What is the role of fibric acid derivatives in the treatment of noncoronary atherosclerosis?

Updated: Dec 23, 2019
  • Author: F Brian Boudi, MD, FACP; Chief Editor: Yasmine S Ali, MD, FACC, FACP, MSCI  more...
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The precise mechanism of action of this class of drugs is complex and incompletely understood. These agents increase the activity of lipoprotein lipase and enhance the catabolism of triglyceride-rich lipoproteins, which is responsible for an increase in the HDL cholesterol fraction.

A decrease in hepatic very low-density lipoprotein (VLDL) synthesis and an increase in cholesterol excretion into bile also appear to occur. The fibrates typically reduce triglyceride levels by 20-50% and increase HDL cholesterol levels by 10-15%. The decrease in VLDL and triglyceride levels results from the ability of fibric acid derivatives to enhance the synthesis of lipoprotein lipase.

The effect of fibric acid derivatives on LDL cholesterol is variable. Levels may be expected to decrease by 10-15%. In patients with marked hypertriglyceridemia, LDL cholesterol levels may increase, which likely reflects the ability of the LDL receptor to clear the increased LDL generated by increased VLDL catabolism.

Fibrate therapy may also be responsible for a decrease in the clotting ability of platelets and fibrinogen levels, which may account for some of the reported clinical benefits.

Fibric acid derivatives include fenofibrate (Tricor) and gemfibrozil (Lopid).

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