Numerous epidemiological and genetic studies using Mendelian randomization support that elevated triglyceride-rich lipoproteins (TRLs) and TRL/remnant cholesterol (remnant-C) are causally associated with atherosclerotic cardiovascular disease (ASCVD), myocardial infarction, ischaemic stroke, aortic valve stenosis, and all-cause mortality.6–8 Although the features of the TRLs that cause atherosclerosis are debated, high plasma triglycerides are a marker of high levels of the cholesterol content of TRLs (=remnant-C). As triglycerides can be degraded by most cells in the body and do not accumulate in atherosclerotic plaques, it is unlikely that triglycerides per se are the cause of atherosclerosis.6 Limitations of solely evaluating plasma triglycerides are that the cholesterol to triglyceride content in TRLs varies and that triglycerides are also found in both LDL and HDL. Therefore, clinically it seems more appropriate to calculate or measure the cholesterol content of TRLs, i.e. TRL/remnant-C. TRL/remnant-C can be calculated as total cholesterol minus LDL-C minus HDL-C (remnant-C = non-HDL-C minus LDL-C), i.e. cholesterol in all TRLs, but requires a direct measurement of LDL-C at triglycerides >4.5 mmol/L (400 mg/dL). In the fasting state, TRL/remnant-C constitutes cholesterol in very-low-density lipoprotein (VLDL), VLDL remnants, and intermediate-density lipoprotein (IDL), whereas in the non-fasting state cholesterol in chylomicron remnants is also included.6 TRL/remnant-C can also be measured directly.