老年冠心病患者颈动脉狭窄筛查的意义及危险因素分析

目的研究老年冠心病患者伴发颈动脉狭窄（CAS）的危险因素。方法根据是否有CAS将775例老年冠心病患者分为CAS组（128例）和非CAS组（647例）,比较2组患者的临床特点,采用Logistic多元回归方法分析冠心病患者的危险因素。结果CAS的发生率为16．5％（128／775）。CAS组年龄高于非CAS组[（69±6）岁比（68±4）岁],差异有统计学意义（P〈0．01）。CAS的发生率随着冠状动脉病变程度加重而增加（x2=11．425,P〈0．01）。左主干病变CAS发生率明显高于其他病变（x2=7．88,P〈0．01）。多因素Logistic回归分析中,只有年龄和冠心病多支病变是CAS的独立危险因素。结论冠心病患者伴发CAS的发生与冠状动脉病变程度相关,高龄是独立的危险因素。     

空腹血糖与青年男性冠心病患者冠状动脉病变的关系

目的 探讨青年男性冠心病患者空腹血糖水平与冠状动脉病变程度的关系.方法 回顾性分析2009年1月至2010年12月于我院住院诊断为冠心病并行冠状动脉造影手术的青年男性(年龄≤44岁)共372例,根据冠状动脉造影结果,分为单支病变组(218例),双支病变组(84例)和三支病变组(70例),观察BMI、SBP、DBP、Hb、BUN、肌酐、血清尿酸、空腹血糖、TG、TC、HDL-C和LDL-C与冠状动脉病变程度的关系.结果 在单支病变、双支病变和三支病变组,空腹血糖水平逐渐升高,两两比较差异有统计学意义[分别为(6.4±2.1)、(7.5±2.5)和(8.4±3.4) mmol/L,均P＜0.05].SBP、TG、TC及HDL-C在单支病变组与其他2组比较存在统计学差异(均P＜0.05);LDL-C在单支病变组与双支病变组比较存在统计学差异(P＜0.05).Logistic回归分析显示,影响冠状动脉多支病变的独立危险因素为TG[4.381(1.221～15.727)]、空腹血糖[1.234(1.117 ～ 1.364)]及SBP[1.035(1.014～1.056)](均P＜0.05).结论 空腹血糖是青年男性冠心病患者冠状动脉多支病变的独立危险因素.     

非酒精性脂肪肝与结直肠腺瘤性息肉发病相关性分析

目的:探讨非酒精性脂肪肝(NAFLD)和结直肠腺瘤性息肉发病的相关性。方法:选择某院2018年2月～2019年2月完善肠镜检查和相关辅助检查资料完整的住院患者608例,划分为结直肠腺瘤性息肉组290例及正常对照组318例;收集性别、年龄、NAFLD患病率及代谢指标等,比较两组有无差异;采用Logistic回归分析NAFLD是否为结直肠腺瘤性息肉危险因素。结果:结直肠腺瘤性息肉组NAFLD患病率明显高于正常对照组;多因素Logistic回归分析显示,NAFLD是结直肠腺瘤性息肉的独立危险因素(OR:2.16;95%CI:1.50～3.10)。结论:NAFLD与结直肠腺瘤性息肉的发病密切相关。     

血清抵抗素与冠状动脉粥样硬化的关系

目的探讨人血清抵抗素水平与冠状动脉粥样硬化病变程度的关系.方法82例临床可疑冠心病患者根据冠状动脉造影结果分为冠状动脉粥样硬化组60例和正常对照组22例,Gensini评分系统对冠状动脉病变狭窄严重程度进行定量评分,酶联免疫吸附法测定血清抵抗素水平,同时获取患者血压、身高、体质量、空腹血糖、胰岛素、血脂等相关指标进行分析.结果(1)冠状动脉粥样硬化组血清抵抗素水平(2.09±1.12)μg/L明显高于正常对照组的(1.43±0.83)μg/L(P＜0.05).(2)Logistic回归显示血清抵抗素水平与冠状动脉狭窄严重程度呈正相关(标准化偏回归系数为0.366,P＜0.05).结论高抵抗素血症与冠状动脉粥样硬化独立相关,可能是动脉粥样硬化发生发展的独立危险因素.     

冠心病发病危险因素的临床分析

目的 探讨冠心病发病主要危险因素及分布特点.方法 分析246例疑诊CHD患者的临床资料,对(CHD)与各危险因素关系作单因素、多因素Logistic回归分析.结果 经冠状动脉造影诊断CHD172例,非CHD 74例.单因素Logistic回归分析显示,年龄、高血压、糖尿病、吸烟、空腹血糖、高低密度脂蛋白胆固醇(LDL-C)血症及血脂异常的比值比(OR)>1.0(P<0.05),CHD与上述因素正相关;载脂蛋白A1(ApoA1)水平OR值<1.0(P<0.05),CHD与APOA1水平负相关.多因素Logistic回归分析显示,依OR值高低排列,糖尿病史、高LDL-C血症、年龄、APOA1水平入选回归方程,其中糖尿病、高LDL-C血症与年龄OR值>1.0(P<0.05),CHD与上述因素呈正相关;ApoAl水平OR值<1.0(P<0.05).另外,患者对高脂血症知晓率低,非CHD组实际血脂异常发生率也高,与CHD组血脂异常分布相似[低高密度脂蛋白胆固醇(HDL-C)、高甘油三酯(TG)、高LDL-C].结论 糖尿病史、高LDL-C血症、年龄可看作CHD危险因素,ApoA1可视为CHD保护因素.非CHD者血脂异常发生率也高,防治工作中不可忽视.     

2型糖尿病患者冠状动脉病变的特点

目的通过冠状动脉造影方法评估2型糖尿病患者的冠状动脉病变状况.方法经冠状动脉造影证实有冠状动脉狭窄的313例冠心病患者,根据有无糖尿病(DM)分为冠心病(CHD)组和DM组,观察各组冠状动脉病变状况的特点.结果两组在年龄及血管病变的分布上无明显差异;DM组女性所占比例高于CHD组;DM组比CHD组血压更高、高脂血症发生率;DM组冠状动脉左主干或多支血管病变发生率、重度狭窄及完全闭塞的发生率均高于CHD组.结论DM合并冠心病患者冠状动脉多支病变及完全闭塞的发生率高,糖尿病可促进冠状动脉病变的发生和发展,是CHD的重要危险因素.     

高血压对青年女性心肌梗死患者的影响及其与冠状动脉病变的关系

目的 探讨高血压对青年女性急性心肌梗死的影响及其与冠状动脉病变程度的关系.方法 收集2003年6-12月在首都医科大学附属北京安贞医院及武装警察部队北京市总队医院住院诊断为急性心肌梗死并行冠状动脉造影的64例青年女性（年龄≤44岁）患者的临床资料进行回顾性分析,根据冠状动脉造影结果,分为单支病变患者（46例）和多支病变患者（18例）;选取同时期住院行冠状动脉造影排除冠心病诊断的青年女性60例作为对照组.观察高血压与冠状动脉病变程度在急性心肌梗死患者中的关系.结果 ①青年女性中,心肌梗死组高血压比例（56.2％,36/64）高于对照组（8.3％,5/60）,多支病变患者高血压比例（77.8％,14/18）高于单支病变患者（47.8％,22/46） （P ＜0.05）.②Logistic回归分析显示,青年女性患者中,高血压[比值比（OR）=16.173,95％置信区间（CI）：4.130 ～ 63.328]、血红蛋白（OR=1.039,95％ CI：1.002 ～1.078）及尿酸（OR=1.008,95％ CI：1.001 ～ 1.016）是急性心肌梗死的独立危险因素（均P＜0.05）.③心肌梗死组中,高血压合并冠状动脉多支病变患者（38.9％,14/36）多于非高血压合并多支病变患者（14.3％,4/28） （P＜0.05）;急性ST段抬高型心肌梗死患者中,高血压合并冠状动脉多支病变（77.8％,14/18）的比例高于单支病变组（46.2％,18/39） （P ＜0.05）.结论 高血压是青年女性急性心肌梗死的独立危险因素,合并高血压的心肌梗死患者冠状动脉病变更为严重.     

血清尿酸水平与冠状动脉病变程度的关系

目的:探讨冠状动脉造影患者血清尿酸(SUA)水平与冠状动脉病变程度的关系.方法:入选我院行冠状动脉造影(CAG)患者474例,根据CAG结果分为冠心病(CAD)组(366例)和非CAD组(108例).冠状动脉病变程度采用冠状动脉病变支数和冠状动脉病变Gensini积分(GS)量化.结果:(1)总体CAD组SUA水平高于非CAD组(P<0.05),亚组分析女性CAD组SUA水平高于女性非CAD组(P<0.05);总体CAD组、男性CAD组、女性CAD组高尿酸(HUA)百分比均高于非CAD组(P<0.05).(2)SUA水平第3、第4四分位的CAD患病率明显高于第1、第2四分位(P<0.05).(3)多因素Logistic回归分析显示HUA是经CAG诊断的CAD的危险因素(OR=2.639,95%CI为1.080～6.443,P=0.033).(4)相关分析提示SUA水平和GS有正相关性(r=0.270,P<0.01),亚组分析男性、女性SUA水平和GS间均有正相关性(r=0.171,P<0.01;r=0.298,P<0.01).结论:SUA可能是CAG诊断的CAD的危险因素.SUA水平和冠状动脉病变程度有一定相关性,女性相关性较男性略显著.     

血尿酸水平与冠心病及其严重程度的关系研究

目的:研究血尿酸(UA)水平与冠心病(CAD)的发生及其严重程度的关系.方法:根据冠状动脉造影结果将患者251例分为CAD组148例和非CAD组103例,以发生病变的血管支数反映冠心病严重程度,将患者分为A、B、C、D4组,分别对应冠状动脉正常、1支、2支、3支病变,比较各组间尿酸水平.根据尿酸水平按四分位数将患者分为第1～4组.结果:(1)CAD组血尿酸水平高于非CAD组(P＜0.01),Logistic多因素同归分析显示年龄、天冬氨酸转氨酶、尿酸水平为冠心病的危险因素.(2)尿酸水平与冠脉病变支数呈正相关(rn=0.229,P＜0.01),其中女性组尿酸水平与冠脉病变支数呈正相关(rn=0.317,P＜ 0.01),而男性组无此相关性(rs=-0.36,P=0.671).(3)血尿酸水平第3、第4四分位的CAD患病率明显高于第1、第2四分位(P＜0.01).结论:血清尿酸水平与冠心病的患病率有关,且与冠状动脉病变程度呈正相关.     

老年和中青年冠心病的临床特点危险因素与冠状动脉造影关系探讨

目的　为了解老年、中青年冠心病 (CHD)的临床特点、危险因素和冠状动脉病变 ,以提高防治效果。方法　将 110例 CHD患者按年龄分两组 ,老年组 72例 (60岁以上 ) ,中青年组 3 8例 (4 5岁以下 ) ,比较组间临床症状、危险因素及冠状动脉病变支数、狭窄程度。结果　中青年组具有典型心绞痛者占 89.5% ,老年组仅占4 7.2 % (P<0 .0 5)。老年组高血压占 4 7.2 % ,而中青年组仅占 15.8% (P<0 .0 1)。中青年组吸烟占 50 % ,老年组仅占 2 7.8% (P<0 .0 5)。家族史中青年组占 3 9.5% ,老年组仅占 9.7% (P<0 .0 1) ,提示吸烟、家族史为中青年组重要的危险因素。冠状动脉病变老年组三支病变占 4 3 .1%且狭窄程度较重 ,中青年组单支病变多占 55.3 % ,其中 7例 (18.4 % )冠状动脉造影正常或轻度狭窄。结论　 CHD患者的年龄对临床症状、危险因素、冠状动脉病变有明显的关系 ,预防冠心病要从儿童做起     

Disease System Analysis: Basic Disease Progression Models in Degenerative Disease

Purpose To describe the disease status of degenerative diseases (i.e., type 2 diabetes mellitus, Parkinson’s disease) as function of disease process and treatment effects, a family of disease progression models is introduced.Methods Disease progression is described using a progression rate (R_dp) acting on the synthesis or elimination parameters of the indirect response model. Symptomatic effects act as disease-dependent or -independent effects on the synthesis or elimination parameters. Protective drug effects act as disease dependent or -independent effects on R_dp.Results Simulations with the ten disease models show distinctly different signature profiles of treatment effects on disease status. Symptomatic effects result in improvement of disease status with a subsequent deterioration. Treatment cessation results in a disease status equal to the situation where treatment had not been applied. Protective effects result in a lasting reduction, or even reversal, of the disease progression rate and the resulting disease status during the treatment period. After cessation of treatment the natural disease course will continue from the disease status at that point.Conclusion Disease system analysis constitutes a scientific basis for the distinction between symptomatic versus protective drug effects in relation to specific disease processes as well as the identification of the exposure-response relationship during the time-course of disease.     

Epigenetic Inheritance of Disease and Disease Risk

Epigenetic marks in an organism can be altered by environmental factors throughout life. Although changes in the epigenetic code can be positive, some are associated with severe diseases, in particular, cancer and neuropsychiatric disorders. Recent evidence has indicated that certain epigenetic marks can be inherited, and reshape developmental and cellular features over generations. This review examines the challenging possibility that epigenetic changes induced by environmental factors can contribute to some of the inheritance of disease and disease risk. This concept has immense implications for the understanding of biological functions and disease etiology, and provides potential novel strategies for diagnosis and treatment. Examples of epigenetic inheritance relevant to human disease, such as the detrimental effects of traumatic stress or drug/toxic exposure on brain functions, are reviewed. Different possible routes of transmission of epigenetic information involving the germline or germline-independent transfer are discussed, and different mechanisms for the maintenance and transmission of epigenetic information like chromatin remodeling and small noncoding RNAs are considered. Future research directions and remaining major challenges in this field are also outlined. Finally, the adaptive value of epigenetic inheritance, and the cost and benefit of allowing acquired epigenetic marks to persist across generations is critically evaluated.     

Tangier Disease

Tangier disease is one of the most severe forms of familial high-density lipoprotein (HDL) deficiency. Since its discovery it has been diagnosed in about 100 patients and is characterized by severe plasma deficiency or absence of HDL, apolipoprotein A-I (apoA-I, the major HDL apolipoprotein) and by accumulation of cholesteryl esters in many tissues throughout the body. The biochemical signs of this condition are plasma HDL concentrations less than 5mg/dL, low total plasma cholesterol (below 150mg/dL), and normal or high plasma triglycerides. Tangier disease is caused by mutations in the ‘ATP-Binding Cassette transporter Al’ (ABCA1) gene, which encodes the membrane transporter ABCA1. This transporter plays a key role in the first step of reverse cholesterol transport, through which the efflux of free cholesterol from peripheral cells is transferred to lipid-poor apoA-I. The Tangier disease clinical phenotype is inherited as an autosomal recessive trait, the biochemical phenotype is inherited as an autosomal co-dominant trait. Nearly all the children affected by Tangier disease were identified on the basis of large, yellow-orange tonsils, while half of the adult patients affected by Tangier disease came to medical attention because of symptoms of neuropathy. Diagnosis in the remaining subjects was related to the clinical features of hepatomegaly, splenomegaly, premature myocardial infarction (about 30% of Tangier disease cases) or stroke, thrombo-cytopenia, anemia, gastrointestinal disorders, corneal opacities, hypocholesterolemia, low HDL cholesterol, or following a familial screening of Tangier patients. To date there is no specific treatment for Tangier disease. Old and recently designed drugs, known to increase HDL levels, have been shown to be ineffective in Tangier patients. The possible and more realistic therapeutic strategy should be designed to obtain a selective increase of mature HDL concentration to restore cholesterol efflux. Recently designed drugs like the cholesteryl ester transfer protein (CETP) inhibitors dalcetrapib and anacetrapib and reconstituted forms of HDL could be considered until the development of gene therapy.