Abstract

BackgroundDiscordance of lipid parameters is closely associated with residual cardiovascular risk. This study investigated the discordance between non-high-density lipoprotein cholesterol (non-HDL-C) or apolipoprotein B (apoB) and low-density lipoprotein cholesterol (LDL-C), and assessed arterial stiffness risk.MethodsThis study included a total of 402 middle-aged and elderly Northern Chinese individuals whose brachial-ankle pulse wave conduction velocity (baPWV), and clinical and biochemical data were measured. Arterial stiffness was defined by inclusion in the upper quartile of the baPWV. All participants were divided into four mutually exclusive concordance/discordance groups based on the lipid goal for high-risk populations, according to the 2019 European Society of Cardiology / European Atherosclerosis Society guidelines. Discordance was defined as LDL-C ≥ 1.81 mmol/L with non-HDL-C < 2.59 mmol/L, or apoB < 0.80 mmol/L, or vice versa.ResultsThe mean age of the participants was 65.9 ± 13.0 years; 59.5% of the participants were male. The mean LDL-C was 2.41 ± 0.81 mmol/L, non-HDL-C: 3.06 ± 0.94 mmol/L, and apoB: 0.84 ± 0.21 mmol/L. LDL-C was observed to be discordant with non-HDL-C (20.1%) and apoB (30.8%). When stratified according to LDL-C levels, the baPWV was greater in those patients with higher non-HDL-C or apoB levels. In the adjusted logistic regression model, low LDL-C and high non-HDL-C or apoB discordance were also associated with the risk of arterial stiffness (OR: 13.412 and OR: 13.054, respectively).ConclusionsThere was discordance between LDL-C and non-HDL-C, or apoB in middle-aged and elderly Chinese individuals; this was associated with a higher risk of arterial stiffness. Non-HDL-C or apoB levels could be used to identify individuals who may benefit from more comprehensive lipid modification.

Highlights

  • Discordance of lipid parameters is closely associated with residual cardiovascular risk

  • Many studies [4,5,6] have shown that in addition to low-density lipoprotein cholesterol (LDL-C), other lipid parameters, such as non-high-density lipoprotein cholesterol or apolipoprotein B can increase the risk of cardiovascular disease (CVD); this is conducive to the assessment and treatment of residual risk, because the major contributing risk factor for residual risk is the difference between the estimated LDL-C value and the actual quantity of circulating atherogenic lipoprotein particles

  • The odds for arterial stiffness were significantly higher when non-highdensity lipoprotein cholesterol (HDL-C) or apolipoprotein B (apoB) was greater than the cut-off value, and not significantly higher than the reference when non-HDL-C or apoB levels were below the cut-off point, suggesting that the risk for arterial stiffness is more strongly influenced by non-HDL-C or apoB than by LDL-C

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Summary

Introduction

Discordance of lipid parameters is closely associated with residual cardiovascular risk. This study investigated the discordance between non-high-density lipoprotein cholesterol (non-HDL-C) or apolipoprotein B (apoB) and low-density lipoprotein cholesterol (LDL-C), and assessed arterial stiffness risk. Many studies [4,5,6] have shown that in addition to LDL-C, other lipid parameters, such as non-high-density lipoprotein cholesterol (non-HDLC) or apolipoprotein B (apoB) can increase the risk of CVD; this is conducive to the assessment and treatment of residual risk, because the major contributing risk factor for residual risk is the difference between the estimated LDL-C value and the actual quantity of circulating atherogenic lipoprotein particles. When the cholesterol content is higher or lower than the average concentration, the cholesterol concentration is discordant with the number of lipoprotein particles, as is the cardiovascular risk predicted by LDL-C, non-HDL-C, and apoB. The 2019 European Society of Cardiology / European Atherosclerosis Society (ESC/EAS) guidelines for the management of dyslipidemia [11] advocate that nonHDL-C and apoB should be evaluated and considered as secondary targets for lipid control

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