Morphological,Functional, and Tissue Characterization of Silent Myocardial Involvement in Patients With Primary Biliary Cholangitis

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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.     

糖尿病患者甘油三酯/高密度脂蛋白胆固醇比值水平与胰岛素抵抗的关系

目的探讨血清甘油三酯/高密度脂蛋白胆固醇(TG/HDL-C)比值水平与胰岛素抵抗的关系。方法对146例2型糖尿病患者测定空腹胰岛素(FINS)、空腹血糖(FBG),TG,HDL-C,低密度脂蛋白胆固醇(LDL-C)水平,计算TG/HDL-C比值,并按TG/HDL-C和FBG水平分组,比较组间差异与胰岛素抵抗指数(HOMA-IR)的关系。结果糖尿病组TG/HDL-C比值水平(2.531±3.741)显著高于正常对照组(0.898±0.487),差异有显著性(t=4.279,P<0.001)。TG/HDL-C比值增高组HOMA-IR(3.291±2.004)明显高于TG/HDL-C比值正常组(2.403±1.789),差异有显著性(t=2.796,P<0.01)。血糖水平>10 mmol/L组HOMA-IR(3.575±2.216)明显大于血糖水平≤10mmol/L组(2.384±1.584),差异有显著性(t=3.760,P<0.001)。结论糖尿病患者TG/HDL-C比值水平与胰岛素抵抗存在着密切的相关性。     

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.     

Close correlation between high-density lipoprotein and triglycerides in normotriglyceridaemia.

The relationship between high-density-lipoprotein (HDL) particle size subclasses and the levels of the major lipoprotein lipids was studied in 74 men consecutively referred to the lipid clinic. HDL (density 1.070-1.21 kg l-1) was separated by polyacrylamide gradient gel electrophoresis (GGE) into five size-defined subclasses, in order of decreasing size as follows: HDL2b, HDL2a, HDL3a, HDL3b and HDL3c. Cholesterol and triglyceride concentrations in very-low-density (VLDL), low-density (LDL) and high-density (HDL) lipoproteins were determined. The level of VLDL triglycerides was negatively correlated with HDL2b (r = -0.66, P less than 0.0001), and positively correlated with HDL3b concentrations (r = 0.65, P less than 0.0001). Both correlations were restricted to subjects with VLDL triglyceride concentrations of less than 1.80 mmol l-1, i.e. those with normotriglyceridaemia. Patients with a history of myocardial infarction and/or angina pectoris (n = 18) had significantly lower HDL2b levels than subjects with asymptomatic hyperlipidaemia (n = 50), i.e. 0.16 vs. 0.22 mg protein ml-1 (P less than 0.05), despite essentially similar cholesterol and triglyceride levels in the VLDL, LDL and HDL fractions, including HDL2 and HDL3 cholesterol.     

Lipids and lipoproteins as risk factors for coronary heart disease in men with abnormal glucose tolerance: the Honolulu Heart Program

Abstract. Objectives. To evaluate lipids and lipoproteins as risk factors for coronary heart disease (CHD) in older men with non-insulin-dependent diabetes (NIDDM) or abnormal glucose tolerance compared with normoglycaemic men. Design. A prospective, population-based cohort study based on the lipoprotein examination (1970–72) of the Honolulu Heart Program. Follow-up was through to December 1988. Setting. Honolulu, Hawaii. Subjects. Japanese-American men, ages 51–72 at baseline: 2042 with 1 h glucose < 12.5 mmol l^?1 (normal group); 376 on oral hypoglycaemic agents or with 1 h glucose ≥ 12.5 mmol l^?1 after 50 g oral glucose challenge (abnormal glucose tolerance group). None had prevalent coronary heart disease (CHD) or stroke at baseline. Main outcome measures. Incident CHD: definite nonfatal myocardial infarction (MI) or fatal CHD. Results. There were 221 incident cases in the normal group, and 65 in the abnormal glucose tolerance group. Total and high-density lipoprotein (HDL) cholesterol were significant predictors of incident CHD in men with NIDDM or abnormal glucose tolerance after controlling for age, body-mass index, systolic blood pressure, pack-years of cigarettes and alcohol consumption (P < 0.05). Total, low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterol were significant predictors in normal men, and HDL cholesterol was of borderline significance. Conclusions. Abnormal lipids and lipoproteins are significant, independent predictors of CHD in subjects with NIDDM or abnormal glucose tolerance. Attention to lipid and lipoproteins as CHD risk factors should be part of clinical management of these patients.     

HDL-C/ApoA1、MCP-1水平与中青年冠心病患者病变程度及炎症反应的相关性

目的 探讨高密度脂蛋白胆固醇（HDL-C）/载脂蛋白A1(ApoA1)及单核细胞趋化蛋白-1(MCP-1)水平与中青年冠状动脉粥样硬化性心脏病（以下简称冠心病）病变程度及炎症反应的相关性。方法 选取2021年10月—2022年10月在南通大学附属医院和如皋市人民医院就诊的中青年冠心病患者130例作为观察组,其中稳定型心绞痛（SAP）42例,不稳定型心绞痛（UAP）50例,急性心肌梗死（AMI）38例;病变支数：单支病变59例,双支病变39例,三支病变32例;按照狭窄程度分为轻度46例,中度54例,重度30例。另取同期该院冠状动脉CT血管造影或冠状动脉造影正常者130例作为对照组。比较各组HDL-C/ApoA1、MCP-1、肌酸激酶同工酶MB(CK-MB)、肌酸激酶（CK）、心肌肌钙蛋白Ⅰ（cTnⅠ）、白细胞计数（WBC）、超敏C反应蛋白（hs-CRP）、生长刺激表达基因2蛋白（ST2）及Gensini评分。结果 观察组HDL-C/ApoA1低于对照组（P <0.05）,MCP-1、CK-MB、CK、cTnⅠ、WBC、hs-CRP、ST2高于对照组（P <0.05）。AMI和...     

Effect of recent alcohol intake on acceptor properties of high-density lipoproteins and their interaction with liver cells

Institute of Therapy, Siberian Branch, Academy of Medical Sciences of the USSR, Novosibirsk. All-Union Preventive Medicine Research Center, Ministry of Health of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR Yu. P. Nikitin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 110, No. 12, pp. 611–613, December, 1990.