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Is a blood pressure rise the only deleterious off-target effect of cholesterol ester transfer protein inhibitors?

Although the effective reduction in low-density lipoprotein (LDL) cholesterol decreases cardiovascular mortality by around 20% per mmol/l (39 mg/dl) reduction [1], a substantial cardiovascular risk remains. In addition, high-density lipoprotein (HDL) cholesterol levels have been shown to predict major cardiovascular events in patients treated with statins, even when LDL cholesterol levels have been reduced to below 70 mg/dl [2]. Because a low serum HDL cholesterol level is one of the strongest predictors of coronary artery disease (CAD) [3], a new exciting therapeutic strategy that uses cholesterol ester transfer protein (CETP) inhibitors has recently been developed [4–6]. CETP inhibitors markedly increase HDL cholesterol and decrease LDL cholesterol when administered as monotherapy or when administered in combination with statins [4–6]. Recently, although torcetrapib therapy was shown to increase HDL cholesterol and decrease LDL cholesterol in the Investigation of Lipid Level Management to Understand its Impact in Atherosclerotic Events (ILLUMINATE) trial [7], this therapy results in an increased risk of mortality and morbidity through some unknown mechanism(s). Post hoc analyses of the ILLUMINATE trial have provided some possible explanations for the adverse outcome with torcetrapib. In this issue of the Journal of Hypertension, Clerc et al. [8] explore the possible mechanism of this increased risk by examining the unique steroidogenic and hypertensive effects of torcetrapib.