The Vytorin debacle has sparked some in the medical community to reassess the importance of controlling LDL – so-called bad –cholesterol in preventing heart and coronary artery disease. It has long been accepted that reducing LDL cholesterol would prevent the build-up of artery clogging plaque. But a study released last month that indicated that Vytorin did nothing to prevent plaque buildup has raised doubts about that theory. The new debate sparked by the Vytorin revelations could have serious implications for the millions of people who use other cholesterol lowering drugs, including statins.
Vytorin, which was developed and marketed jointly by Merck and Schering-Plough, was approved for use by the Food & Drug Administration in 2004. Vytorin is a combination of cholesterol-lowering Zetia and the statin Zocor. Statins like Zocor reduce the amount of cholesterol produced by the liver, while Zetia lessens the amount of cholesterol in food that is absorbed in the intestines. High cholesterol levels are thought to put a person at risk of developing clogged arteries – a major risk factor for heart attacks and strokes. Doctors and Vytorin users were led to believe that the drug would effectively reduce both sources of cholesterol, thereby lessening the amount of plaque build up in the arteries, as well as the risk of having heart attacks and strokes.
The ENHANCE study, which began in June 2002, focused on a group of 720 patients with a rare condition predisposing them to high cholesterol. The patients were given either Vytorin or a high dose of simvastatin, the generic form of Zocor. The ENHANCE study found that Vytorin worked no better to reduce clogged arteries than a high dose of a less-expensive, generically available statin alone. In fact, some of the Vytorin patients in ENHANCE actually developed more arterial plaque than those taking Zocor alone, putting them at an even greater risk of heart attacks and strokes.
As a result of the ENHANCE study, some of the world’s leading heart doctors have begun to question whether the lower-is-better theory of cholesterol management still holds. But ENHANCE was not the first study to do spark such doubts. Studies of the experimental Pfizer drug torcetrapib had earlier called the theory into question. Torcetrapib represented a new class of cholesterol medicine designed not only to lower LDL cholesterol but also to boost HDL, or “good” cholesterol. But the results of two large-scale studies linked torcetrapib to deaths and showed it failed to prevent the buildup of arterial plaque. Soon after, Pfizer gave up on the drug.
No one is suggesting that cholesterol-lowering medicines be abandoned, but many are now questioning whether the pharmaceutical industry’s longtime focus on bad cholesterol is fully supported by scientific evidence.