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Randomised controlled trial
CETP inhibition improves the lipid profile but has no effect on clinical cardiovascular outcomes in high-risk patients
  1. Robert S Rosenson
  1. Cardiometabolics Unit, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai, New York City, New York, USA
  1. Correspondence to Professor Robert S Rosenson, Cardiometabolics Unit, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Hospital Box 1031, New York, NY 10029, USA; robert.rosenson{at}mssm.edu

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Commentary on: Lincoff AM, Nicholls SJ, Riesmeyer JS, et al. Evacetrapib and cardiovascular outcomes in high-risk vascular disease. N Engl J Med 2017;376:1933–42.

Context

High-density lipoprotein (HDL) cholesterol (HDL-C) is a robust predictor of cardiovascular disease (CVD) events; however, research into both rare monogenic HDL disorders and Mendelian randomisation studies of dysfunctional traits associated with HDL-C demonstrate that this biomarker is not involved in the causal pathway for atherosclerosis.1 Small-effect variants in the gene encoding cholesteryl ester transfer protein (CETP) associate with higher HDL-C and lower myocardial infarction rates, whereas large-effect variants associate with reduced survival. CETP loss-of-function variants also associate with low levels of low-density lipoprotein (LDL) cholesterol (LDL-C), which confounds the attribution of the atheroprotective effect of CETP-mediated HDL changes.

Small molecules that inhibit CETP activity have been previously investigated in two randomised clinical trials of CVD outcomes.2 3 Treatment with torcetrapib, in combination with atorvastatin increased HDL-C …

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