Professor Chris J Packard, Professor of Vascular Biochemistry, University of Glasgow, UK
Recent research has reinforced the association between triglyceride-rich lipoproteins (TRLs) and plasma TG with atherosclerotic cardiovascular disease (ASCVD). This evidence comes from a variety of sources. First, genetic studies show that TRLs are causally associated with coronary heart disease risk and that TRLs are four to five times more atherogenic than LDL-C on a per particle basis.1-2 Second, further exploration of clinical trial data reveals that when LDL-C levels are very low, for example in the ODYSSEY OUTCOMES study with a PCSK9 inhibitor, there is still a substantial residual risk associated with plasma TG levels.3 Thirdly, recent studies have demonstrated that TRLs appear to influence the risk of ASCVD in part via multiple pro-inflammatory effects such a upregulation of production of pro-inflammatory cytokines and enhanced endothelial inflammatory responses.1 Addressing the TG-associated risk in patients with well-treated LDL-C levels should therefore be a part of our overall strategy for reducing cardiovascular disease.
