Although lipoprotein(a) [Lp(a)] was first described more than 35 years ago,
adequate prospective data have only recently supported Lp(a) as an indepen
dent risk factor for coronary heart disease (CHD). in vitro studies suggest
that Lp(a) contributes to atherogenesis directly by cholesterol uptake and
indirectly by the inhibition of fibrinolysis. In patients with CHD or a si
gnificant risk for CHD, Lp(a) should be measured and treated with either ni
acin or estrogen if the patient has Lp(a) cholesterol levels of more than 1
0 mg/dL or an Lp(a) mass of more than 30 mg/dL. In addition, homocysteine a
nd remnant-like lipoprotein cholesterol are strongly supported by prospecti
ve or population-based prevalence data as independent risk factors for CHD.
Homocysteine revels of more than 14 mu mol/L should be treated with vitami
n supplements of folate, B-6, and B-12. Remnantlike lipoprotein cholesterol
is the product of a novel immunoassay that separates the partially hydroly
zed triglyceride-rich remnant particles. The association of these particles
with CHD risk in women may explain the small independent CHD risk that tri
glycerides have in women in the Framingham Heart Study. A clear therapeutic
intervention has not been documented but may include diet, fibric acid der
ivatives, or hydroxymethylglutamyl coenzyme A reductase inhibitors.