Dyslipidemias in patients with coronary heart disease confer a greater
risk of ischemic cardiac events than comparable dyslipidemias in peop
le free of disease. A major dyslipidemia can be diagnosed in more than
80% of patients with established premature coronary heart disease. Th
ese dyslipidemias constitute not only elevations of low-density lipopr
otein cholesterol (hypercholesterolemia) but also indicate abnormaliti
es in the metabolism of triglyceride-rich lipoproteins, high-density l
ipoproteins, and lipoprotein(a). Clinical trials have demonstrated tha
t therapy to lower low-density lipoprotein levels can delay angiograph
ic progression of coronary stenoses and reduce recurrent cardiac event
rates. These clinical benefits from low-density lipoprotein cholester
ol lowering may occur as early as 6 to 12 months after initiation of t
herapy. Intervention strategies for dyslipidemias are directed toward
lowering the low-density lipoprotein cholesterol fraction to 90 to 100
mg/dl. This approach begins with dietary modification, weight loss, s
moking cessation, and aerobic exercise. Patients with hypercholesterol
emia refractory to nonpharmacologic intervention require lipid-lowerin
g agents. The choice of lipid-lowering medications is influenced by co
ncomitant abnormalities of lipoprotein metabolism, such as hypertrigly
ceridemia or hypoalphalipoproteinemia. Treatment of primary dyslipidem
ias other than hypercholesterolemia may be warranted in die presence o
f other cardiac risk factors; however, a broader spectrum of clinical
trial data is needed to support or refute this contention.