: In chronic venous insufficiency (CVI), an increase in venous pressure causes the passage of intravascular blood cells and molecules into the surrounding tissues and induces histopathological changes in the lower extremities, leading to increased pigmentation in the legs, ulceration, and
tissue loss to various degrees. This study aimed to investigate whether an increase in venous pressure in the coronary veins can lead to the aforementioned histopathological changes. Material and methods: Twenty-four New Zealand rabbits were divided into the following three groups: experimental model of coronary venous hypertension (CVH) (n= 8), sham group (n= 8), and control group (n= 8). After 21 days postoperatively, tissue samples from each group were compared for perivascular inflammation, erythrocyte extravasation, macrophage infiltration, and hemosiderin deposits by histopathological scoring under a light microscope. Matrix metalloproteinase-2 (MMP-2) activation was evaluated using immunohistochemical staining.
Results: In the CVH group, hemosiderin accumulation was significantly higher than in the sham and control groups (1.0 (1.0–3.0), 0.0 (0.0–1.0), 0.0 (0.0–0.0); p< 0.001). Immunohistochemically, in the CVH group, MMP-2 levels were significantly higher than in the sham and control groups (2.0 (1.0–3.0), 0.0 (0.0–1.0), 0.0 (0.0–0.0); p< 0.001).
Conclusions: This experimental study showed for the first time the histopathological and immunohistochemical changes in myocardial tissue, similar to those observed in CVI, as a result of increased coronary venous pressure due to coronary vein ligation. Further studies are needed to understand the clinical implications of these results.
Keywords: coronary veins, hemosiderin, Thebesian valve, vein occlusion, venous insufficiency.