It is possible that in subjects with
elevated triglyceride levels, the postprandial state not only
redistributes apo(a) to VLDL; it may also extend the plasma
residence of apo(a) relative to apoB-100 within Lp(a), thereby,
enhancing the profile of Lp(a) particles, especially
in individuals with apo(a) isoforms of lower molecular weight.
Future studies need to be done in hypertriglyceridemic
subjects while in the fed state, with therapeutic agents
known to affect the synthesis and catabolism of the individual
apolipoprotein components of Lp(a).