Homocysteine modifies fibrin clot deformability: another possible explanation of harm.

ROJAS A. M.; KORDICH L.; LAURICELLA A. M.

BIORHEOLOGY

IOS PRESS

Lugar: Nieuwe Hemweg 6B, 1013 BG Amsterdam, The Netherlands.; Año: 2009 vol. 46 p. 379 - 387

0006-355X

Several studies have associated elevated plasma homocysteine (Hcy) levels with higher risk of thrombosis. In order to understand the mechanism(s) involved with homocysteine harmful action, we have studied the effect of this amino-acid on plasma fibrin-clot, measuring the viscoelastic clots’ response as a function of Hcy-concentration added to plasma (0, 50, 100, 250 and 500 mM). Storage (G') and loss (G") moduli were significantly higher than control at all Hcy concentrations evaluated in a dose-independent way (G’Hcy 50 µM 254±10 Pa vs 178±30 Pa, p=0,012; G”Hcy 50 µM 32±1 Pa vs 24±2 Pa, p=0,012). Increases observed in G' and G" values, as well as unchanged tan d (G’/G”) obtained from Hcy-clots with respect to control system (tan d Hcy 50 µM 0,130±0,007 Pa vs 0,150±0,020 Pa, NS), allowed us to conclude that Hcy action led to the stiffening of the clots formed. The higher linked fibrin network (higher G') contributed both to this structural behavior and to a higher compartmentalization and viscosity of the fluid phase (higher G") of the gel. The lower deformability of the clots formed after Hcy addition was also detected through deformation sweep assays. This material’s characteristics may lead to pathological behavior, increasing blood vessels’ obstruction.