Rh. Gandhi et al., ANALYSIS OF THE CONNECTIVE-TISSUE MATRIX AND PROTEOLYTIC ACTIVITY OF PRIMARY VARICOSE-VEINS, Journal of vascular surgery, 18(5), 1993, pp. 814-820
Purpose: Valvular incompetence and venous wall abnormalities have been
suggested as primary etiologic factors responsible for the developmen
t of varicose veins. This study was conducted to evaluate the connecti
ve tissue constituents of greater saphenous varicosities. Proteolytic
activity, a factor that can lead to matrix degradation and cause weake
ning and dilation of the venous wall, was also assessed. Methods: The
collagen and elastin contents of 16 nonthrombophlebitic greater saphen
ous varicose veins (VV) and seven normal greater saphenous veins (NV)
were quantified. In addition, four duplex scanning-confirmed competent
segments of greater saphenous veins (i.e., potential varicose veins [
PV]) affected by varicosis at alternate sites were analyzed. Proteolyt
ic activity was determined by zymography and radiolabeled substrate as
say. Results: The content of collagen was significantly increased in t
he VV and PV compared with NV (VV = 189 +/- 7 mg/gm, PV = 189 +/- 9 mg
/gm vs NV = 144 +/- 10 mg/gm, p < 0.05). Conversely, the elastin conte
nt in the VV and PV was significantly reduced (VV = 53 +/- 3 mg/gm, PV
= 50 +/- 4 mg/gm vs NV = 74 +/- 4 mg/gm, p < 0.05). The collagen to e
lastin ratio demonstrated an alteration in VV and PV compared with NV
(VV = 3.7 +/- 0.3, PV = 3.9 +/- 0.4 vs NV = 2.0 +/- 0.2, p < 0.05). Ca
sein and gelatin zymography did not demonstrate significant qualitativ
e differences in the enzymatic activities among the three groups. Quan
titative analysis of the elastase activity in the venous tissues was s
imilarly not appreciably altered (VV = 5.1 +/- 0.2 U/gm, PV 5.3 +/- 0.
2 U/gm vs NV = 5.7 +/- 0.3 U/gm). Conclusion: A significant increase i
n the collagen content and a significant reduction in the elastin cont
ent of VV were demonstrated. The net increase in the collagen/elastin
ratio is indicative of an imbalance in the connective tissue matrix. T
he biochemical profile of PV was similar to VV and significantly diffe
rent from NV. These preliminary data support the presence of connectiv
e tissue abnormalities before valvular insufficiency. In addition, the
absence of an increase in the proteolytic activity excludes enzymatic
matrix degradation as an essential component in the formation of veno
us varicosities.