Hypertriglyceridemia
Background
Triglyceride (TG) metabolism can produce a by-product called remnant lipoproteins, which can be atherogenic. Most guidelines consider hypertriglyceridemia to start at values ≥ 150 mg/dl. It is the most common dyslipidemia, as it can occur in 30% of the general population. Although fasting levels are usually obtained per the current US protocol, there is evidence that non-fasting TG levels might be a better indicator of cardiovascular (CV) risk as these levels may better reflect the usual levels that the body is exposed to.
Causes of HyperTG
- primary
- familial hyperTG
- familial combined hyperlipidemia
- familial dysbetalipoproteinemia
- familial chylomicronemia
- lipodystrophic syndromes
- secondary
- diet, decreased physical activity, smoking
- diabetes, alcohol abuse, hypothyroidism, pregnancy
- thiazides, non-selective beta blockers, antipsychotics, glucocorticoids
- estrogen and estrogen receptor blockers
- propofol
- interferon
- cancer therapies
Treatment
In summary, consider addition of EPA when triglycerides are still elevated on maximally tolerated statin therapy. As well, address underlying possible causes of hyperTG as above.
- JELIS (2007) - 19% relative risk reduction in cardiovascular events when 1.8g daily of eicosapentaenoic acid (EPA) was added to low-intensity statin therapy, for patients with hypercholesteremia and age 40-75
- REDUCE-IT (2018) - icosapent ethyl ester (EPA) led to a reduction in ASCVD events in secondary prevention patients and high risk primary prevention patients with DM and residual elevated TGs on top of maximally tolerated statin therapy
- STRENGTH (2021) - omega-3 CA (EPA+DHA) in addition to statin for patients with DLD and high ASCVD risk did NOT reduce MACE
References
- Triglycerides - Pathophysiology to Clinical Outcomes with Dr. Matthew Budoff
- 207. Lipids: REDUCE-IT Versus STRENGTH Trials - EPA in Clinical Practice with Dr. Peter Toth
- Japan EPA Lipid Intervention Study - American College of Cardiology