Abstract
In light of the success of the statin drugs, interest in preventive cardiology has shifted to new frontiers of pharmacologic intervention: defining optimal levels of low-density lipoprotein (LDL) cholesterol, inhibiting cholesterol absorption, addressing the inflammatory component of atherosclerosis, and increasing the levels of protective high-density lipoprotein (HDL) cholesterol. This last approach attracted attention last year when it was reported that a new drug, torcetrapib, could substantially increase levels of HDL cholesterol by inhibiting cholesteryl ester transfer protein.1 The drug was heralded as a novel weapon against heart disease that could be an important clinical tool if its effect on lipids . . .