If LDL cholesterol is well-controlled with statins, adding high doses of extended-release niacin to increase low levels of HDL cholesterol won't further lower your risk of myocardial infarction or stroke, according to late-breaking research presented at the American Heart Association's Scientific Sessions 2011 and published in the New England Journal of Medicine.

Many patients with stable heart and vascular disease are still at substantial risk for cardiac death, heart attack or stroke even after their LDL cholesterol has reached therapeutic levels (40-80 mg/dL) on statin therapy. It is suggested that this may be due to the presence of too little HDL cholesterol along with high levels of triglycerides, another blood fat. This lipid pattern is consistent with abnormalities seen in metabolic syndrome.

In the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health (AIM-HIGH) study, 1,718 patients were randomized to receive high-dose (1,500 to 2,000 mg/day), extended-release niacin, while 1,696 patients received placebo.

At two years, HDL and triglycerides levels continued to be improved in the niacin group, with a 25 percent increase in HDL and a 29 percent drop in triglycerides. In the placebo group, there was a modest change of a 10 percent increase in HDL and an 8 percent drop in triglyceride levels.

The niacin group experienced a decrease in LDL by approximately 12 percent.

However, the improved lipid changes in the niacin group didn't translate into fewer heart attacks, strokes or heart-related deaths or hospitalizations, which occurred in 16.4 percent of patients taking niacin and 16.2 percent of those on placebo ― a difference that was not statistically significant (P=0.80).

Because of the lack of benefit, the National Heart, Lung, and Blood Institute, in agreement with the recommendations of its Data Safety Monitoring Committee, decided to stop the trial 18 months before the planned completion.

"If you are a patient with stable cardiovascular disease who has achieved and maintained very low levels of LDL cholesterol on a statin, these research findings indicate the addition of high-dose niacin does not improve your risk for future events and is therefore not needed," said William E. Boden, M.D., lead researcher and professor of medicine and public health at the University at Buffalo in New York.

However, the AIM-HIGH results apply only to the 20 percent of heart disease patients who actually achieve very low LDL levels, Boden said. "At this point, we don't know whether HDL-raising would be beneficial for the other 80 percent of patients who are unable to lower their LDL this much."

"Also, by including only stable patients, AIM-HIGH didn't address the possible benefit of niacin therapy in patients who have experienced a recent heart attack or heart-related chest pain," said Jeffrey Probstfield, M.D., AIM-HIGH co-principal investigator and professor of medicine and cardiology at the University of Washington in Seattle. "Thus, it remains unclear whether such higher-risk patients with low HDL levels may benefit from niacin or other drugs which raise HDL levels."

The co-authors are writing on behalf of the AIM-HIGH trial research group.

The study was primarily funded by the National Heart, Lung, and Blood Institute. Abbott Laboratories gave a supplemental unrestricted research grant to the NHLBI and provided the extended-release niacin (Niaspan®). Merck provided the simvastatin used in the trial.