Table 1.
Drug | Action on TGs Levels |
---|---|
Statins | Lower TGs levels by 20% [18,54] First-line therapy |
Fibrates (e.g., pemafibrate) | The most potent drugs in managing hypertriglyceridemia Produce a decrease of up to 50% in TGs concentrations [58] Pemafibrate is non-inferior to other fibrates and has a more favorable safety profile Their potency to decrease overall cardiovascular risk is modest |
Omega 3 fatty acids (e.g., Icosapent Ethyl) | Demonstrated a 25% relative risk reduction in adverse cardiovascular events both in primary and secondary prevention when administrated at a high dose [63] Exert a beneficial effect on endothelial function assessed via flow-mediated dilation [66] |
Ezetimibe | Produces only a slight decrease in TGs levels [59] |
PCSK9 inhibitors (e.g., evolocumab) | Controversial data Reduction in VLDL, IDL, LDL, and Lp(a) levels The decrease in VLDL levels is dependent on baseline Lp(a) values [67] The lowering effect is more pronounced on VLDL2 levels than on VLDL1 [68] |
Volanesorsen | A second-generation chimeric antisense therapeutic oligonucleotide that decreases plasma apoCIII and TGs levels in a dose-dependent manner [71] |
Inclisiran | Small interfering RNA agent Majorly effective in reducing LDL concentration but also lowered TGs levels in ORION 9, 10, and 11 trials [72,73] |
GLP-1 receptor agonists (e.g., liraglutide) |
Decreases apoB48 synthesis in CMs Apparently decreased production of atherogenic remnants in diabetic patients [74] |
SGLT2 inhibitors (e.g., empagliflozin) |
Decrease in fasting and post-prandial TGs concentration and a flow-mediated dilation improvement [75] |
TG: triglyceride; VLDL: very-low-density lipoproteins; IDL: intermediate-density lipoprotein; Lp(a): lipoprotein(a); RNA: ribonucleic acid; CMs: chylomicrons.