Abstract
Background: atherosclerotic process inexorably advances in patients reaching low-density lipoprotein cholesterol (LDL-C) targets. An attractive hypothesis is that lipoprotein particles (very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL)), could contribute to residual risk. The present study aims to investigate the relationship between carotid intima-media thickness (IMT) and different lipoprotein subfractions in a cohort of healthy postmenopausal women. Methods: 75 postmenopausal women, at LDL-C target levels without overt cardiovascular disease, underwent biochemical analyses (including subfraction assay of plasma lipoproteins) and carotid ultrasound examination. Results: a statistically significant correlation between VLDL and carotid IMT (p < 0.001) was found. No significant correlation was found between carotid IMT and LDL-C (p = 0.179), IDL-C (p = 0.815), high-density lipoprotein (HDL) (p = 0.855), and LDL score (p = 0.240). Moreover, IMT is significantly correlated to LDL particle diameter (p = 0.044). After adjusting for age, systolic blood pressure, body mass index, smoking habits, glucose plasma concentration, and Lipoprotein(a) (Lpa) levels, multivariate analysis showed that women in the third tertile of VLDL-C, compared with those in the first tertile, were significantly associated to the highest IMT (p = 0.04). Conclusions: in this cohort of postmenopausal women, VLDL-C was significantly associated to carotid IMT, independent of main cardiovascular risk factors. These findings pave the way for targeting circulating concentrations of VLDL-C to reduce cardiovascular events in patients with target LDL-C levels.
Highlights
The role of statins and other lipid-lowering drugs in lowering low-density lipoprotein cholesterol (LDL-C) and reducing cardiovascular disease (CVD) has been well established in trials of both primary and secondary prevention [1,2].Despite the significant reductions in Low-density lipoprotein (LDL)-C and successive CVD reduction, residual atherosclerotic cardiovascular disease (ASCVD) persists, especially among high-risk subjects with type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity, where atherogenic dyslipidemia is associated, in particular, with elevated levels of triglycerides (TG), low levels of high-density lipoprotein cholesterol (HDL-C), and increased remnant lipoproteins
The present study aims at evaluating the relationship between lipid profile biomarkers (VLDL-C, LDL-C, intermediate-density lipoprotein cholesterol (IDL-C), and HDL) and other cardiovascular risk factors with subclinical atherosclerosis in a cohort of postmenopausal women, without overt CVD and at target LDL-C levels
The present study demonstrated an independent association between very low-density Lipoprotein (VLDL)-C and carotid intima-media thickness (IMT) in a cohort of postmenopausal women without overt cardiovascular disease, and with on-target LDL-C levels
Summary
The role of statins and other lipid-lowering drugs in lowering low-density lipoprotein cholesterol (LDL-C) and reducing cardiovascular disease (CVD) has been well established in trials of both primary and secondary prevention [1,2]. Despite the significant reductions in LDL-C and successive CVD reduction, residual atherosclerotic cardiovascular disease (ASCVD) persists, especially among high-risk subjects with type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity, where atherogenic dyslipidemia is associated, in particular, with elevated levels of triglycerides (TG), low levels of high-density lipoprotein cholesterol (HDL-C), and increased remnant lipoproteins. Clinical studies indicate that a focus solely on the assessment and management of LDL-C is not an optimal strategy for all patients; emerging evidence has established that very low-density Lipoprotein (VLDL), their remnants, and Lipoprotein(a) (Lpa), likewise, are causally related to CVD [5,6]. An attractive hypothesis is that other lipoprotein particles (VLDL, intermediate-density lipoprotein (IDL)), and their remnants, Lpa, could contribute to the residual risk in subjects at LDL-C goal
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