LPA and metabolic syndrome: Whether this is due to an intensified influx and adhesiveness of Lp(a)-LDL particles into the vessel matrix (subendothelium) or insufficient pleiotropic of statins is not known and deserves further investigation, such as adding another arm in the comparison, namely AntiSense Oligonucleotide and siRNA targeting LPA. One speculation on the early age of events in a comparable dyslipidemia (LDL-cholesterol) setting is that Lp(a) might hinder an antiatherogenic mechanism which could be the release of LDL complex from the subendothelial layer of lesion prone arteries.