Could non-HDL-cholesterol be a better marker of atherogenic dyslipidemia in obstructive sleep apnea?

Background/objectiveObstructive 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.MethodsWe retrospectively evaluated treatment naïve 2361 subjects admitted to the sleep laboratory of a university hospital for polysomnography. All subjects’ lipid profile including total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, and non-HDL-cholesterol were measured.ResultsOut 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, non-HDL-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.ConclusionsAtherogenic dyslipidemia is highly prevalent and non-HDL-cholesterol levels are significantly 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.     

Inadequate dietary magnesium intake increases atherosclerotic plaque development in rabbits

Epidemiological studies have shown dietary magnesium (Mg) intake and serum Mg levels to be inversely correlated with the development of atherosclerosis. We hypothesized that low levels of Mg would promote atherosclerotic plaque development in rabbits. New Zealand white rabbits (4 months old, n = 22) were fed an atherogenic diet containing 0.12% (−Mg), 0.27% (control), or 0.43% (+Mg) Mg for 8 weeks. Blood samples were obtained at baseline, 2, 4, 6, and 8 weeks and were assayed for total cholesterol, high-density lipoprotein (HDL), non-HDL, triglycerides (TG), C-reactive protein, serum Mg, and erythrocyte Mg. Aortas from −Mg had significantly more plaque, with an intima thickness 42% greater than control and 36% greater than +Mg. Serum cholesterol levels rose over time, and at 8 weeks, −Mg had the highest and +Mg the lowest total and non-HDL cholesterol and TG levels, although these results did not reach significance. Over time, serum Mg levels increased, and erythrocyte Mg levels decreased. C-reactive protein significantly increased in all groups at 4 and 6 weeks but returned to baseline levels by 8 weeks. This study supports the hypothesis that inadequate intake of Mg results in an increase in atherosclerotic plaque development in rabbits.     

Low-density lipoprotein subfraction profiles in dialysis patients

Summary: Uraemic dyslipidaemia is a major risk factor for cardiovascular disease in end-stage renal failure patients. In patients without renal failure, high levels and qualitative abnormalities of low-density lipoprotein (LDL) are known to be atherogenic. Recently, LDL subfraction analysis has associated premature coronary artery disease with a high prevalence of small, dense LDL particles characterizing the LDL subclass phenotype B. We therefore examined the lipid profiles, LDL subfraction distribution and phenotypes in our population of haemodialysis (HD; n = 30) and peritoneal dialysis patients (PD; n = 17), and compared them to 40 asymptomatic, non-uraemic volunteers. Dialysis patients had significantly higher triglyceride and VLDL cholesterol concentrations and lower HDL cholesterol and smaller LDL peak particle diameters. PD patients had significantly higher total cholesterol, glycated haemoglobin and fasting blood glucose levels with smaller LDL peak particle diameters (24.4 [0.1] vs 24.8 [0.1 nm] than HD. Both groups showed significant negative correlations between plasma triglyceride and LDL peak particle diameter, and positive correlations between HDL cholesterol and LDL peak particle diameter. All the PD patients expressed the B phenotype (LDL peak diameter ± 25.5 nm) compared to 73% of HD patients. This study demonstrates that HD and especially PD patients have atherogenic lipid profiles which are associated with a predominance of small dense LDL particles and the highly atherogenic LDL subclass phenotype B.     

Acute infections in children are accompanied by oxidative modification of LDL and decrease of HDL cholesterol, and are followed by thickening of carotid intima-media.

BACKGROUND: Atherosclerosis begins early in life. Infections might contribute to the pathogenesis of atherosclerosis. In this study, we investigated whether acute infections in children could alter the carotid wall morphology and the lipid profile. METHODS: Mean carotid intima-media thickness (IMT) was measured by high-resolution ultrasound in 28 hospitalised children (mean age: 5+/-2 years), who fulfilled the diagnostic criteria of acute infections (body temperature, >38 degrees C; C-reactive protein, >15mg/ml, and clinical), and in 20 age- and gender-matched controls. Antibodies against oxidised low-density lipoprotein (anti-oxLDL antibodies), as well as total and high-density lipoprotein cholesterol (HDL-C) were analysed in all children. The infection group was investigated both during the acute illness and 3 months after clinical recovery (post-infection). RESULTS: During the acute illness, the infection group had elevated anti-oxLDL antibodies and decreased HDL-C, as compared to those obtained at 3 months and in controls (p<0.05). These changes in the infection group were followed, at 3 months, by thickening of carotid intima-media. Those who received antibiotics during their acute illness had less carotid thickening than those who were not treated with antibiotics (p<0.05). CONCLUSION: Acute infections in children seem to be accompanied by enhanced oxidative modification of LDL and by decrease in HDL-C. These lipid changes may be followed by thickening of carotid artery intima-media. These findings suggest that, in childhood, acute infections could be associated with increased risk of atherosclerosis, and warrant further studies on this topic.     

从TNT研究看稳定性冠心病患者的强化降脂治疗

4 背景 强化降脂使低密度脂蛋白胆固醇（low-density lipoprotein cholesterol，LDL-C）低于指南推荐的水平将使急性冠脉综合征患者获益。但强化降脂使稳定性冠心病患者的LDL-C低于100mg／dL是否安全和有效尚不清楚。     

The Levels of Serum Low-Density Lipoprotein Cholesterol Using Direct Measurement in Healthy Japanese School Children

This study aimed to investigate the levels of serum low-density lipoprotein cholesterol (LDLC) using direct measurement in healthy Japanese school children. The subjects were 621 children (325 boys and 296 girls) aged 9 to 10 in the 4th grade, and 688 children (334 boys and 354 girls) aged 12 to 13 in the 7th grade. The levels of serum LDLC and high-density lipoprotein cholesterol were measured by direct determination (Cholestest LDL and Cholestest NHDL; Daiichi Pure Chemicals Co., Ltd., Tokyo, Japan). In boys in the 4th grade, the mean, the 75th, the 90th and the 95th percentiles of LDLC levels (mg/dl) were 91.6, 104, 124 and 134, respectively. In girls in the 4th grade, they were 92.8, 108, 122 and 130. In boys in the 7th grade, they were 83.4, 96, 113 and 123. In girls in the 7th grade, they were 93.0, 106, 126 and 137. Serum LDLC levels in boys in the 7th grade were lower than those of other groups. The direct measurement of serum LDLC level is useful for evaluation of dyslipidemia in healthy school children, because the method is applicable to non-fasting serum.     

脑梗死患者血浆氧化低密度脂蛋白与一氧化氮、假性血友病因子及血浆颗粒膜蛋白的关系研究

目的探讨动脉粥样硬化性脑梗死患者血浆氧化低密度脂蛋白与血管内皮损伤及血小板活化程度的关系。方法用酶联免疫吸附测定（ELISA）的方法检测49例脑梗死患者和50例相匹配的对照组血浆氧化低密度脂蛋白（OX-LDL）、血管性假血友病因子（VWF）、血浆颗粒膜蛋白（GMP-140）水平，同时用硝酸还原酶比色法测定血清一氧化氮（NO）水平，并把、VWF、GMP-140、NO与OX-LDL作相关分析。结果脑梗死组血浆OX-LDL、、VWF、GMP-140明显高于对照组（t=2．91，P〈0．01；t=3．94，P〈0．001；t=2．08，P〈0．05），而脑梗死组血清NO水平明显低于对照组（t=4．02，P〈0．001）；相关分析表明血浆OX-LDL水平与血清NO水平呈负相关（r=-0．204，P〈0．05），与血浆懈呈正相关（r=0．60，P〈0．01），与血浆GMP-140呈正相关（r=0．430，P〈0．01）。结论脑梗死患者的血浆OX-LDL明显增高，而OX-LDL增高可能是脑梗死的危险因素。     

硫酸酯化葡甘聚糖凝胶颗粒的微观形貌及其吸附行为研究

制备了硫酸酯化魔芋葡甘聚糖凝胶颗粒血液低密度脂蛋白吸附剂，扫描电镜观察产物呈交联网状多孔结构。体外静态吸附实验表明：在37℃振荡吸附2h后，对总胆固醇（TC）、低密度脂蛋白及超低密度脂蛋白胆固醇（LDL＋VLDL-C）、高密度脂蛋白胆固醇（HDL-C）的吸附率分别为52．68％、54．76％、27．78％。通过吸附动力学曲线和吸附等温线分析，吸附剂对LDL＋VLDL-C的作用包括类似分子筛的吸附和电荷间静电相互作用两种方式。