The authors review the pathophysiology of hypertriglyceridemic hyperapoB, focusing on the changes in lipoprotein particle
number and composition rather than lipoprotein lipid levels; summarize the in vitro and in vivo evidence that small, dense
low-density lipoprotein (LDL) are more atherogenic than normal larger, buoyant LDL; and delineate the particularly high-risk
state conferred by increased numbers of small, dense LDL.