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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.
Abstract:
Although statins significantly decrease the incidence of cardiovascular disease (CVD), residual CVD risk remains high. This may partly be due to uncorrected atherogenic dyslipidaemia. The driving force behind atherogenic dyslipidaemia is hypertriglyceridaemia, which results from hepatic oversecretion and/or hypocatabolism of triglyceride-rich lipoproteins, and is typical of type 2 diabetes and metabolic syndrome. Persistent atherogenic dyslipidaemia in patients treated with a statin according to low-density lipoprotein-cholesterol goals may be corrected with niacin, fibrates or n-3 fatty acids. Clinical trial evidence to inform best practice is limited, but new data support adding fenofibrate to a statin. A consistent feature of fibrate clinical trials is the specific benefit of these agents in dyslipidaemic patients and the improvement in diabetic retinopathy with fenofibrate. Ongoing clinical trials may provide good evidence for adding niacin to a statin. Low-dose n-3 fatty acids could be used routinely after a myocardial infarction, but the value of higher doses of n-3 fatty acids in reducing CVD risk remains to be demonstrated.
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