VASCULAR REMODELING IN VARICOSE-VEINS

The present study describes the histopathologic aspects of varicose (n =29; mean age, 52 +/- 12 years) and normal saphenous veins (n=17; mean age, 51 +/- 12 years) of patients from a similar age group. We focuse d on the changes that occur in the circular layer of the venous wall. We examined the venous walls by light microscopy and transmission elec tronmicroscopy. A semiquantitative grading system was used to assess t he smooth muscle cell (SMC) hypertrophy and the change that occurs in the elastin pattern. The volume densities (V-v) of SMC and collagen we re measured as well as the diameter of the SMC, and the nuclei of SMC per fixed area were counted. The varicose vein wall differed from the normal saphenous vein by the presence of hypertrophic SMC as well as d isorganized elastin patterns. A correlation between the hypertrophic S MC and an abnormal elastin pattern was observed (r=0.658, p<0.001). Ul trastructurally, the SMC show prominent microherniations and vesicles that bud from the cell. These vesicles contain microfilaments and micr otubuli, although no other organelles could be detected. The elastin f ibers are disrupted from the hypertrophic SMC. No significant differen ce could be detected in both the V-v of SMC and the V-v of collagen. T he diameter of the SMC in the varicose vein (d=9.45 +/- 1.22 mu m) dif fers significantly from that in the normal saphenous vein (d=6.22 +/- 1.47 mu m) (p<0.001). Also, the nuclei of SMC per fixed area differs s ignificantly between the varicose (87 +/- 18) and nonvaricose (117 +/- 24) veins (p<0.001). We conclude that the cellular hypertrophy of the SMC and the microherniations could be the basis for disruption of the elastin fibers connected to the SMC in varicose veins. Disrupted conn ections between SMC and elastin fibers could in turn induce the weakne ss of the venous wall observed in varicose vein disease.