TY - JOUR

T1 - Triglyceride-rich remnant lipoproteins are more atherogenic than LDL per particle

T2 - is this important?

AU - Tybjærg-Hansen, Anne

AU - Nordestgaard, Børge G.

AU - Christoffersen, Mette

PY - 2023

Y1 - 2023

N2 - 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.

AB - 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.

U2 - 10.1093/eurheartj/ehad419

DO - 10.1093/eurheartj/ehad419

M3 - Review

C2 - 37403539

AN - SCOPUS:85172879247

VL - 44

SP - 4196

EP - 4198

JO - European Heart Journal

JF - European Heart Journal

SN - 0195-668X

IS - 39

ER -