Abstract
Triglycerides (TGs) are measured as part of routine lipid profiles but their relationship to cardiovascular disease (CVD) risk has been controversial and overshadowed by high-density lipoprotein cholesterol (HDL-C). Epidemiological studies show a clear relationship of TG-containing lipoproteins including remnant particles with CVD risk with the effect being most clearly demonstrated through the excess risk captured by non-HDL-C compared with low-density lipoprotein-cholesterol (LDL-C). Mendelian randomisation studies show a consistent relationship of gene variants linked to TG metabolism with rates of CVD. Furthermore, meta-analyses of intervention trials with statins and other nonstatin drugs also suggest that reducing TGs is associated with benefits on rates of CVD events. Historical subgroup data from fibrate trials suggest benefits in patients with high TG:HDL ratios but seem to add little to optimized statin therapy. Recent trials with omega-3 fatty acids (specifically eicosapentaenoic acid) have suggested that high-dose formulations in contrast to low dose formulations have benefits on CVD outcomes. Further studies with newer agents are required to determine the place of TG-lowering drugs in therapeutic pathways. Trials with agents such as pemafibrate and vupanorsen may finally answer these questions.
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