脂蛋白(a)与动脉粥样硬化研究进展

脂蛋白(a)由低密度脂蛋白和载脂蛋白(a)组成.高血浆脂蛋白(a)水平是动脉粥样硬化和心血管疾病的独立危险因素.脂蛋白(a)不但能参与动脉粥样硬化斑块的形成,还能影响抗炎机制和血管壁中促凝与抗凝因子的平衡.血浆脂蛋白(a)水平的个体差异很大,主要受遗传因素控制.血浆脂蛋白(a)水平对药理和非药理因素都不敏感,临床上缺乏高效安全降低脂蛋白(a)水平的治疗方法.近年,科研工作者发现反义寡核苷酸链和人工合成的肽链等可以降低脂蛋白(a)水平,但用于临床治疗还需进一步研究.本文拟对近年来脂蛋白(a)与动脉粥样硬化研究的新进展进行综述.     

脂蛋白(a)的研究进展

脂蛋白(a)是动脉粥样硬化形成与进展的高危因素,外周血中高浓度的脂蛋白(a)已成为冠心病公认的预测因子。由于它主要受遗传调控,饮食、运动、生活方式、传统降脂药物等对脂蛋白(a)水平的影响很小。随着研究的深入,脂蛋白(a)的代谢、致病机制和危害逐渐被人们了解,氧化修饰后的脂蛋白(a)具有更强的致动脉粥样硬化作用。此外,可降低脂蛋白(a)的新型降脂药物已经被研发出来,它们降低脂蛋白(a)的强度和作用靶点各不相同,对疾病的预后的影响也仍有待观察。本文就脂蛋白(a)的代谢、遗传调控、氧化修饰、临床干预手段等研究进展作一综述。     

脂蛋白(a)与钙化性主动脉瓣疾病的研究进展

钙化性主动脉瓣疾病是常见的心血管疾病,随着人口老龄化的日益加剧其逐渐成为主要的医疗负担.瓣膜置换术是该病的主要治疗方法,但高龄群体手术风险较大,并发症发生率高.且目前仍缺少预防或减缓疾病进展的有效药物.研究发现,脂蛋白(a)在瓣膜钙化的病理过程中起关键作用,脂蛋白(a)水平升高是钙化性主动脉瓣疾病的重要危险因素,显著增...     

脂蛋白(a)与糖尿病肾病相关性的研究进展

大量证据表明,脂蛋白(a)[LP(a)]与冠心病、脑卒中和钙化性主动脉瓣狭窄等心脑血管疾病密切相关.随着研究的深入,发现LP(a)与糖尿病肾病也有一定的相关性,可能在其发生发展、临床诊断及治疗上发挥一定的作用.本文就脂蛋白(a)的结构特点、遗传、代谢及与糖尿病肾病的相关性最新进展予以综述.     

中老年女性脂蛋白(a)含量测定及临床意义

目的　观察中老年女性血清脂蛋白 (a)〔LP(a)〕及血脂含量与心、脑血管疾病的发生、发展的关系。方法　采用电泳法和酶法检测30 5例中老年女性血清LP(a)及血脂含量。结果　中老年女性绝经后组 ,血清中LP(a)、LDL C、TC、TG含量高于绝经前组 (P <0 .0 1或P <0 .0 5) ;HDL C、和E2 低于绝经前组 (P <0 .0 1或P <0 .0 5)。心、脑血管疾病组LP(a)、LDL C、TC、TG均明显高于对照组 (P <0 .0 1或P <0 .0 5) ,HDL C低于对照组 (P <0 .0 5)。结论　中老年女性绝经后血清中LP(a)、LDL C、TC、TG含量升高 ,HDL C含量降低使中老年女性增加了患心脑血管疾病的危险。     

脂蛋白(a)致动脉粥样硬化作用机制研究进展

脂蛋白 (a)被认为是动脉粥样硬化疾病的独立危险因素 ,但是脂蛋白 (a)在动脉粥样硬化形成中的作用机制尚不完全清楚。本文从其结构特点和遗传特性及其致动脉粥样硬化作用机制两个方面进行综述 ,分析了脂蛋白 (a)可能参与动脉粥样硬化形成的机制 ,为临床预防和治疗动脉粥样硬化性心脑血管疾病提供理论依据     

脂蛋白(a)与冠心病的研究

脂蛋白(a)[Lp(a)]由低密度脂蛋白(LDL)和载脂蛋白(a)组成.Lp(a)的血浆浓度主要由遗传因素决定,并与其基因多态性相关,具有个体及种族差异.Lp(a)有促动脉粥样硬化(AS)作用,其血浆浓度与冠心病(CHD)密切相关,是AS及CHD的独立危险因素.烟酸缓释制剂是目前治疗高Lp(a)血症最有效的药物.     

脂蛋白(a)与冠心病的研究

脂蛋白(a)[Lp(a)]由低密度脂蛋白(LDL)和载脂蛋白(a)组成。Lp(a)的血浆浓度主要由遗传因素决定,并与其基因多态性相关,具有个体及种族差异。Lp(a)有促动脉粥样硬化(AS)作用,其血浆浓度与冠心病(CHD)密切相关,是AS及CHD的独立危险因素。烟酸缓释制剂是目前治疗高Lp(a)血症最有效的药物。     

脂蛋白(a)与心血管疾病的关系

脂蛋白(a)[Lp(a)]结构类似于低密度脂蛋白(LDL),高水平Lp(a)是一种公认的心血管疾病危险因子。体内存在氧化型Lp(a)更易于促进动脉粥样硬化的发生发展。Lp(a)中的载脂蛋白(a)[apo(a)]存在异质性,研究显示其危险性可能是由于apo(a)等位基因水平差异引起的,而且apo(a)的多态性影响到Lp(a)水平的临床测定,如何降低apo(a)对结果的影响还需要更多深入研究。目前针对高Lp(a)水平的人群尚无统一的治疗标准,但降脂治疗有益于预防心脑血管疾病的发生。     

老年肾脏疾病血清脂蛋白(a)检测的临床意义

肾脏疾病患者常存在脂类代谢紊乱 ,不仅加重肾脏本身病变。同时与心血管病变关系密切。近年国内外研究表明血清脂蛋白 (a) [Lp(a) ]是导致心脑血管疾病的独立危险因素[1]。为早期发现并预防肾脏疾病患者的心血管并发症 ,作者对 52例老年肾脏疾病患者及 2 8例健康人进行血清Lp(a     

The role of Lipoprotein(a) in cardiovascular disease: Current concepts and future perspectives

High lipoprotein(a) [Lp(a)] levels are associated with the development of atherosclerotic cardiovascular disease (ASCVD) and with calcific aortic valve stenosis (CAVS) both observationally and causally from human genetic studies. The mechanisms are not well characterized but likely involve its role as a carrier of oxidized phospholipids (OxPLs), which are known to be increased in pro-inflammatory states, to induce pro-inflammatory changes in monocytes leading to plaque instability, and to impair vascular endothelial cell function, a driver of acute and recurrent ischemic events. In addition, Lp(a) itself has prothrombotic activity. Current lipid-lowering strategies do not sufficiently lower Lp(a) serum levels. Lp(a)-specific-lowering drugs, targeting apolipoprotein(a) synthesis, lower Lp(a) by up to 90% and are being evaluated in ongoing clinical outcome trials. This review summarizes the current knowledge on the associations of Lp(a) with ASCVD and CAVS, the current role of Lp(a) assessment in the clinical setting, and emerging Lp(a)-specific-lowering therapies.     

Relationship Between Lipoprotein(a) and Angiographic Severity of Femoropopliteal Lesions

Aim: High levels of lipoprotein(a) [Lp(a)] are a risk factor for peripheral artery disease (PAD). However, the relationship between Lp(a) levels and the severity of femoropopliteal lesions in patients with PAD has not been systematically studied. This study aimed to assess the impact of Lp(a) levels on angiographic severity of femoropopliteal lesions in patients with PAD. Methods: We retrospectively analyzed a single-center database including 108 patients who underwent endovascular therapy for de novo femoropopliteal lesions and measured the Lp(a) levels before therapy between June 2016 and September 2019. Patients were divided into low Lp(a) [Lp(a) ＜30 mg/dL; 77 patients] and high Lp(a) [Lp(a) ≥ 30 mg/dL; 31 patients] groups. Trans-Atlantic Inter-Society Consensus (TASC) II classification, calcification [referring to the peripheral arterial calcium scoring system (PACSS) classification], and lesion length were compared between the groups. Results: The prevalence of TASC II class D (13% vs 38%, P ＜0.01) and severe calcification (PACSS 4) (6% vs 23%, P =0.02) was significantly higher and the lesion length longer (123±88 mm vs 175±102 mm, P ＜0.01) in the high Lp(a) group than in the low Lp(a) group. In multivariate analysis, Lp(a) ≥ 30 was an independent predictor for the prevalence of TASC II class D (HR=3.67, 95% CI 1.27–10.6, P =0.02) and PACSS 4 (HR=4.97, 95% CI 1.27–19.4, P =0.02). Conclusion: The prevalence of TASC II class D and severe calcification of femoropopliteal lesions was higher in patients with high Lp(a) than those with low Lp(a).     

Lipoprotein(a) in Type 1 Diabetic Patients with Renal Disease

Lp(a) was measured in 64 normoalbuminuric, 52 microalbuminuric, and 37 proteinuric Type 1 diabetic patients and 54 healthy subjects. Microalbuminuric and proteinuric Type 1 diabetic patients had higher median Lp(a) values (133 (16–1932) and 169 (17–1149) mg I^?1) than patients with normal AER (73 (15–1078) mg I^?1; p=0.048 and p=0.027). Lp(a) in healthy subjects (110 (15–1630)mg I^?1) did not differ from the diabetic subgroups. The frequency of Lp(a) values in the upper quarter of the normal distribution was similar in the diabetic groups and did not differ between diabetic and control subjects. The cumulative distribution of Lp(a) was similar in all groups. Lp(a) concentrations were not related to AER, age, gender, duration of diabetes, body mass index, glycaemic control, serum creatinine, free insulin or systolic blood pressure. Cholesterol, LDL-cholesterol, triglycerides, and apo B were higher in microalbuminuric and proteinuric than in normoalbuminuric Type 1 diabetic patients. Lp(a) was independently related to diastolic blood pressure, fibrinogen, and macroangiopathy. In conclusion, median Lp(a) concentrations tend to be higher in Type 1 diabetic patients with early and established renal disease, although the differences are small and the overlap between groups large. Lp(a) is related to diastolic blood pressure and fibrinogen, and this association of powerful risk factors suggests that Lp(a) may play a role in the pathogenesis of cardiovascular disease in Type 1 diabetic patients with proteinuria. Whether Lp(a) is an independent determinant of increased cardiovascular risk in these patients needs to be elucidated by prospective studies.     

胱硫醚β-合酶活性的测定及应用

为探讨姜黄素的降血脂和抗动脉粥样硬化作用是否通过影响低密度脂蛋白和脂蛋白（ａ）的代谢来实现的,用姜黄素经刺猥腋下静脉注入,２ｍｉｎ后注射＾１２５Ｉ－低密度脂蛋白、＾１２５Ｉ－低密度脂蛋白、＾１２５Ｉ－脂蛋白（ａ）、＾１２５Ｉ－去唾液酸低密度脂蛋白或＾１２５Ｉ－去唾液酸脂蛋白（ａ）,１小时后处死动物,测定血、肝、肾、脾、胆汁和肾上腺中的放射性含量。实验发现,姜黄素使低密度脂蛋白进入肝脏和肾上腺增多胆     

Lipoprotein (a) Immunapheresis in the Treatment of Familial Lipoprotein (a) Hyperlipoproteinemia in a Patient with Coronary Heart Disease

Abstract: This paper reports 2 years' experience with lipoprotein (a) (Lp[a]) immunapheresis which was successfully handled on a now 40-year-old patient with familial Lp(a) hyperlipoproteinemia inducing severe coronary heart disease with 2 myocardial infarctions and diffuse coronary sclerosis. Continued treatment by Lp(a) immun-absorption with specific sheep antibodies reduced stenosis in coronary vessels more than 50% and stopped the progression of coronary heart disease. A special apheresis technique and the results of continued absorption effects are described.