Non-HDL-cholesterol in dyslipidemia: Review of the state-of-the-art literature and outlook

Raja, Vikrama; Aguiar, Carlos; Alsayed, Nasreen; Chibber, Yogeyaa S.; ElBadawi, Hussein; Ezhov, Marat; Hermans, Michel P.; Pandey, Ramesh Chandra; Ray, Kausik K.; Tokgözoglu, Lale; Zambon, Alberto; Berrou, Jean-Pascal; Farnier, Michel

doi:10.1016/j.atherosclerosis.2023.117312

Cited by 11 publications

(3 citation statements)

References 66 publications

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“…Introducing a new or additional measure with yet-to-be-defined reference values and concerns over added costs and standardization—though these have largely been addressed [ 72 , 73 ]—might exacerbate the reluctance and difficulties in implementation among physicians [ 71 , 73 , 74 ]. These concerns may be less pertinent for non-HDL cholesterol, which can be accurately calculated from a standard lipid panel and is increasingly favored for ASCVD health and risk reduction [ 6 – 9 , 14 , 75 , 76 ]. Decisive factors in the uptake of any lipid measurement(s) in pediatric care will hinge on its predictive utility and the subsequent physician education around it [ 71 ].…”

Section: Discussionmentioning

confidence: 99%

Tracking of apolipoprotein B levels measured in childhood and adolescence: systematic review and meta-analysis

Stanesby,

Zhou,

Fonseca

et al. 2023

Eur J Pediatr

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To quantify the tracking of apolipoprotein B (apoB) levels from childhood and adolescence and compare the tracking of apoB with low-density lipoprotein (LDL) cholesterol, a systematic search of MEDLINE, Embase, Web of Science, and Google Scholar was performed in October 2023 (PROSPERO protocol: CRD42022298663). Cohort studies that measured tracking of apoB from childhood/adolescence (< 19 years) with a minimum follow-up of 1 year, using tracking estimates such as correlation coefficients or tracking coefficients, were eligible. Pooled correlations were estimated using random-effects meta-analysis. Risk of bias was assessed with a review-specific tool. Ten studies of eight unique cohorts involving 4677 participants met the inclusion criteria. Tracking of apoB was observed (pooled r = 0.63; 95% confidence interval [CI] = 0.53–0.71; I2 = 96%) with no significant sources of heterogeneity identified. Data from five cohorts with tracking data for both lipids showed the degree of tracking was similar for apoB (pooled r = 0.59; 95% CI = 0.55–0.63) and LDL cholesterol (pooled r = 0.58; 95% CI = 0.47–0.68). Study risk of bias was moderate, mostly due to attrition and insufficient reporting.Conclusion: ApoB levels track strongly from childhood, but do not surpass LDL cholesterol in this regard. While there is strong evidence that apoB is more effective at predicting ASCVD risk than LDL cholesterol in adults, there is currently insufficient evidence to support its increased utility in pediatric settings. This also applies to tracking data, where more comprehensive data are required. What is known:• Apolipoprotein B is a known cause of atherosclerotic cardiovascular disease.• Apolipoprotein B levels are not typically measured in pediatric settings, where low-density lipoprotein cholesterol remains the primary lipid screening measure. What is new:• This meta-analysis of 10 studies showed apolipoprotein B levels tracked strongly from childhood but did not exceed low-density lipoprotein cholesterol in this regard.• More comprehensive tracking data are needed to provide sufficient evidence for increased utility of apolipoprotein B in pediatric settings.

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Section: Discussionmentioning

confidence: 99%

Tracking of apolipoprotein B levels measured in childhood and adolescence: systematic review and meta-analysis

Stanesby,

Zhou,

Fonseca

et al. 2023

Eur J Pediatr

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“…Additional pro-atherogenic lipid parameters, such as RC, nonHDL-C, apoB, and Lp(a), provide important predictive information for ASCVD risk assessment and management [ 23 ]. In particular, a meta-analysis found that in statin-treated patients, treatment levels of LDL-C, nonHDL-C, and apoB were all associated with the risk of future MACE, but the association was significantly stronger for nonHDL-C than for LDL- C ( P = 0.002) and apoB ( P = 0.02) [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

The effect of lipid-lowering therapy on lipid-related residual risk factors: a prospective study

Li,

Gao,

et al. 2024

Lipids Health Dis

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Background Remnant cholesterol (RC) and nonhigh-density lipoprotein cholesterol (nonHDL-C) are key risk factors for atherosclerotic cardiovascular disease (ASCVD), with apolipoprotein B (apoB) and lipoprotein(a) [Lp(a)] also contributing to its residual risk. However, real-world population-based evidence regarding the impact of current clinical LDL-C-centric lipid-lowering therapy (LLT) on achieving RC and nonHDL-C goals, as well as on modifying residual CVD risk factors is limited. Methods This prospective observational study enrolled 897 CVD patients from September, 2020 to July, 2021. All participants had previously received low-/moderate-intensity LLT and were discharged with either low-/moderate-intensity LLT or high-intensity LLT. After a median follow-up of 3 months, changes in RC, nonHDL-C, and other biomarkers were assessed. Multivariate logistic regression was performed to analyze the impact of the LLT on goal attainment. Results Among all patients, 83.50% transitioned to high-intensity LLT from low or moderate. After follow-up, the high-intensity group saw significantly greater reductions in RC (-20.51% vs. -3.90%, P = 0.025), nonHDL-C (-25.12% vs. 0.00%, P < 0.001), apoB (-19.35% vs. -3.17%, P < 0.001), triglycerides (-17.82% vs. -6.62%, P < 0.001), and LDL-C and total cholesterol. Spearman correlation analysis revealed that LDL-C reduction from current LLT was strongly correlated with nonHDL-C reduction (r = 0.87, P < 0.001). Patients who received high-intensity LLT had significant improvements in attainment of RC (from 44.2% to 60.7%, χ² = 39.23, P < 0.001) and nonHDL-C (from 19.4% to 56.9%, χ² = 226.06, P < 0.001) goals. Furthermore, multivariate logistic regression showed that high-intensity LLT was a protective factor for RC [odds ratio (OR) = 0.66; 95% confidence intervals (CI), 0.45–0.97; P = 0.033] and nonHDL-C goal attainment (OR = 0.51; 95% CI, 0.34–0.75; P < 0.001), without a significant increase of adverse reactions. Conclusion Current levels of clinically prescribed LDL-C-centric treatment can reduce RC and other lipid-related residual risk factors, but high-intensity LLT is better at achieving nonHDL-C and RC goals than low-/moderate-intensity LLT, with a good safety profile. More targeted RC treatments are still needed to reduce residual lipid risk further.

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“…Atherosclerosis is an important pathogenic mechanism for both ischemic and hemorrhagic stroke [ 39 – 41 ]. Reduced HDL-C levels impede effective cholesterol transport, leading to deposition within arterial walls and promoting the formation of atherosclerotic plaques [ 42 ] An elevated PC enhances blood coagulability, facilitating thrombus formation at sites of arterial injury and thereby contributing to the development of atherosclerotic lesions [ 43 ]. Research by Jialal et al [ 20 ] demonstrated a significant correlation between the PHR and elevated triglycerides and coagulation factors, suggesting that an elevated PHR may reflect an imbalance in coagulation homeostasis.…”

Section: Discussionmentioning

confidence: 99%

The association of the platelet/high-density lipoprotein cholesterol ratio with self-reported stroke and cardiovascular mortality: a population-based observational study

Zhang,

Xu,

2024

Lipids Health Dis

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Background Previous studies have shown that the relationship between high-density lipoprotein cholesterol (HDL-C) and stroke is controversial, and the association between the platelet/high-density lipoprotein cholesterol ratio (PHR), a novel marker for inflammation and hypercoagulability states, and stroke has not been established. Methods This study presents an analysis of cross-sectional data from the 2005–2018 National Health and Nutrition Examination Survey (NHANES). Stroke history, HDL-C levels, and platelet counts were obtained during cross-sectional surveys. The PHR was calculated as the ratio of the number of platelets to HDL-C concentration. Weighted logistic regression was used to assess the associations of HDL-C and the PHR with stroke. Nonlinearity of this relationship was determined through restricted cubic splines (RCSs) and two-piecewise linear regression for identifying inflection points. Furthermore, Cox regression was utilized to prospectively analyze the associations of the PHR and HDL-C concentration with cardiovascular disease (CVD) mortality in stroke survivors. Results A total of 27,301 eligible participants were included in the study; mean age, 47.28 years and 50.57% were female, among whom 1,040 had a history of stroke. After full adjustment, the odds ratio (OR) of stroke associated with a per standard deviation (SD) increase in the PHR was estimated at 1.13 (95% confidence interval (CI): 1.03 − 1.24, P = 0.01), and the OR of stroke associated with a per SD increase in HDL-C was 0.95 (95% CI: 0.86–1.05, P = 0.30). The RCS indicated a nonlinear relationship for both variables (PPHR = 0.018 and PHDL-C = 0.003), and further piecewise linear regression identified inflection points at PHR = 223.684 and HDL-C = 1.4 mmol/L. Segmental regression indicated that in the PHR ≥ 223.684 segment, the estimated OR of stroke associated with a per-SD increase in the PHR was 1.20 (95% CI: 1.09 − 1.31, P < 0.001), while the association of stroke with HDL-C was not significant before or after the inflection point (P > 0.05). Furthermore, Cox regression and RCS showed that a per-SD increase in the PHR was linearly associated with a greater risk of CVD mortality among stroke survivors (HR: 1.14, 95% CI: 1.06 − 1.22, P < 0.001; nonlinear, P = 0.956), while HDL-C was not significantly associated with CVD mortality. Conclusion The association between the PHR and stroke incidence exhibited a significant threshold effect, with an inflection point at 223.684. A PHR exceeding 223.684 was positively associated with stroke, while the association between HDL-C and stroke was not significant. Additionally, the PHR was positively and linearly associated with CVD mortality among stroke survivors.

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Non-HDL-cholesterol in dyslipidemia: Review of the state-of-the-art literature and outlook

Cited by 11 publications

References 66 publications

Tracking of apolipoprotein B levels measured in childhood and adolescence: systematic review and meta-analysis

Tracking of apolipoprotein B levels measured in childhood and adolescence: systematic review and meta-analysis

The effect of lipid-lowering therapy on lipid-related residual risk factors: a prospective study

The association of the platelet/high-density lipoprotein cholesterol ratio with self-reported stroke and cardiovascular mortality: a population-based observational study

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