Search

Aim: Issuance of the WHO Housing and health guidelines has paralleled growing interest in the housing environment. Despite accumulating evidence of an association between outdoor temperature and serum cholesterol, indoor temperature has not been well investigated. This study examined the association between indoor temperature and serum cholesterol. Methods: We collected valid health checkup data of 2004 participants (1333 households), measured the indoor temperature for 2 weeks in winter, and divided participants according to whether they lived in a warm (average bedroom temperature ≥ 18℃), slightly cold (12–18℃) or cold house (＜12˚C). The relationship between bedroom temperature and serum cholesterol was analyzed using multivariate logistic regression models, adjusting for demographics, lifestyle habits and the season in which the health checkup was conducted, with a random effect of climate areas in Japan. Results: The sample sizes for warm, slightly cold, and cold houses were 206, 940, and 858, respectively. Compared to those in warm houses, the odds ratio of total cholesterol exceeding 220 mg/dL was 1.83 (95%CI: 1.23–2.71, p=0.003) for participants in slightly cold houses and 1.87 (95%CI: 1.25–2.80, p=0.002) in cold houses. Similarly, the odds ratio of LDL/non-HDL cholesterol exceeding the standard range was 1.49 (p=0.056)/1.67 (p=0.035) for those in slightly cold houses and 1.64 (p=0.020)/1.77 (p=0.021) in cold houses. HDL cholesterol and triglycerides were not significantly associated with bedroom temperature. Conclusion: Besides lifestyle modification, improving indoor thermal environment through strategies such as installing high thermal insulation and appropriate use of heating devices may contribute to better serum cholesterol condition.

AimsThe 2019 vs. 2016 European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) dyslipidaemia guidelines contains new recommendations for primary prevention with statins; however, the potential impact of these changes is unclear. We compared the 2019 and 2016 guidelines regarding statin eligibility and potential impact on prevention of atherosclerotic cardiovascular disease (ASCVD) in the general population.Methods and resultsWe examined 45 750 individuals aged 40–75 from the Copenhagen General Population Study, all free of ASCVD and statin use at baseline. During the 9.2-year follow-up, 3337 experienced ASCVD (myocardial infarction, stroke, and cardiovascular death). For Class I/A recommendations, 32.3% (95% confidence interval: 31.8–32.7) and 15.4% (15.1–15.7) of individuals were statin eligible according to the 2019 and 2016 guidelines. The increased statin eligibility by the 2019 guidelines was explained by lower low-density lipoprotein cholesterol (LDL-C) thresholds alone (explaining 33.2%), older age range alone (49.4%), older age range in combination with lower LDL-C thresholds (14.7%), and updated SCORE risk algorithm (2.8%). If fully implemented, the estimated percentage of ASCVD events that can be prevented by using high-intensity statins for 10 years were 25% and 11% with the 2019 and 2016 guidelines. Mainly because of older age range in the 2019 guidelines, the corresponding estimated numbers needed to treat (NNT) to prevent one ASCVD event were 19 and 20.ConclusionDue to lower LDL-C threshold and older age range, the 2019 vs. 2016 ESC/EAS guidelines doubles the number of individuals eligible for primary prevention with statins. This considerably improves the potential for ASCVD prevention in the general population, with similar NNT to prevent one event.

Súhrn Stručný komentár k návrhu fenotypovej klasifikácie dyslipidémií, ktorá vychádza zo stanovenia triacylglycerolov a non-HDL cholesterolu a delí dyslipidémie do 6 tried podľa Fredericksonovej klasifikácie a zavádza 3 nové triedy s hodnotami vyšetrení v normálnom rozmedzí. Abstract Short commentary on the proposal of a new phenotypic classification system for dyslipidemias based on triacylglycerol and non-HDL cholesterol values. The classification divides dyslipidemias to 6 types according to Frederickson classification and introduces 3 new types with values in the normal range., {"references":["Clouet-Foraison, N. et al. (2017) Advanced lipoprotein testing for cardiovascular diseases risk assessment: a review of the novel approaches in lipoprotein profiling. Clin Chem Lab Med 55, 1453-1464 doi10.1515/cclm-2017-0091","Ďurovcová E. a kol. (2020) Klinická biochémia, vybrané kapitoly. Osveta Martin. 301 s, ISBN 978-80-8063-489-6","Fredrickson, D.S., Levy, R.I., Lees, R.S. (1967) Fat transport in lipoproteins--an integrated approach to mechanisms and disorders, New Engl J Med, 276, 34-42.","Gaško, R., Hefler, M., Pirošková Z. (2022) Nový fenotypový klasifikačný systém dyslipidémií (Sampson) založený na štandardnom lipidovom paneli. Laboratórna Diagnostika, 27(1)","Gorabi, A.M. et al. (2020) Epigenetic control of atherosclerosis via DNA methylation: a new therapeutic target? Life Sci 253:117682. doi 10.1016/lfs.2020.117682","Khoury, S. et al. (2018) Quantification of lipids: model, reality, and compromise. Biomolecules 8:174. doi 10.3390/biom8040174","Jabor, A., Franeková, J. Kubíček, Z. (2020) Principy interpretace laboratorních testů: 2., přepracované a doplněné vydání, Praha, Grada Publishing, 456 s. ISBN 978-80-271-1272-2.","Josefs, T., Boon, R.A. (2020) The long non-coding road to atherosclerosis. Curr Atherosclerosis Rep 22:55 doi 10/1007/s1883-020-00872-6","Koplev, S. et al. (2022) A mechanistic framework for cardiometabolic and coronary artery diseases. Nature Cardiovasc Res 1, 85-100. doi 10.1038/s44131-021-00009-1","Langlois, M.R. et al. (2020) \"European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) Joint Consensus Initiative. Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM\", Clin Chem Lab Med. 58(4):496-517. doi: 10.1515/cclm-2019-1253.","Libby, P. The changing landscape of atherosclerosis (2021) Nature 592, 524-533. doi 10.1038/s41586-021-03392-8.","Sampson, M. et al. (2021) A new phenotypic classification system for dyslipidemias based on the standard lipid panel Lipids Health Dis 20, 170. doi.org/10.1186/s12944-021-01585-8","Tada, H., Takamura M., Kawashiri M.A. (2020) What is the mechanism of genetic contribution to atherosclerosis? J Atherosclerosis 307, 72-74 doi 10.1016/j.atherosclerois.2020.05.006"]}

To explore whether non-high-density-lipoprotein cholesterol (non-HDL-c) is associated with depression, a total of 26 819 Canadians aged 45–85 from the Canadian Longitudinal Study on Aging (CLSA) were included in analysis. Non-HDL-c, the difference between total-c and HDL-c, was categorized into five levels, i.e.

Suboptimal blood pressure (BP) control in patients with type 2 diabetes is associated with adverse micro‐ and macrovascular complications. This study aimed to investigate the predictors of uncontrolled hypertension in an Iranian population with type 2 diabetes. This is a cross‐sectional study of 2612 patients with type 2 diabetes, including 944 patients with hypertension. Controlled and uncontrolled hypertension were assessed. Multivariate logistic regression modeling was used to determined independent predictors of uncontrolled hypertension. Of 2612 patients with type 2 diabetes, 944 (36.1%) patients had hypertension. Of all patients with hypertension, 580 (61.4%) were still on monotherapy. Uncontrolled hypertension was detected in 536 participants (56.8%). Patients with uncontrolled hypertension had significantly higher body mass index (BMI) (29.8±4.8 vs. 28.6±4.6), waist circumference (99.11±10.95 vs. 96.68±10.92), pulse pressure (67.3±17.3 vs. 48.4±10.7), total cholesterol (177.1±45.5 vs. 164.3±40.5), non‐HDL cholesterol (133.0±43.5 vs. 120.1±38.7), triglycerides (175.7±80.3 vs. 157.4±76.7), and Atherogenic Index of Plasma (AIP) (0.57±0.23 vs. 0.52±0.24) (p 200 mg/dl non‐HDL cholesterol had a significant correlation with uncontrolled hypertension (OR = 4.635, CI95%:1.781–12.064, p = .002). In conclusion, BMI, pulse pressure, total cholesterol, and non‐HDL cholesterol are significant predictors of uncontrolled hypertension in patients with type 2 diabetes. Also, ineffective monotherapy, medical inertia and patients’ non‐compliance were other contributors to the uncontrolled hypertension.

Background/objective: Obstructive sleep apnea (OSA) is independently associated with dyslipidemia, a surrogate marker of atherosclerosis. Low-density lipoprotein (LDL)-cholesterol is accepted as a major independent risk factor for cardiovascular disease. However, non-high-density lipoprotein (HDL)cholesterol is a better marker of atherogenic dyslipidemia and recommended as a target of lipid lowering therapy. We aimed to assess the prevalence of atherogenic dyslipidemia, and relationship between OSA severity and serum LDL-cholesterol and non-HDL cholesterol levels in OSA patients. Methods: We retrospectively evaluated treatment naive 2361 subjects admitted to the sleep laboratory of a university hospital for polysomnography. All subjects' lipid profile including total cholesterol, LDLcholesterol, HDL-cholesterol, triglycerides, and non-HDL-cholesterol were measured. Results: Out of 2361 patients (mean age 49.6 +/- 11.9 years; 68.9% male, apnea-hypopnea index 36.6 +/- 28.4/h), 185 (7.8%) had no OSA and 2176 (92.2%) had OSA. Atherogenic dyslipidemia prevalence was high (57-66%) in OSA patients, and especially increased in severe OSA compared to other groups (p < 0.05). Though total and LDL-cholesterol did not differ between those with and without OSA, nonHDL-cholesterol (p = 0.020), and triglycerides (p = 0.001) were higher and HDL-cholesterol levels (p = 0.018) were lower in OSA patients than non-OSA. Non-HDL-cholesterol was significantly correlated with OSA severity (p < 0.001) and hypoxia parameters (p < 0.01), whereas LDL-cholesterol showed no correlation. Conclusions: Atherogenic dyslipidemia is highly prevalent and non-HDL-cholesterol levels are signifi-cantly increased, predominantly in severe OSA patients. Non-HDL-cholesterol but not LDL-cholesterol, is significantly correlated with OSA severity and hypoxia parameters. Therefore, it could be better to use non-HDL-cholesterol, which is a guideline recommended target of lipid therapy, as a marker of atherosclerotic cardiovascular risk in OSA patients. (c) 2021 Elsevier B.V. All rights reserved.

Background A distorted blood lipid profile is an important risk factor for ischemic heart disease (IHD) but the predictive ability of the different lipid measures has rarely been studied. Our aim was to examine and compare, in a large sample of women, the predictive ability of total cholesterol/HDL cholesterol ratio (TC/HDL-C) and non-HDL-C in relation to IHD, adjusted for age, exercise, smoking, waist-hip ratio, blood pressure, and diabetes mellitus. Methods Between 1995 and 2000, a total of 6537 women aged 50–59 years from the Women’s Health in Lund area (WHILA) study in southern Sweden were included and underwent a baseline examination. The women were followed through national registers for incidence of IHD during a mean follow-up of 17 years. The prediction accuracy was estimated through Harrell’s C and Akaike Information Criterion (AIC). Results Increasing TC/HDL-C as well as non-HDL-C showed strong associations with IHD, with the highest risk in the 5th quintile, where the HR was 2.30 (95% CI: 1.70–3.11) for TC/HDL-C and 1.67 (95% CI: 1.25–2.24) for non-HDL-C, after adjustments. Comparisons using Harrell’s C and AIC indicated that TC/HDL-C has a slightly higher predictive ability than that of non-HDL-C (Harrell’s C 0.62 and 0.59 respectively, p = 0.003 for difference, age-adjusted model; AIC for TC/HDL-C Conclusions TC/HDL-C ratio and non-HDL-C are both clinical predictors for IHD in middle-aged women. The results indicate that the predictive ability of TC/HDL-C was higher than that of non-HDL-C; however, non-HDL-C was linearly related to IHD (p = 0.58) and may be easier to calculate and interpret in clinical practice, for early identification of future IHD in women.

Aims Guidelines recommend targeting non-high-density lipoprotein cholesterol to reduce cardiovascular risk. We assessed the impact of baseline triglycerides on non-high-density lipoprotein cholesterol goal attainment in 10 phase 3 trials with alirocumab versus control ( n = 4983). Methods Trials were grouped into four pools based on alirocumab dose (75–150 mg every 2 weeks), control (placebo/ezetimibe) and statin use. Baseline triglyceride quintiles were built within each pool. Non-high-density lipoprotein cholesterol goal attainment (very high risk: Results Higher baseline triglycerides were associated with a worse cardiovascular risk profile. Low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol increased with higher triglycerides, but the magnitude in non-high-density lipoprotein cholesterol was three- to four-fold higher compared with the increase in low-density lipoprotein cholesterol. Non-high-density lipoprotein cholesterol and low-density lipoprotein cholesterol percentage reductions from baseline with alirocumab were similar regardless of baseline triglycerides. A greater proportion of alirocumab-treated patients attained non-high-density lipoprotein cholesterol and low-density lipoprotein cholesterol goals compared with placebo or ezetimibe. Unlike low-density lipoprotein cholesterol goal attainment, non-high-density lipoprotein cholesterol goal attainment significantly declined with increasing baseline triglycerides ( p Conclusion Individuals with increased triglycerides have higher non-high-density lipoprotein cholesterol levels and lower rates of non-high-density lipoprotein cholesterol goal attainment (unlike low-density lipoprotein cholesterol goal attainment). Alirocumab improves non-high-density lipoprotein cholesterol goal attainment in this population. These results highlight the impact of triglycerides on non-high-density lipoprotein cholesterol and the need for novel therapies targeting triglyceride-related pathways.

The article discusses a new approach to assessing cardiovascular risk in clinical practice, presented in the European guidelines 2021. Two novel risk charts (SCORE2 and SCORE2-OP) have been proposed that have undergone significant revision and require significant changes in primary care practice. It has been suggested that in modern conditions their practical introduction is premature, since the healthcare system is not ready for renewal. Therefore, time is needed to adapt it to the practical healthcare conditions and to revise the medical screening protocols, which will require financial costs. The implementation of these recommendations should be taken responsibly so as not to harm the existing system of preventive care.

Context Calculated non–high-density lipoprotein (HDL) cholesterol (non-HDLC) should selectively include cholesterol from atherogenic lipoproteins to be a reliable risk marker of cardiovascular disease. In hypertriglyceridemia (HTG), there is increased abundance of larger and less atherogenic triglyceride-rich lipoproteins (TRL), namely, larger very-low-density lipoproteins (VLDL), and chylomicrons. Objective We aim to demonstrate that serum triglyceride (TG) level has a substantial impact on non-HDLC’s ability to represent cholesterol from atherogenic lipoproteins, even though TG is not part of the calculation for non-HDLC. Design Analysis of lipid profile data Settings Lipid Clinic patient cohort, and Biochemistry Laboratory patient cohort Patients or Other Participants 7,492 patients in the Lipid Clinic cohort with baseline lipid profiles documented prior to starting lipid-lowering medications and 156,311 lipid profiles from The Ottawa Hospital Biochemistry Laboratory cohort. Intervention None Main Outcome Measure Our modeling process includes derivation of TG-interval–specific lipoprotein composition factor (LCF) for TRL, which represents the mass ratio of cholesterol to TG in TRL. A high LCF indicates that the TRLs are mainly the cholesterol-rich atherogenic remnant lipoproteins. A low LCF indicates that the TRLs are mainly the TG-rich larger VLDL and chylomicrons. Results As serum TG increases, there is progressive decline in the LCF for TRL, which indicates that the calculated non-HDLC level reflects progressive inclusion of cholesterol from larger TRL. This is shown in both cohorts. Conclusions Calculated non-HDLC is influenced by TG level. As TG increases, non-HDLC gradually includes more cholesterol from larger TRL, which are less atherogenic than LDL and remnant lipoproteins.

We evaluated the control of cardiovascular disease (CVD) risk factors among patients with atherosclerotic cardiovascular disease (ASCVD) in the Centralized Pan-Middle East Survey on the undertreatment of hypercholesterolaemia (CEPHEUS) in the Arabian Gulf. Of the 4398 enrolled patients, overall mean age was 57 ± 11 years, 60% were males, 13% were smokers, 76% had diabetes, 71% had metabolic syndrome and 78% had very high ASCVD risk status. The proportion of subjects with body mass index

BackgroundAtherogenic dyslipidemia is highly prevalent in the Arabian Gulf. Non–high-density lipoprotein cholesterol (non-HDL-C) reduction has been proposed as an additional goal to low-density lipoprotein cholesterol (LDL-C) lowering to prevent atherosclerotic cardiovascular disease (ASCVD). Data on non–HDL-C goal attainment in patients with high triglycerides (TGs) on lipid-lowering drugs (LLDs) in the region is scarce.ObjectiveEvaluate non–HDL-C target attainment according to the National Lipid Association in patients on LLDs stratified by TG (200 [2.26] mg/dL [mmol/L]) levels in the Arabian Gulf.MethodsOverall, 4383 patients on LLD treatment from 6 Middle Eastern countries participating in the Centralized Pan-Middle East Survey on the Undertreatment of Hypercholesterolemia study were evaluated. Patients were classified according to TG levels and ASCVD risk.ResultsThe overall non–HDL-C goal attainment was 41% of the subjects. Non–HDL-C goal was less likely attained in patients with high TGs (12% vs 27% vs 55%; P

There is no doubt about the relationship between LDL-c and cardiovascular risk, as well as about the benefits of statin treatment. Once the objective of LDL-c has been achieved, the evidences that demonstrate the persistence of a high cardiovascular risk, a concept called residual risk, are notable. The residual risk of lipid origin is based on atherogenic dyslipidemia, characterized by an increase in triglycerides and triglyceride-rich lipoproteins, a decrease in HDL-c and qualitative alterations in LDL particles. The most commonly used measures to identify this dyslipidemia are based on the determination of total cholesterol, triglycerides, HDL, non-HDL cholesterol and remaining cholesterol, as well as apolipoprotein B100 and lipoprotein (a) in certain cases. The treatment of atherogenic dyslipidemia is based on weight loss and physical exercise. Regarding pharmacological treatment, we have no evidence of cardiovascular benefit with drugs aimed at lowering triglycerides and HDL-c, fenofibrate seems to be effective in situations of atherogenic dyslipidemia. (C) 2018 Sociedad Espanola de Arteriosclerosis. Published by Elsevier Espana, S.L.U. All rights reserved.

Although cholesterol linked to low-density lipoproteins (c-LDL) is well established as a risk factor for cardiovascular disease, there is often a more complex dyslipidaemia pattern that contributes to the formation of atherosclerotic plaque. Non-HDL cholesterol (c-NO-HDL) is used to estimate the total amount of atherogenic lipoproteins in plasma, some of which are not usually determined in daily clinical practice. c-NO-HDL is easily calculated from the subtraction of total plasma cholesterol from the cholesterol content carried by high density lipoproteins. The c-NO-HDL has a predictive value superior to that of C-LDL to estimate the risk of major cardiovascular events in epidemiological studies. Genetic studies by analysis of the complete genome, together with those based on Mendelian randomisation, point to the aetiological character of c-NO-HDL on ischaemic heart disease (IHD). Intervention studies, and the meta-analyses derived from them, close the causal circle between c-NO-HDL and IHD, by demonstrating that any intervention that decreases the concentrations of the former reduces the incidence of arteriosclerotic heart disease. The European ESC/EAS 2016 guide for the management of dystipidaemia considers c-NO-HDL as a therapeutic target with a Class I la recommendation (should be performed) Level B (data from a single randomised clinical trial [RCT]) or from several non-RCTs), and sets its target at less than 100 or 130 mg/dL for those patients with very high risk or high risk, respectively. These achievable c-NO-HDL values are easily calculated by adding 30 mg/dL to the c-LDL targets. (C) 2019 Sociedad Espanola de Arteriosclerosis. Published by Elsevier Espana, S.L.U. All rights reserved.

It is uncertain whether omega-3 fatty acids are beneficial in statin-treated patients. Epanova is a mix of omega-3 free fatty acids, not requiring co-ingestion with food, which can lower triglycerides by up to 31%. STRENGTH will examine whether Epanova 4 g daily reduces the rate of cardiovascular events in statin-treated patients with hypertriglyceridemia and low levels of HDL-C at high risk for developing cardiovascular events. STRENGTH is a randomized, double-blind, placebo-controlled trial. Patients had a triglyceride level ≥ 180 to 4 weeks, and have LDL-C < 100 mg/dL, but were also eligible if LDL-C was ≥100 mg/dL while on maximum tolerated statin therapy. The study will extend from October 30, 2014 to October 30, 2019. 13 086 patients were randomized to Epanova 4 g or placebo daily in addition to standard medical therapy. The primary efficacy outcome is time to first event of cardiovascular death, myocardial infarction, stroke, coronary revascularization or hospitalization for unstable angina. The trial will continue until 1600 patients reach the primary endpoint, with a median duration of therapy of 3 years. STRENGTH will determine whether Epanova 4 g daily will reduce cardiovascular events in statin-treated high-risk patients with hypertriglyceridemia and low HDL-C levels.

Background—Mendelian randomization data suggest genetic determinants of lifetime higher triglyceride-rich lipoprotein-cholesterol (TRL-C) are causally related to cardiovascular disease and therefore a potential therapeutic target. The relevance of TRL-C among patients receiving statins is unknown. We assessed the relationship between TRL-C and cardiovascular risk, and whether this risk was modifiable among patients receiving statins in the TNT trial. Methods—Patients with coronary heart disease [CHD] and LDL-C 130-250mg/dL entered an 8-week run-in phase with atorvastatin 10mg/day (ATV10). After this period, participants with LDL-C

Background Apolipoprotein B (apoB) is known to be a more powerful predictor of cardiovascular disease than conventional lipids. We aimed to determine the clinical relevance of a newly developed equation to estimate serum apoB levels based on total cholesterol, HDL cholesterol, and triglycerides in patients with high cardiovascular risk. Methods The occurrence of a major cardiovascular event (MCVE) was assessed using the data from the Treating to New Targets (TNT) and Incremental Decrease in End points through Aggressive Lipid lowering (IDEAL) trials. Results Pooled analysis of these two data sets showed that both directly-measured apoB (HR per 1-SD (95% CI): 1.16 (1.11–1.21), P

Background Circulating lipid concentrations are among the strongest modifiable risk factors for coronary artery disease (CAD). Most genetic studies have focused on Caucasian populations with little information available for populations of African ancestry. Methods Using a cohort of ~2,800 African-Americans (AAs) from a biobank at Vanderbilt University (BioVU), we sought to trans-ethnically replicate genetic variants reported by the Global Lipids Genetics Consortium to be associated with lipid traits in Caucasians, followed by fine-mapping those loci using all available variants on the MetaboChip. Results In AAs, we replicated one of 56 SNPs for total cholesterol (TC) (rs6511720 in LDLR, p=2.15×10−8), one of 63 SNPs for high-density lipoprotein cholesterol (HDL-C) (rs3764261 in CETP, p=1.13×10−5), two of 46 SNPs for low-density lipoprotein cholesterol (LDL-C) (rs629301 in CELSR2/SORT1, p=1.11×10−5 and rs6511720 in LDLR, p=2.47×10−5) and one of 34 SNPs for TG (rs645040 in MSL2L1, p=4.29×10−4). Using all available variants on MetaboChip for fine mapping, we identified additional variants associated with TC (APOE), HDL-C (LPL and CETP) and LDL-C (APOE). Furthermore, we identified two loci significantly associated with non-HDL-C: APOE/APOC1/TOMM40 and PCSK9. Conclusions The genetic architecture of lipid traits in AAs differs substantially from that in Caucasians and it remains poorly characterized.

[Objective] To evaluate some risk factors for cardiovascular diseases in feeding and eating disorders, the degree of lipid abnormalities was investigated in a large Japanese cohort of different groups of feeding and eating disorders, according to the Japan Atherosclerosis Society Guidelines for the Prevention of Atherosclerotic Cardiovascular Diseases 2012 (JAS Guidelines 2012). [Methods] Participants in the current study included 732 women divided into four groups of feeding and eating disorders: anorexia nervosa, restricting type (AN-R); anorexia nervosa, binge-eating/purging type; bulimia nervosa (BN); and binge-eating disorder (BED). We measured the serum levels of total cholesterol, high-density-lipoprotein (HDL) cholesterol, and triglyceride in these participants. Low-density-lipoprotein (LDL) cholesterol and non-HDL cholesterol levels were also calculated. [Results] The concentrations of LDL cholesterol and non-HDL cholesterol were widely distributed in all groups. When the LDL cholesterol risk was defined as ≥120 mg/dL and the non-HDL cholesterol risk as ≥150 mg/dL, according to the JAS Guidelines 2012, the proportion of LDL cholesterol risk ranged from 29.6% (BN) to 38.6% (AN-R), and the proportion of non-HDL cholesterol risk ranged from 17.8% (BN) to 30.1% (BED). [Conclusion] The present findings suggest the existence of LDL cholesterol risk and non-HDL cholesterol risk in all groups of eating disorders. Given the chronicity of this condition, the development of elevated concentrations of LDL cholesterol and non-HDL cholesterol at an early age may increase the risk of cardiovascular diseases.

Background This study investigated associations between type 2 diabetes mellitus and non-traditional lipid measures (total cholesterol (TC)/high-density lipoprotein cholesterol (HDL-C), triglycerides (TG)/HDL-C, and non-HDL-C). Methods We conducted a community-based, cross-sectional study of 9 078 participants aged 18 years or older (4 768 men and 4 310 women) who lived in the Jidong community, Tangshan, China. The adjusted odds ratios for type 2 diabetes were calculated for every standard deviation change in TC, log-transformed TG, HDL-C, LDL-C, non-HDL-C, TC/HDL-C, and log-transformed TG/HDL-C using multivariate logistic regression analysis. Receiver operating characteristic (ROC) curve analysis was used to define the points of maximum sum of sensitivity and specificity for each lipid measure as a predictor for type 2 diabetes. Results Prevalence of type 2 diabetes was 6.29 %. Higher TC, TG, LDL-C, non-HDL-C, TC/HDL-C, and TG/HDL-C, and lower HDL-C levels were individually associated with type 2 diabetes in multivariate analyses (all P

Aim: The Japan Atherosclerosis Society (JAS) guidelines for the diagnosis and treatment of hyperlipidemia in Japanese adults recommend using low-density lipoprotein cholesterol (LDL-C) calculated by Friedewald formula (F_LDL-C) for subjects with triglyceride (TG) levels

Abundant evidence over past decades shows that foods with added plant sterols and plant stanols lower serum LDL cholesterol concentrations. However, despite the overwhelming data, numerous scientific questions still remain. The objective of this paper is to summarize the considerations of 60 academic and industrial experts who participated in the scientific meeting in Maastricht, the Netherlands, on issues related to the health effects of plant sterols and plant stanols. The meeting participants discussed issues including efficacy profiling, heterogeneity in responsiveness, effects beyond LDL-C lowering, and food formulation aspects of plant sterol and stanol consumption. Furthermore, aspects related to the potential atherogenicity of elevated circulatory plant sterol concentrations were discussed. Until the potential atherogenicity of plant sterols is resolved, based on the results >200 clinical trials, the risk to benefit of plant sterol use is favorable. Evidence on these topics in plant sterol and plant stanol research was presented and used to reach consensus where possible. It was concluded that endpoint studies looking at plant sterol and plant stanol efficacy are needed, however, there was no clear opinion on the best marker and best design for such a study. Based on the current scientific evidence, plant sterols and plant stanols are recommended for use as dietary options to lower serum cholesterol. Refereed/Peer-reviewed

Context The value of assessing various emerging lipid-related markers for prediction of first cardiovascular events is debated. Objective To determine whether adding information on apolipoprotein B and apolipoprotein A-I, lipoprotein(a), or lipoprotein-associated phospholipase A(2) to total cholesterol and high-density lipoprotein cholesterol (HDL-C) improves cardiovascular disease (CVD) risk prediction. Design, Setting, and Participants Individual records were available for 165 544 participants without baseline CVD in 37 prospective cohorts (calendar years of recruitment: 1968-2007) with up to 15 126 incident fatal or nonfatal CVD outcomes (10 132 CHD and 4994 stroke outcomes) during a median follow-up of 10.4 years (interquartile range, 7.6-14 years). Main Outcome Measures Discrimination of CVD outcomes and reclassification of participants across predicted 10-year risk categories of low ( = 20%) risk. Results The addition of information on various lipid-related markers to total cholesterol, HDL-C, and other conventional risk factors yielded improvement in the model's discrimination: C-index change, 0.0006 (95% CI, 0.0002-0.0009) for the combination of apolipoprotein B and A-I; 0.0016 (95% CI, 0.0009-0.0023) for lipoprotein(a); and 0.0018 (95% CI, 0.0010-0.0026) for lipoprotein-associated phospholipase A(2) mass. Net reclassification improvements were less than 1% with the addition of each of these markers to risk scores containing conventional risk factors. We estimated that for 100 000 adults aged 40 years or older, 15 436 would be initially classified at intermediate risk using conventional risk factors alone. Additional testing with a combination of apolipoprotein B and A-I would reclassify 1.1%; lipoprotein(a), 4.1%; and lipoprotein-associated phospholipase A(2) mass, 2.7% of people to a 20% or higher predicted CVD risk category and, therefore, in need of statin treatment under Adult Treatment Panel III guidelines. Conclusion In a study of individuals without known CVD, the addition of information on the combination of apolipoprotein B and A-I, lipoprotein(a), or lipoprotein-associated phospholipase A(2) mass to risk scores containing total cholesterol and HDL-C led to slight improvement in CVD prediction. JAMA. 2012; 307(23):2499-2506 www.jama.com

Background HIV infected patients, especially those treated with antiretroviral (ARV) drugs, show an increased risk and incidence of cardiovascular disease. Objectives The aim of this study was to evaluate the progression of subclinical atherosclerosis in the carotid arteries, expressed as the value of carotid intima-media thickness (cIMT) and the amount of atherosclerotic plaques, and to analyze the correlation between cIMT and risk factors for cardiovascular diseases in a cohort of HIV infected patients. Methods The analysis included 72 HIV infected patients, mean age 39.4 years, and 27 healthy HIV negative individuals, matched for age and sex. The data collected included evaluation of the infection, ARV treatment, past cardiovascular events, assessment of traditional and nontraditional risk factors for cardiovascular diseases, cIMT measurements and amount of atherosclerotic plaques in the carotid arteries. Results HIV infected patients show more advanced subclinical atherosclerosis in the carotid arteries (cIMT and plaques incidence). The cardiovascular risk profile of the HIV infected patients is significantly different from HIV negative people. Among the HIV positive group lower body mass index (BMI) and higher waist/hip ratio (WHR) are observed. The concentration of all cholesterol fractions is lower, whereas the concentration of triglycerides is higher. Cigarette smoking is more common among HIV-infected individuals. A strong statistical correlation between cIMT and age, hypertension, non-high-density lipoprotein (non-HDL) cholesterol and ARV time were found. Total and LDL cholesterol, and lifetime smoking exposure also affect the cIMT. The relationship between cIMT and current HIV RNA may indicate the impact of the current infection status on the cIMT dynamics in this subpopulation.

Aims To determine whether specific lipid parameters are better predictors of cardiovascular disease (CVD) in Japanese mild-to-moderate hypercholesterolemic patients with and without diabetes. Methods Mildly or moderately hypercholesterolemic patients with no history of CVD received diet therapy or diet therapy plus pravastatin. In this post-hoc subanalysis, 5-year data from 3170 patients (668 diabetes, 2502 non-diabetes) on diet therapy alone were used to compare lipid parameters as predictors of CVD. We examined the data by tertiles, using hazard ratio (HR) per one-standard deviation (SD) increment (decrease for high-density lipoprotein cholesterol, HDL-C), χ 2 value, receiver operating characteristic curve analysis, and spline analysis. Results In mild-to-moderate hypercholesterolemic patients with diabetes, increased total cholesterol (TC)/HDL-C, low-density lipoprotein cholesterol (LDL-C)/HDL-C and decreased HDL-C were strongly associated with increased incidence of CVD (tertile analysis). In non-diabetes, increased non-HDL-C, and LDL-C/HDL-C were significantly associated with increased incidence of CVD. A one-SD decrease in HDL-C and a one-SD increment in non-HDL-C, TC/HDL-C, and LDL-C/HDL-C were significantly associated with increased HRs for CVD in both diabetes and non-diabetes. Linear CVD risk increases were found for non-HDL-C in diabetes and for non-HDL-C and HDL-C in non-diabetes (spline analysis). Conclusions In mild-to-moderate hypercholesterolemia, CVD risk prediction by stratifications of single or combination of traditional lipid parameter values illustrates various patterns. Parameters including HDL-C are better predictors of cardiovascular risk than only using TC or LDL-C alone. Non-HDL-C could be the most useful lipid parameter to assess CVD risk, considering it is easy to calculate and less affected by food intake.

Atherosclerosis is a chronic inflammatory vascular disease, and an association between elevated blood lipids and atherosclerosis has previously been recognized. Low-density lipoprotein cholesterol (LDLc) levels have also been recognized as indicators of cardiovascular complications, but two people who have exactly the same LDLc concentrations may have different risk factors, and the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines recommend patching non-high-density lipoprotein cholesterol (non-HDLc) as another indicator. The present study investigated diabetic dyslipidemia to determine if there is a correlation between dyslipidemia and C-reactive protein (CRP). The data shows that non-HDLc was an independent risk factor for cardiovascular events in patients with diabetes and that CRP could indicate the risk of future cardiovascular events in both high-risk and healthy individuals.

Adult studies have reported associations of low 25-hydroxyvitamin D (25OHD) with dyslipidemia and cardiovascular disease; however, there are scarce pediatric data regarding relationships between vitamin D status and specific lipid markers affecting cardiovascular risk. In this cross-sectional study of children evaluated at university-based pediatric endocrinology clinics, 178 patients meeting criteria for overweight or obesity had 25OHD levels assessed over a 2-year period; 60 of 178 had non-HDL (high-density lipoprotein) cholesterol and fasting lipid parameters performed. Patients with 25OHD

Background: Animal studies have demonstrated that an inhibition of DPP-4 has an impact on the secretion of cholesterol and apoB by the small intestine. However, there is no consensus about the changes of the lipid profile following administration of sitagliptin. Methods: Accordingly, we treated patients who had type 2 diabetes complicated by dyslipidemia with sitagliptin and evaluated its effects on the profile of lipid parameters. A total of 248 outpatients with type 2 diabetes complicated by dyslipidemia were treated with sitagliptin at a daily dose of 50 mg. The levels and percent changes of lipid and glucose metabolism markers were measured at baseline and at 12 weeks after the initiation of treatment. Results: Both plasma glucose and HbA 1 c were significantly decreased. Among the lipid parameters, total cholesterol (TC) and non-high-density lipoprotein cholesterol (non-HDL-C) showed a significant decrease (TC 3.6 ± 15.6%, non-HDL-C 2.9 ± 19.7%; P < 0.05). Stratified analysis revealed a significant decrease of TC, low-density lipoprotein cholesterol (LDL-C) and non-HDL-C in the high triglyceride (TG) group ( ≥ 150 mg/dL) (P < 0.05). Analysis stratified by demographic factors demonstrated significant differences in the changes of TC, LDL-C and non-HDL-C. Multivariate analysis showed a significant decrease of the TC, LDL-C and non-HDL-C levels in the high TG group ( ≥ 150 mg/dL), as well as a significant decrease of TC and LDL-C in patients using strong statins. Conclusions: The results suggested that sitagliptin caused a significant decrease of TC, LDL-C and non-HDL-C, particularly in patients with high baseline TG levels and those using strong statins. J Clin Med Res. 2014;6(5):327-335 doi: http://dx.doi.org/10.14740/jocmr1889w

ObjectiveThis study evaluated the success in attaining non-HDL-cholesterol (non-HDL-C) goals in the multinational L-TAP 2 study.Methods9955 patients ≥20 years of age with dyslipidemia on stable lipid-lowering therapy were enrolled from nine countries.ResultsSuccess rates for non-HDL-C goals were 86% in low, 70% in moderate, and 52% in high-risk patients (63% overall). In patients with triglycerides of >200 mg/dL success rates for non-HDL-C goals were 35% vs. 69% in those with ≤200 mg/dL (p < 0.0001). Among patients attaining their LDL-C goal, 18% did not attain their non-HDL-C goal. In those with coronary disease and at least two risk factors, only 34% and 30% attained respectively their non-HDL-C and LDL-C goals. Rates of failure in attaining both LDL-C and non-HDL-C goals were highest in Latin America.ConclusionsNon-HDL-C goal attainment lagged behind LDL-C goal attainment; this gap was greatest in higher-risk patients.

Objective: This study evaluated the success in attaining non-HDL-cholesterol (non-HDL-C) goals in the multinational L-TAP 2 study. Methods: 9955 patients ≥20 years of age with dyslipidemia on stable lipid-lowering therapy were enrolled from nine countries. Results: Success rates for non-HDL-C goals were 86% in low, 70% in moderate, and 52% in high-risk patients (63% overall). In patients with triglycerides of >200 mg/dL success rates for non-HDL-C goals were 35% vs. 69% in those with ≤200 mg/dL (p < 0.0001). Among patients attaining their LDL-C goal, 18% did not attain their non-HDL-C goal. In those with coronary disease and at least two risk factors, only 34% and 30% attained respectively their non-HDL-C and LDL-C goals. Rates of failure in attaining both LDL-C and non-HDL-C goals were highest in Latin America. Conclusions: Non-HDL-C goal attainment lagged behind LDL-C goal attainment; this gap was greatest in higher-risk patients. © 2012 Elsevier Ireland Ltd.

Non-high-density lipoprotein (non-HDL) cholesterol [total cholesterol minus high-density lipoprotein (HDL) cholesterol] is considered a better predictor of coronary heart disease (CHD) risk than low-density lipoprotein (LDL) cholesterol. The Slovak Roma population have approximately 2.5-fold higher premature CHD mortality than the overall population. It is agreed that detection of dyslipidemia and prevention of atherosclerosis by controlling CHD risk factors should begin in childhood. However, only limited population-based data are available for non-HDL cholesterol in children. Hence the aim of the present cross-sectional study has been to determine population frequency data and correlations of non-HDL cholesterol in 788 Roma and Caucasian children (42% Roma, 51% male), aged 7-17, from Central Slovakia, as part of the Slovak Lipid Community Study. Roma children, compared to Caucasians, had higher serum levels of total cholesterol, LDL cholesterol and HDL cholesterol, were less physically active, smoked more, and had lower body mass index and blood pressure (all at p0.05). Serum non-HDL cholesterol levels were similar in Roma and Caucasians (in mmol/L: 2.74 vs. 2.65, p = 0.062) and similar too in boys and girls (2.66 vs. 2.73, p = 0.092), but higher in the younger (7-11 yrs.) than in the older (12-17 yrs.) age group (2.77 vs. 2.62, p0.001). Non-HDL cholesterol was negatively associated with age and cigarette smoking (r = -0.09 and -0.11 respectively, p0.05), whereas general obesity as measured by body mass index, waist circumference and per capita income were positively correlated with non-HDL cholesterol (r = 0.09-0.14, p0.05). Intermediate or strong positive correlations were found with other lipid variables under study: triglycerides, total and LDL cholesterol and apoliporotein (Apo) B (r = 0.43-0.93, p0.001). No significant association was noted between non-HDL cholesterol and blood pressure, physical activity status, and HDL cholesterol and Apo AI. In a multivariate analysis: body mass index, age and cigarette smoking accounted for 3.3% of the variance in non-HDL cholesterol. The non-HDL cholesterol cut-off points identified as corresponding to the recommended cut-off points of LDL cholesterol for CHD risk assessment and treatment of dyslipidemia in pediatric population were: acceptable3.30, borderline 3.31-3.81 and highor = 3.82 mmol/L. The prevalence of dyslipidemia according to the high non-HDL cholesterol value was 5.4% in Roma and 4.2% in Caucasian children (p = 0.098). In conclusion, our results confirm no ethnic-, gender- or age-related differences in non-HDL cholesterol levels between Slovak Roma and Caucasian children. In both ethnic groups, overweight and obesity and also higher socio-economic status--but not cigarette smoking--are adversely associated with non-HDL cholesterol levels in childhood.

Lipid abnormalities associated with urinary albumin excretion rate in Taiwanese type 2 diabetic patients.BackgroundThe purpose of this study was to examine the lipid abnormalities associated with urinary albumin excretion rate (UAER) in type 2 diabetic patients.MethodsA total of 275 (122 men and 153 women; aged 60.6 ± 11.1 years) patients were selected with stringent criteria to prevent confounders. Normoalbuminuria (N = 152) and albuminuria (N = 123) were defined as urinary albumin-to-creatinine ratio (ACR) of