He was in for his annual check up. No complaints, no new issues since last year. He still had some knee pain at the end of the day - osteoarthritis. He'd tried losing some weight but was disappointed that he'd only managed a couple pounds. Of course there was the high blood pressure and the high cholesterol, for which he was taking his medications regularly. His parents both died in their 50s from heart attacks and, as someone in his mid-50s himself, he took this matter seriously.
We reviewed his vital signs, physical exam findings and laboratory results to determine if we should make any changes to his medications. One set of numbers on the list, his cholesterol levels: LDL 92, HDL 23. The LDL level was at our goal, below 100. The HDL, on the other hand, was too low. He was already on a statin which we knew was helping, but what else could we suggest?
The links between cholesterol and heart disease have been well-established. There are two main forms of cholesterol circulating in the blood stream: LDL and HDL. LDL is commonly referred to as "bad" cholesterol because it accumulates in blood vessel walls, preventing the flow of blood to the heartand leading to heart attacks. HDL is called "good" cholesterol because, at least in part, it seems to do the opposite by reducing LDL. It participates in a process called reverse cholesterol transport whereby it helps to remove cholesterol from the blood vessel wall. In keeping with these roles, elevated levels of LDL but decreased levels of HDL are each associated with increased risk for heart disease.
As one might expect, LDL and HDL levels have both been high-interest targets for drug development. Statins, or HMG-CoA reductase inhibitors, prevent cholesterol synthesis and have been successfully used primarily to lower LDL levels by 20 to 60 percent. More importantly, treatment with statins has also been shown to prevent heart attacks and improve survival. HDL level, however, has proven to be a more difficult target. In an article in a recent issue of The Journal of the American Medical Association, Stephen Nicholls, assistant medical school professor at Case Western University, and colleagues outlined the results of a study of a new drug in an emerging class called CETP inhibitors. In this study, the CETP inhibitor called evacetrapib increased HDL levels by as much as 128 percent.
Yet it remains to be seen whether these new CETP inhibitors will actually prevent heart attacks and improve survival. In 2006, a large clinical trial of an early CETP inhibitor called torcetrapib was stopped because, though it increased HDL levels, it actually increased mortality. In other words, raising HDL levels may help physicians feel better, but the real question is: Will it help our patient?
Jeffrey Sturek is a University Medical student. He can be reached at jms3hk@virginia.edu.
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