While two large clinical trials recently showed that adding niacin to statin therapy failed to improve clinical outcomes despite a significant increase in HDL-C levels, little is known about exactly why the increased HDL-C levels did not reduce the risk of cardiovascular events, including heart attack and stroke. Now, a small study from researchers the Perelman School of Medicine at the University of Pennsylvania, has shown that while niacin increased measured levels of HDL-C, it did not improve the functionality of HDL. This may provide an explanation for the failure of niacin to further reduce cardiovascular risk. The study results were reported today at the 62nd Annual Scientific Session of the American College of Cardiology in San Francisco (Abstract # 919-7).
"There is a major need to identify additional agents to target residual cardiovascular risk beyond the use of statins," said senior study author Daniel J. Rader, MD, professor of Medicine and chief, Division of Translational Medicine and Human Genetics, at Penn. "Niacin is one of the oldest players in this field and is often used clinically to increase HDL cholesterol levels. However, much to the disappointment of the medical community, recent trials of niacin added to standard LDL-lowering therapy with statins failed to show benefit in improving cardiovascular outcomes. There has been substantial recent interest in the function of HDL independent of HDL cholesterol levels. We performed a small trial to examine how niacin modulated a classic function of HDL, namely its ability to promote cholesterol removal from cells."
Previous work from Penn investigators has shown that a measure of HDL function, cholesterol efflux capacity, is more strongly related to coronary artery disease than HDL cholesterol levels.