-transparent.png){kind=logo}
OBJECTIVE Valvular incompetence and venous wall abnormalities have been suggested as primary etiologic factors responsible for the development of varicose veins. This study was conducted to evaluate the connective tissue constituents of greater saphenous varicosities. Proteolytic activity, a factor that can lead to matrix degradation and cause weakening and dilation of the venous wall, was also assessed. METHODS The collagen and elastin contents of 16 nonthrombophlebitic greater saphenous 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. Proteolytic activity was determined by zymography and radiolabeled substrate assay. RESULTS The content of collagen was significantly increased in the 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 content 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 elastin 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). Casein and gelatin zymography did not demonstrate significant qualitative differences in the enzymatic activities among the three groups. Quantitative analysis of the elastase activity in the venous tissues was similarly 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). CONCLUSIONS A significant increase in the collagen content and a significant reduction in the elastin content of VV were demonstrated. The net increase in the collagen/elastin ratio is indicative of an imbalance in the connective tissue matrix. The biochemical profile of PV was similar to VV and significantly different from NV. These preliminary data support the presence of connective 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 venous varicosities.
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
December 1979,
Angiology,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
May 1985,
Angiology,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
November 1976,
Sovetskaia meditsina,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
September 1964,
British medical bulletin,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
March 1995,
Angiology,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
March 1990,
Journal of vascular surgery,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
January 2016,
Angiologiia i sosudistaia khirurgiia = Angiology and vascular surgery,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
October 1986,
Angiology,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
March 1956,
Canadian Medical Association journal,
R H Gandhi, and
E Irizarry, and
G B Nackman, and
V J Halpern, and
R J Mulcare, and
M D Tilson
January 1983,
Blood vessels,
