Triglycerides and atherogenic dyslipidaemia: extending treatment beyond statins in the high-risk cardiovascular

Gerald F Watts1, Fredrik Karpe

  • 1School of Medicine and Pharmacology, University of Western Australia, Perth, WA 6847, Western Australia. gerald.watts@uwa.edu.au

Insights

Statins reduce cardiovascular disease (CVD) risk, but residual risk persists due to uncorrected atherogenic dyslipidaemia. Adding fenofibrate to statins shows promise for improving lipid profiles and outcomes in high-risk patients.

Area of Science:

  • Cardiology
  • Metabolic Disorders
  • Pharmacology

Background:

  • Cardiovascular disease (CVD) risk remains high despite statin therapy.
  • Atherogenic dyslipidaemia, driven by hypertriglyceridaemia, contributes to residual CVD risk.
  • Hypertriglyceridaemia is common in type 2 diabetes and metabolic syndrome.

Purpose of the Study:

  • To evaluate strategies for correcting persistent atherogenic dyslipidaemia in patients on statin therapy.
  • To review clinical trial evidence for agents like niacin, fibrates, and n-3 fatty acids in managing residual CVD risk.

Main Methods:

  • Review of clinical trial evidence for add-on therapies to statins.
  • Analysis of data on fenofibrate, niacin, and n-3 fatty acids in dyslipidaemic patients.
  • Focus on outcomes in patients with type 2 diabetes and metabolic syndrome.

Main Results:

  • New data support adding fenofibrate to statin therapy.
  • Fenofibrates demonstrate specific benefits in dyslipidaemic patients and improve diabetic retinopathy.
  • Ongoing trials may provide evidence for niacin as an add-on therapy.
  • Low-dose n-3 fatty acids may be beneficial post-myocardial infarction, but higher doses require further evidence.

Conclusions:

  • Fenofibrate is a viable option to add to statins for managing residual CVD risk.
  • Niacin and n-3 fatty acids may also play roles, with ongoing research.
  • Addressing atherogenic dyslipidaemia is crucial for reducing residual CVD risk.

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