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HDL hypothesis: where do we stand now?

Sayed M Tariq1, Mandeep S Sidhu, Peter P Toth

  • 1Department of Medicine, Albany Medical Center, Albany Medical College, Albany, NY, USA, TariqS@mail.amc.edu.

Current Atherosclerosis Reports
|March 13, 2014
PubMed

Insights

Despite evidence linking high-density lipoprotein cholesterol (HDL-C) to lower coronary artery disease (CAD) risk, therapies to raise HDL-C have not consistently reduced cardiovascular events. Current trials show insufficient evidence to recommend HDL-targeted therapy for CAD event reduction.

Area of Science:

  • Cardiology
  • Biochemistry
  • Epidemiology

Background:

  • Epidemiological studies, including the Framingham Heart Study, show an inverse relationship between high-density lipoprotein cholesterol (HDL-C) and coronary artery disease (CAD) risk.
  • Low HDL-C levels are an independent predictor of subsequent CAD events.
  • Despite this, therapeutic attempts to raise HDL-C have not consistently reduced major adverse cardiovascular events like death, myocardial infarction (MI), or stroke.

Purpose of the Study:

  • To evaluate the scientific viability of the "HDL hypothesis" which posits that raising HDL-C can lower cardiovascular events.
  • To review recent major randomized trials investigating HDL-C-raising therapies and their impact on cardiovascular outcomes.
  • To discuss the clinical implications of these findings for modern pharmacotherapy in managing cardiovascular risk.

Main Methods:

  • Review of data from major randomized controlled trials including AIM-HIGH, HPS2-THRIVE, ILLUMINATE, and dal-OUTCOMES.
  • Analysis of trial outcomes concerning cardiovascular event reduction in patients receiving HDL-C-targeted therapies.
  • Consideration of specific patient populations and baseline treatment parameters within these trials.

Main Results:

  • Recent trials (AIM-HIGH, HPS2-THRIVE) did not demonstrate a reduction in cardiovascular events in patients with stable ischemic heart disease treated with extended-release niacin and simvastatin.
  • These trials excluded specific populations, such as those with acute coronary syndromes or significant residual dyslipidemia on suboptimal statin therapy, limiting extrapolation of findings.
  • Current clinical trial evidence is insufficient to support HDL-targeted therapy for additional event reduction in CAD patients.

Conclusions:

  • The efficacy of raising HDL-C to reduce cardiovascular events remains uncertain.
  • Recent trial data raise concerns about the "HDL hypothesis" and its clinical application.
  • Further research and careful consideration of patient populations are needed to clarify the role of HDL-C-targeted therapies in cardiovascular disease management.

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