New experimental evidence in vivo suggests that, upon entrance into the arterial intima, IDL and VLDL become trapped at least to the same extent as LDL, and that lipoprotein(a) in normal arteries becomes trapped to the same extent as LDL. In the injured vessel, however, lipoprotein(a) seems to be trapped more than LDL. Further, new evidence also suggests that mildly oxidized LDL may circulate in plasma for a period long enough to enter, accumulate, and be degraded in the arterial intima in preference to normal LDL.