药物预防动脉粥样硬化的研究进展

动脉粥样硬化是导致心血管疾病及死亡的主要原因，严重危害人类健康。目前预防动脉粥样硬化
的机制众多，以调脂代谢降低炎症反应为基础较多。本文将近几年他啶类、贝特类、烟酸类以及中药等调脂药物
对预防动脉粥样硬化的药理作用以及临床应用研究现状做一综述。     

同型半胱氨酸与绝经后女性颈动脉粥样硬化的相关性研究

目的 研究同型半胱氨酸(homocysteine,Hcy)是否为绝经后女性颈动脉粥样硬化的独立风险因素。 方法 对2017年12月—2018年12月北京协和医院健康体检的1 204名55岁以上绝经后女性,进行Hcy检测和颈动脉超声检查。使用多变量logistic回归方法分析Hcy及其他传统风险因素对颈动脉粥样硬化的影响。 结果 Hcy平均值(12.4±3.3)μmol/L,高Hcy血症176人(14.62%)。Hcy与年龄和BMI正相关(分别r=0.19,P<0.001;r=0.11, P<0.001)。颈动脉粥样硬化患者的Hcy显著升高(Z=-2.56,P=0.011)。logistic回归显示,对于颈动脉粥样硬化只有年龄(OR=1.11,95%CI:1.09~1.14)和收缩压(OR=1.02,95%CI:1.01~1.02)是独立风险因素;对颈动脉斑块形成年龄(OR=1.10,95%CI:1.08~1.12)、收缩压(OR=1.02,95%CI:1.01~1.03)、糖化血红蛋白(OR=1.27,95%CI:1.07~1.50)和高血压病史(OR=1.40,95%CI:1.06~1.87)是独立危险因素。 结论 在绝经后女性,Hcy不是动脉粥样硬化发生的独立风险因素,筛查高Hcy血症在预防该人群颈动脉粥样硬化的意义仍需进一步证明。     

Lysophosphatidylcholine‐induced cytotoxicity and protection by heparin in mouse brain bEND.3 endothelial cells

A pathological feature in atherosclerosis is the dysfunction and death of vascular endothelial cells (EC). Oxidized low‐density lipoprotein (LDL), known to accumulate in the atherosclerotic arterial walls, impairs endothelium‐dependent relaxation and causes EC apoptosis. A major bioactive ingredient of the oxidized LDL is lysophosphatidylcholine (LPC), which at higher concentrations causes apoptosis and necrosis in various EC. There is hitherto no report on LPC‐induced cytotoxicity in brain EC. In this work, we found that LPC caused cytosolic Ca²⁺ overload, mitochondrial membrane potential decrease, p38 activation, caspase 3 activation and eventually apoptotic death in mouse cerebral bEND.3 EC. In contrast to reported reactive oxygen species (ROS) generation by LPC in other EC, LPC did not trigger ROS formation in bEND.3 cells. Pharmacological inhibition of p38 alleviated LPC‐inflicted cell death. We examined whether heparin could be cytoprotective: although it could not suppress LPC‐triggered Ca²⁺ signal, p38 activation and mitochondrial membrane potential drop, it did suppress LPC‐induced caspase 3 activation and alleviate LPC‐inflicted cytotoxicity. Our data suggest LPC apoptotic death mechanisms in bEND.3 might involve mitochondrial membrane potential decrease and p38 activation. Heparin is protective against LPC cytotoxicity and might intervene steps between mitochondrial membrane potential drop/p38 activation and caspase 3 activation.     

鞘磷脂类信号通路与动脉粥样硬化的研究进展

动脉粥样硬化是临床常见的冠心病和脑梗死等缺血性心脑血管疾病的主要病理基础,其病因复杂,发病机制尚未完全阐明。近年来,越来越多的研究显示鞘磷脂类信号通路可通过调节脂代谢、炎症和血管内皮功能等影响动脉粥样硬化的发生发展。文章综述了鞘磷脂类信号通路关键分子鞘磷脂、神经酰胺和1-磷酸鞘氨醇与动脉粥样硬化的关系,旨在为防治疾病提供新思路。     

How accurate is atherosclerosis imaging by coronary computed tomography angiography?

Invasive coronary plaque imaging such as intravascular ultrasound and optical coherence tomography has been widely used to observe culprit or non-culprit coronary atherosclerosis, as well as optimize stent sizing, apposition and deployment. Coronary computed tomographic angiography (CTA) is non-invasively available to assess coronary artery disease (CAD) and has become an appropriate strategy to evaluate patients with suspected CAD. Given recent technologies, semi-automated plaque software is available to identify coronary plaque stenosis, volume and characteristics and potentially allows to be used for the assessment of more details of plaque information, progression and future risk as a surrogate tool of the invasive imaging modalities. This review article aims to focus on various evidence in coronary plaque imaging by coronary CTA and describes how accurate coronary CTA can classify coronary atherosclerosis.     

Ex vivo identification of atherosclerotic plaque calcification by a 31P solid-state magnetic resonance imaging technique.

Calcified tissue is a common component of atherosclerotic plaques, and occurs most often in mature plaques. The process of calcification is a poorly understood risk factor that may contribute to a plaque's vulnerability to sudden rupture. In this study a solid-state imaging sequence, termed single-point imaging (SPI), was used to observe calcification directly in ex vivo atherosclerotic plaques. Standards were used to validate the ability of (31)P SPI to detect and differentiate calcification from crystalline cholesterol, phospholipids, and other plaque components. After suitable experimental parameters were found, human carotid specimens obtained by endarterectomy were imaged ex vivo by (31)P solid-state imaging and standard (1)H methods. In contrast to (1)H imaging methods, (31)P imaging detected only the calcification in the plaque.     

氯吡格雷防治动脉粥样硬化缺血性疾病的研究进展

氯吡格雷防治动脉粥样硬化斑块破裂后血栓形成尤其是冠状动脉疾病及其经皮冠脉介入性治疗有了充足的临床试验证据,对于粥样斑块的形成和发展的相关依据正在进行,现就氯吡格雷全面预防和治疗动脉粥样硬化缺血性疾病的研究进展作一综述。