Remnants, LDL, and the Quantification of Lipoprotein-Associated Risk in Atherosclerotic Cardiovascular Disease

Purpose of Review Implementation of intensive LDL cholesterol (LDL-C) lowering strategies and recognition of the role of triglyceride-rich lipoproteins (TRL) in atherosclerosis has prompted re-evaluation of the suitability of current lipid profile measurements for future clinical practice. Recent Findings At low concentrations of LDL-C (< 1 8 mmol/1/70 mg/dl), the Friedewald equation yields estimates with substantial negative bias. New equations provide a more accurate means of calculating LDL-C. Recent reports indicate that the increase in risk per unit increment in TRL/remnant cholesterol may be greater than that of LDL-C. Hence, specific measurement of TRL/remnant cholesterol may be of importance in determining risk. Non-HDL cholesterol and plasma apolipoprotein B have been shown in discordancy analyses to identify individuals at high risk even when LDL-C is low. Summary There is a need to adopt updated methods for determining LDL-C and to develop better biomarkers that more accurately reflect the abundance of TRL remnant particles.

Automated summary

The implementation of intensive LDL-C lowering strategies and recognition of TRL's role in atherosclerosis have prompted a re-evaluation of current lipid profile measurements for future clinical practice. New equations for calculating LDL-C and specific measurement of TRL/remnant cholesterol may be important in determining risk. Updated methods for determining LDL-C and development of better biomarkers reflecting TRL particles abundance are necessary.