Factors influencing the accumulation in fibrous plaques of lipid derived from low density lipoprotein. I. Relation between fibrin and immobilization of apo B-containing lipoprotein.

The lipid that accumulates in some fibrous atherosclerotic lesions appears to be derived from plasma low density lipoprotein (LDL). An early stage in lipid accumulation may be immobilization of a fraction of the LDL, and this is released by incubation with proteolytic enzymes, of which the most effective is the fibrinolytic enzyme, plasmin. We have examined the relationship between release of fibrin degradation products (FDP) and LDL in controlled plasmin incubations of 42 samples of normal intima and atherosclerotic lesions from aortas of 10 patients. In three patients (group 1) no LDL was released from any of the 11 tissue samples although they comprised lesions as well as normal intima. In 2 more patients (group 2) LDL was consistently low. However, in 5 patients (group 3) substantial amounts of LDL were released from all 21 tissue samples, and there was a significant correlation between the amounts of FDP and LDL (P less than 0.001). In spite of this correlation there were marked differences in the ratio FDP/LDL, but analysis by SDS-polyacrylamide gel electrophoresis and immuno blotting of the FDP released showed no consistent pattern related to LDL binding. Although the ratio FDP/LDL showed a 4-fold range, in 6 lesions subjected to successive 2-h incubations with plasmin the ratio within each lesion remained constant, supporting the concept that fibrin and LDL are linked.