Managing the residual cardiovascular disease risk associated with HDL-cholesterol and triglycerides in statin-treated...

Area of Science:

• Cardiology
• Endocrinology
• Pharmacology

Background:

• Cardiovascular disease (CVD) is a leading cause of death in Europe, with type 2 diabetes (T2D) significantly increasing this risk.
• Dyslipidaemia, characterized by abnormal lipid levels, is a primary CVD risk factor, necessitating effective management.
• Despite statin therapy, many T2D patients with dyslipidaemia face residual CVD risk due to high triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C).

Purpose of the Study:

• To review current and novel pharmacotherapies for managing residual CVD risk in high-risk patients, particularly those with T2D and dyslipidaemia.
• To evaluate the role of add-on therapies to statins for optimizing lipid management beyond LDL-C reduction.

Main Methods:

• Review of evidence supporting add-on therapies to statins for dyslipidaemia management in high-risk patients.
• Discussion of fibrates (e.g., fenofibrate) and niacin as established add-on treatments.
• Exploration of emerging novel approaches for TG and HDL-C management, including CETP inhibitors, Apo A-1 analogues, mipomersen, lomitapide, and PCSK9 inhibitors.

Main Results:

• Fibrates, particularly fenofibrate, are recommended as add-on therapy to statins for elevated TG or low HDL-C in high-risk T2D patients.
• Combination therapy with statins and fibrates shows significant benefit in reducing residual CVD risk.
• Novel agents targeting HDL-C and TG offer promising future therapeutic avenues for complex dyslipidaemia.

Conclusions:

• Optimizing statin therapy is crucial, but add-on pharmacotherapy is essential for managing residual CVD risk in high-risk T2D patients.
• Fibrates represent a key therapeutic option for addressing TG and HDL-C abnormalities when statins alone are insufficient.
• Ongoing research into novel lipid-modulating agents holds potential for further advancements in CVD risk reduction.