Abstract
Diffuse atherosclerosis is the primary reason for late graft failure after cardiac transplantation. Because there is increasing evidence that imbalances in the hemostatic and fibrinolytic pathways are associated with allogeneic rejection, we hypothesized that atherothrombotic risk factors may contribute to accelerated atherosclerosis. We therefore prospectively evaluated the burden of coronary atherosclerosis by intravascular ultrasound (IVUS) in 20 patients and measured plasma fibrinogen (FGN). lipoprotein (a) (Lp(a)) and net fibrinolytic activity of plasma using a standard fibrin plate assay. Intimal thickening was quantified using IVUS by measuring the intimal index (li = intimal area/[intimal area + luminal area]) in 2–5 segments of the LAD using planimetry. The maximal Ii per patient was calculated and indexed to the time post-transplant (Mxli/Yr). FGN predicted severity of Mxli/Yr (r 2 = 0.41, p = 0.008). In patients with decreased plasma fibrinolytic activity (lytic zone < 100 mm 2 ). Mxli/Yr was increased ten-fold (0.21 ± 0.17 vs. 0.02 ± 0.02, p = 0.002). Because Lp(a) colocalizes with fibrinogen in the vessel wall and inhibits fibrinolysis, we correlated plasma Lp(a) levels with the degree of intimal thickening. Lp(a) did not predict Mxli/Yr (p = NS). In conclusion, these data suggest that plasma FGN and net fibrinolytic activity predict the degree of intimal thickening and that fibrin deposition may play an integral role in diffuse coronary atherosclerosis after cardiac transplantation.
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