Assessing Atherosclerotic Cardiovascular Disease Risk with Advanced Lipid Testing: State of the Science

Abstract

Cardiovascular disease is the number one cause of death and disability worldwide. While substantial gains have been made in reducing cardiovascular mortality, future projections suggest that we have reached a nadir and may be at an inflection point, given the rising tide of obesity and diabetes. Evaluation and management of plasma lipids is central to the prevention of atherosclerotic cardiovascular disease. Although the standard lipid panel represents a well-established platform to assess risk, this test alone can be insufficient and/or misleading. Advances in our understanding of atherosclerosis have led to the development of lipid-based biomarkers that help to discriminate the risk of cardiovascular disease when it is unclear. While these biomarkers provide novel information, their implementation into clinical medicine remains difficult given discrepancies in the literature, lack of assay standardisation, poor accessibility and high cost. However, additional measures of atherogenic lipoproteins or their surrogates may offer insight beyond the standard lipid panel, providing a more precise assessment of risk and more accurate assessment of lipid-lowering therapy.

The association of fasting plasma thiol fractions with body fat compartments, biomarker profile, and adipose tissue gene expression

“…In line with its association with android adiposity, tCys correlated positively with the atherogenic apolipoprotein apoB, and inversely with apoA1, the main antiatherogenic protein component of HDL particles (German and Shapiro 2020). A higher ratio of apoB to apoA1 is a recognized risk factor for cardiovascular disease (Walldius and Jungner 2006).…”

Precision medicine in secondary prevention of ischemic stroke: how may blood-based biomarkers help in clinical routine? An expert opinion

“…,51]. Levels of Apolipoprotein A-I (ApoA-I) are correlated to HDL concentration, and low ApoA-I levels seem to have a loose association with increased cardiovascular risk [52].…”

Glucose induced ApoB100/ApoAI ratio changes in cultured HepG2 cells in vitro

“…1 Conventionally, it was thought that increases in plasma low-density lipoprotein cholesterol (LDL-C) and decreases in high-density lipoprotein cholesterol (HDL-C) were the major factors causing CHD. 2 However, numerous in vivo human cohort studies have suggested that another factor in CHD risk might be the apolipoprotein B100/ apolipoprotein AI (ApoB100/ApoAI) ratio. [3][4][5][6][7] ApoB100 is a large surface protein present on low-density lipoprotein (LDL) and serves as a ligand for the LDL receptor, which facilitates its clearance from the plasma.…”

“…Apolipoprotein AI (ApoAI) is the major protein constituent on highdensity lipoprotein (HDL) and plays a central role in reverse cholesterol transport by stabilizing the HDL particle, interacting with the ATP-binding cassette transporter I, activating lecithin cholesterol acyl transferase and acting as a ligand for the hepatic scavenger receptor. 2 In order to prove those in vivo human cohort findings that ApoB100/ApoAI ratio is a CHD risk factor and understand the molecular mechanism of how ApoB100/ApoAI ratios are modulated in atherosclerosis, an in vitro cell assay model was built in the current study. Extracellular expression of ApoB100 and ApoAI were measured in cultured HepG2 cells in response to different concentrations of glucose.…”