Pathological changes of chronic venous insufficiency is characterized by intimal and medial fibrosis of venous wall. Our aim was to link the correlation between Doppler sonography data and the degree of intimal and medial lesions in varicose saphenous veins at different locations.
Saphenous veins from ten patients were evaluated by Doppler sonography and inmunohistochemestry. smooth muscular actin, and vimentin were studied from normal to pathological vein lesions. Collagen fibers distribution and extracellular matrix were also studied by Red Sirius Stain. Elastogenesis was studied by confocal microscopy and orcein stain. The evaluation of each molecule was explored using almost two slides per case. Quantification of these molecules and structures were made by Image J software.
In initial lesions of varicose vein, intimal layer double their size compared to normal wall vein. Present a progressive increase of extracellular matrix and myofibroblast (vimentin+ and SMA+) proliferation. At severe intimal varicose lesions, lumen of vein decreased, and Doppler sonography blood flow was lower. In this field we observed thickness in intimal wall, corresponding to significatilly increase of SMA+ cells and elastics fibers deposition.
The morphometric data showed that SMA+ area at intimal layer is correlated negatively to intimal thickness. In addition, quantification of elastic fibers at intimal varicose veins is significantly high compared to normal vein. Correlation between elastics fibers area and intimal high were negative. In the intima, a deposition of elastic fibers, which were shorter and disorganized was observed. The vascular medial layer shows atrophy of smooth muscular cells and presence of fibrous tissue. The intimal and medial fibrotic changes were not related to mast cell or immunocompetent cells proliferation.
These data suggest a progressive transformation from normal to pathological varicose vein. In the eco Doppler sonography area reflux of varicose veins, we found a well established intimal and medial lesions characterized by fibrotic tissue and loss of SMA cells. These lesions are an irreversible fibrotic process in patients with leg chronic venous insufficiency.