脂质三联征:血脂异常相关疾病的重要预测因子及其治疗干预

Shafeeque Ahmad, M. Hossain, Muhammad Anas
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引用次数: 5

摘要

心血管疾病(CVD)是全球过早死亡的主要原因。2005年全球总死亡人数的30%,即1750万人死于这种心血管疾病。如果不采取适当和迅速的行动,估计到2015年将有2000万人死亡,其中包括中风。Lavie等人[bbb]指出,关于心血管疾病,特别是冠心病(CHD)的财政负担,大多数医学治疗都针对主要的冠心病危险因素。心血管疾病是指任何与心脏和血管有关的疾病。有许多已知的致病因素直接或间接地导致心血管疾病。脂质三联症主要指三种脂质异常:血浆甘油三酯和小密度低密度脂蛋白(sd-LDL)升高,高密度脂蛋白胆固醇(HDL-C)浓度降低。由于脂质三联体在本质上是引起心血管疾病的高度致动脉粥样硬化,也称为致动脉粥样硬化的脂蛋白表型。肝脏分泌富含甘油三酯的极低密度脂蛋白(VLDL)。当这些脂蛋白与位于毛细血管内皮细胞上的脂蛋白脂肪酶接触时,水解甘油三酯,留下VLDL残留物。许多胆固醇水平在200-240毫克/分升范围内的早衰冠心病患者表现出其他危险因素,如高血压、肥胖或甘油三酯代谢异常。但上述异常常见于高密度脂蛋白[3]浓度降低。富含胆固醇的低密度脂蛋白胆固醇(LDL-C)已被广泛研究,并因其有害胆固醇而闻名,因为它被认为是心血管疾病风险评估的良好标志,其在人体内的水平应低于130 mg/dl。高密度脂蛋白c在35-40毫克/分升之间被认为是好胆固醇,因为它有助于去除胆固醇,同时它也显示出抗氧化特性,携带芳基酯酶/对氧氧化酶抗氧化酶。高水平的高密度脂蛋白c(约60毫克/分升)被认为对人体健康起着良好的保护作用,因为它能有效地保护心脏免受危险的攻击。以往的多项研究都清楚地表明,高浓度的LDL- c及LDL / HDL比值的大幅升高是促进动脉粥样硬化[5]的重要危险因素。英国糖尿病进展研究表明,在这一人群中,LDL-C是冠心病的最大危险因素,其次是HDL-C。因此,研究表明,HDL-C升高0.1 mM可使冠心病发病率降低15%。LDL颗粒可分为大浮力LDL (lb-LDL)和小致密LDL (sd-LDL)。这些亚组分与大小、密度、物理化学成分、代谢行为和动脉粥样硬化性的差异有关。不同的已知技术,如密度梯度、超离心、聚丙烯酰胺凝胶电泳、核磁共振等,用于将LDL分离成sd-LDL和lb-LDL亚组分[7-9]。Lb-LDL颗粒呈>25.5 nm, sd-LDL颗粒呈≤25.5 nm。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lipid Triad: An Important Predictor of Dyslipidemia Related Disorders and its Therapeutic Intervention
Cardiovascular disease (CVD) is leading cause of premature death worldwide. 30% of all global deaths in 2005, i.e. 17.5 million people died from this CVD. If proper and quick actions are not taken, an estimated number of 20 million people will die by 2015, including stroke [1]. Lavie et al. [2] stated regarding fiscal burden of CVD and, especially, coronary heart disease (CHD), most medical treatments are directed at the major CHD risk factors. CVD implies to any medical disorders related to heart and blood vessels. There are a number of known causative factors that are directly or indirectly responsible for CVD. The lipid triad refers basically to three lipid abnormalities: increased plasma triglycerides and small dense low density lipoprotein (sd-LDL), and decreased high density lipoprotein cholesterol (HDL-C) concentrations. Since lipid triad is highly atherogenic in nature causing CVD, also called as atherogenic lipoprotein phenotype. The liver secretes lipoproteins called very-low-density lipoproteins (VLDL) rich in triglycerides. As these lipoproteins come into contact with lipoprotein lipase situated on capillary endothelial cell, hydrolyzes the triglycerides leaving VLDL remnant. Many patients with premature CHD having cholesterol levels in the range of 200-240 mg/dl show other risk factors like hypertension, obesity or abnormalities in triglycerides metabolism. But these above anomalies are often seen in reduced concentration of HDL [3]. Low density lipoprotein cholesterol (LDL-C) rich in cholesterol has been extensively studied and known for its bad cholesterol because it is considered as a good marker for cardiovascular disease risk assessment [4] and its level in human body should be below 130 mg/dl. HDL-C ranging between 35-40 mg/dl is considered as good cholesterol as it helps in the removal of cholesterol along with it also shows antioxidant property carrying arylesterase/ paraoxonase antioxidant enzyme. High level about 60 mg/dl of HDL-C is believed to be played a good protective role in human health protection as it protects efficiently heart from dangerous attack on it. The various previous studies clearly indicate that high concentration of LDL-C and substantially increased ratio of LDL and HDL are important risk factors which promote atherosclerosis [5]. The study for UK Progression of Diabetes Study showed that LDL-C is the strongest risk factor for coronary heart disease followed by HDL-C in this population [6]. Thus it suggested that 0.1 mM rise in HDL-C would decrease coronary heart disease by 15%. LDL particles are differentiated into large buoyant LDL (lb-LDL) and small dense LDL (sd-LDL). These subfractions are associated with difference in size, density, physico-chemical composition, metabolic behavior and atherogenicity. Different known techniques such as density gradient, ultracentrifugation, polyacrylamide gel electrophoresis, nuclear magnetic resonance, etc. are employed for fractionation of LDL into sd-LDL and lb-LDL subfractions [7-9]. Lb-LDL particle shows >25.5 nm while sd-LDL particle shows ≤ 25.5 nm.
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