Article Text

Download PDFPDF
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}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

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.


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 …

View Full Text


  • Competing interests RR received funding for a steering committee on the use of PCSK9 inhibitors in familial hypercholesterolaemia for Eli Lilly. This development program was terminated earlier this year.

  • Provenance and peer review Commissioned; internally peer reviewed.