3/29/2007 - Study offers mixed results on medicine to raise "good" cholesterol levels NEW ORLEANS, March 29, 2007—A new study has dealt another blow to the hopes of a class of drugs designed to raise levels of good cholesterol. The study, which was presented at the 56th Annual Scientific Session of the American College of Cardiology (ACC), found that while the drug torcetrapib raised people's levels of high-density lipoprotein (HDL) cholesterol, it didn't slow the buildup of artery-clogging plaque. Torcetrapib made news in December 2006 when its development was halted after it was linked to an unexpected increase in the risk of death. Results of the current study—which took place before the drug's development was stopped—are considered pivotal in determining whether the failure of the drug was a result of a problem specific to the medication or a failure of the entire class of similar drugs. Torcetrapib was developed to raise levels of HDL cholesterol, which is called "good" because it helps the body get rid of artery-clogging cholesterol (low-density lipoprotein, or LDL, cholesterol). Development of drugs to raise HDL has been a research priority because, despite the success of statin drugs at lowering LDL, many people continue to experience heart attacks, stroke or sudden cardiac death. The study involved 1,888 people with coronary artery disease. At the beginning of the study, each person had an intravascular ultrasound (IVUS), which uses sound waves to measure plaque buildup in the coronary arteries. People also received statins in order to bring their LDL levels down. Participants were then randomly assigned to receive either 60 milligrams of torcetrapib or a placebo for two years. Researchers then gave each person a second IVUS test and compared the two sets of test results. They also measured the participants’ blood cholesterol levels at several points during the study. Results showed that people who received torcetrapib experienced a 61 percent relative increase in HDL levels and a 20 percent relative decrease in LDL levels, compared with those who received the placebo. But despite these results, there was no statistical difference between the two groups in plaque volume changes—both groups showed slight increases. What’s more, torcetrapib increased systolic blood pressure—the pressure that occurs when the heart is beating, as opposed to when it’s at rest—by an average of 4.6 mm Hg. Lead author of the study, Steven Nissen, M.D., who is also a former president of the ACC, theorized that the disappointing results might be due to several potential factors: The treatment may not generate HDL particles that function normally in helping remove cholesterol from the body. The increase in blood pressure associated with torcetrapib may have counterbalanced any favorable effects of the drug on cholesterol. The increased blood pressure may have been a sign of a more generalized problem with the medication that simultaneously prevents beneficial effects on plaque progression and increases the adverse reactions of the drug. Because of the problems associated with torcetrapib, new similar medications will clearly have to be carefully scrutinized. But the class of drugs deserves further investigation, Dr. Nissen said, noting that early trials of statin drugs also raised concerns. In the meantime, there are ways to help raise HDL levels other than taking a medication. According to the American Heart Association, lifestyle factors that may improve HDL levels include exercising regularly and not smoking. Back