老年冠心病患者踝臂血压指数与冠脉病变相关性研究

目的探讨老年冠心病患者踝臂血压指数与冠脉病变相关性研究。方法造影剂均选用威视派克,按照几支冠状动脉血管存在≥50%的狭窄,分为一支、二支和三支病变,比较冠心病患者的各项指标。结果 2组患者ABI有显著差异(P<0.05)。结论 ABI和冠状动脉病变严重程度呈负相关,是预测冠状动脉硬化程度的一种简单可靠的指标。     

脉压、收缩压与冠状动脉病变程度相关性研究

目的 探讨冠心病患者脉压(PP)、收缩压(SBP)与冠状功脉病变程度相关性.方法 选择心内科行冠状动脉造影的患者241例,根据冠状动脉造影结果分为冠状动脉狭窄组(n=135)与非冠状动脉狭窄组(n=106).比较冠状动脉狭窄组与非冠状动脉狭窄组以及不同病变支数患者的血压参数.分析各血压参数与冠状动脉狭窄发生率的关系,各血压参数与冠状动脉病变程度的相关性.结果 ①冠状动脉狭窄组冠状动脉狭窄评分、年龄、收缩压、脉压显著高于非冠状动脉狭窄纽(P＜0.05～0.01),且年龄.冠状动脉狭窄评分、SBP.PP随着狭窄支数的增加而逐渐增高,尤其以3支病变患者更为显著(P＜0.05).而DBP低于非冠状动脉狭窄组(P＜0.05).且随着狭窄支数的增加有逐渐降低趋势,但没有统计学意义(P＜0.05).②Pearson直线相关分析年龄、糖尿病史、吸烟、SBP、PP、总胆固醇.低密度脂蛋白胆固醇与冠状动脉病变支数.冠状动脉狭窄记分呈正相关(r分别为0.325,0.241,0.227,0.385,0.517,0.087,0.053,P＜0.05～0.01).③多因素Logistic逐步回归分析SBP.PP.年龄、糖尿病史、吸烟与冠状动脉3支病变的发生有相关性(ON分别为1.283,1.787,1.535,1.950,I.779,P＜0.05).④多元线性回归分析显示年龄、SBP、PP、吸烟、与冠状动脉狭窄记分呈正相关(β=0.301,1.955,0.107,0.240,P＜0.05～0.01).结论 PP、SBP增高,冠状动脉挟窄性病变的发生率增加,冠状动脉狭窄程度加重.冠状动脉狭窄程度与PP,SBP呈正相关,PP是冠状动脉病变程度的独立预测因子.     

急性冠状动脉综合征患者血清中基质金属蛋白酶-2的表达

目的探讨急性冠状动脉综合征与血清基质金属蛋白酶-2(MMP-2)的相关性。方法应用酶图(SDS-PAGE en-zymograph)和Western blot方法检测50名急性冠脉综合征患者(27名ST段抬高急性心肌梗塞患者和23名不稳定性心绞痛患者)、20名稳定性心绞痛患者及40名正常对照者的血清MMP-2水平。结果急性心肌梗塞组血清MMP-2水平明显高于不稳定性心绞痛组;急性心肌梗塞组及不稳定性心绞痛组血清MMP-2水平明显高于正常对照组;稳定性心绞痛组与正常对照组差异无显著意义;急性心肌梗塞组及不稳定性心绞痛组血清MMP-2水平高于稳定性心绞痛组。结论急性冠脉综合征患者血清MMP-2水平明显升高,其水平可能与冠状动脉斑块的稳定性相关。     

C反应蛋白在急性冠脉综合征中的临床意义

目的探讨C反应蛋白(CRP)与急性冠脉综合征(Acute coronary syndromesACS的)关系。方法测定经冠脉造影确诊的冠心病患者60例(其中急性冠脉综合征患者30例,非急性冠脉综合征的冠心病患者30例)和冠脉造影排除冠心病患者30例的血CRP浓度。结果ACS患者组(A组)血CRP浓度为(14.53±16.87)mg/dL;非ACS患者组(B组)血CRP浓度为(4.07±4.56)mg/dL;对照组(C组)血CRP浓度为(3.67±4.43)mg/dL,A组与B组之间CRP浓度有显著性差异(P<0.001);B组与C组之间CRP浓度无显著性差异。结论急性冠脉综合征患者血CRP浓度明显升高,提示炎症反应与急性冠脉综合征密切相关,CRP浓度测定可作为急性冠脉综合征的监测指标。     

C反应蛋白对冠脉病变稳定性评估

目的探讨C反应蛋白(CRP)与冠脉病变稳定性的关系。方法选择稳定性心绞痛25例,不稳定性心绞痛35例,入院后即刻0、6、24、48h和7d检验CRP和肌钙蛋白(TnT),根据患者是否发生心脏不良事件(MACE)进行分类研究。结果不稳定性心绞痛患者CRP的水平明显高于稳定性心绞痛患者,P<0.01,发生心脏不良事件的患者其CRP和TnT水平在任何时点均高于未发生者,P<0.01。结论 C反应蛋白与冠脉病变稳定性相关,CRP和TnT联合检验可用于急性冠脉综合症的危险分层。     

老年人心电图及冠脉造影分析

目的探讨老年人心电图及冠脉造影分析。方法回顾分析我院对234例65岁以上老年人冠状动脉造影检查,对检查结果进行分析。结果 234例中心电图阳性180例,冠状动脉造影阳性144例,冠状动脉造影阴性36例;心电图阴性54例,冠状动脉造影阳性32例,冠状动脉造影阴性22例。在不同年龄组中,男和女性冠状动脉造影阳性率和心电图阳性率,差异均无显著性(P>0.05);随着年龄的增长,心电图和冠状动脉造影阳性率也逐步增高(P<0.05)。显示随着冠脉病变支数的增多,心电图诊断冠心病的阳性率也增高(P<0.05)。结论和冠状动脉造影相对比较,体表心电图作为诊断老年人冠心病有着一定的价值。     

冠状动脉内旋磨术的疗效观察及临床随访

目的观察冠状动脉内旋磨术对钙化、纤维化病变的疗效及临床随访结果。方法对30例冠心病患者的钙化或纤维化病变进行冠脉内旋磨术、冠脉球囊扩张及冠脉支架术,观察患者的手术成功率、围术期并发症及临床随访结果。结果行冠脉内旋磨术的30例患者冠脉造影结果均为B2、C型钙化或纤维化病变。其中1例患者旋磨头未成功通过病变,成功率96.67%;14例(46.67%)病例仅用1.25mm的旋磨头,13例(43.33%)病例仅用1.5mm的旋磨头,仅有1例(3.33%)病例选用1.75mm旋磨头,2例(6.67%)病例分别使用了1.25mm、1.5mm的旋磨头。旋磨术成功的29例患者(96.67%)均应用经皮冠脉血管成形术(PTCA),其中28例(93.33%)在旋磨术后置入支架(均为药物洗脱支架),共植入支架49枚,平均每例患者植入支架1.75枚;平均每例患者植入支架长度(52.2±30.97)mm。2例(6.67%)在术中发生轻度冠脉痉挛;1例(3.33%)发生无血流现象;1例发生一过性三度房室传导阻滞(3.33%),无围术期急性心肌梗死、死亡、冠脉穿孔及急诊冠脉旁路移植术(CABG)。对30例患者进行了(15.9±11.2)个...     

缺血性脑卒中患者急性期C反应蛋白水平与病情及预后的相关性分析

目的探讨缺血性脑卒中患者急性期C反应蛋白(CRP)水平与病情严重程度、预后的相关性。方法对符合入选标准的75例缺血性脑卒中患者,在发病后24h内抽取血清测定CRP水平,按脑卒中患者临床神经功能缺损程度评分标准(CNFDS)进行评分,所有患者行CT或MRI检查,在出院时对预后进行评定。结果CRP异常组脑梗死28例,明显高于腔隙性梗死13例;CRP异常组患者CNFDS评分较高,中位数为17(5~34),且预后不良。结论缺血性脑卒中患者急性期C反应蛋白水平可作为反映脑卒中病情严重程度及预后的一个重要指标。     

颈动脉超声和运动平板试验与冠状动脉造影的相关性

目的探讨颈动脉超声、运动平板试验与冠状动脉造影(CAG)的相关性。方法研究对象经CAG分为冠心病组和非冠心病组,超声观察颈动脉IMT及运动平板试验结果,与CAG结果对照。结果非冠心病组、冠心病不同分支病变组患者颈动脉IMT和冠状动脉记分随CAG严重程度的增加显著增加(P<0.05或<0.01),颈动脉IMT对冠心病诊断有较高的敏感性、特异性和Kappa值;运动平板试验结果对冠心病诊断有较高的敏感性、特异性和Kappa值。结论颈动脉超声和运动平板试验是冠心病诊断的一项重要的辅助检查手段。     

散射免疫比浊法检测类风湿性关节炎患者血清CRP和免疫球蛋白研究

目的探讨散射免疫比浊法检测类风湿性关节炎患者血清CRP和免疫球蛋白的意义。方法采用散射免疫比浊法对63例类风湿性关节炎患者血清CRP和血清免疫球蛋白(IgG、IgA、IgM)进行检测,同时35例健康体检者作为对照,分析其结果。结果类风湿性关节炎患者与正常人比较血清CRP、IgG、IgA、IgM水平升高,活动期患者与正常组相比差异有统计学意义(P<0.01);非活动期患者与正常组相比差异也存在统计学意义(P<0.05)。经治疗后,患者治疗后血清CRP显著低于治疗前(P<0.01),而血清免疫球蛋白(IgG、IgA和IgM)无显著变化(P>0.05)。结论检测类风湿性关节炎患者血清CRP和免疫球蛋白(IgG、IgA、IgM)水平的变化规律,对临床诊断、评价疗效和预后提供一定的参考依据。     

Circulating Levels of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 are Associated with Inflammatory Markers

Lectin-like oxidized-low-density lipoprotein receptor-1 (LOX-1) is increasingly linked to atherosclerotic plaque formation and the soluble form of this receptor may reflect activities of disease. We investigated the associations among levels of sLOX-1, oxidized-low-density lipoprotein (ox-LDL), cytokines and the extension of atherosclerosis in patients with coronary artery disease (CAD). Lipid, TNF-alpha, IL-6, C reactive protein (CRP), ox-LDL, peroxy radical and sLOX-1 levels were measured in 29 controls and 60 patients with CAD, 30 of which with one or two vessels involved (group 1), and 30 patients with three or four vessels involved (group 2). The serum levels of sLOX-1 were significantly and progressively higher in group 1 [611 (346-1,313) pg/ml, median (interquartile range)] and in group 2 [2,143 (824-3,201) pg/ml] than in control subjects [268 (111-767) pg/ml]. LOX-1 levels positively correlated with IL-6 (r = 0.38, P = 0.0042), TNF-alpha (r = 0.38, P = 0.0037), CRP levels (r = 0.32, P = 0.027) and age (r = 0.25, P = 0.048). In the multivariate analysis TNF-alpha resulted the only independent determinant of LOX-1 serum levels (beta-value = 0.304, P = 0.017). These findings suggest that sLOX-1 levels are up-regulated during CAD progression and are associated with inflammatory markers. The measurement of the circulating soluble form of this receptor may be potentially useful in predicting CAD progression in humans.     

The rs2516839 Polymorphism of the USF1 Gene May Modulate Serum Triglyceride Levels in Response to Cigarette Smoking

Single nucleotide polymorphisms (SNPs) of the USF1 gene (upstream stimulatory factor 1) influence plasma lipid levels. This study aims to determine whether USF1 SNPs interact with traditional risk factors of atherosclerosis to increase coronary artery disease (CAD) risk. In the present study serum lipid levels and USF1 gene polymorphisms (rs2516839 and rs3737787) were determined in 470 subjects: 235 patients with premature CAD and 235 controls. A trend of increasing triglycerides (TG) levels in relation to the C allele dose of rs2516839 SNP was observed. The synergistic effect of cigarette smoking and C allele carrier state on CAD risk was also found (SIM = 2.69, p = 0.015). TG levels differentiated significantly particular genotypes in smokers (1.53 mmol/L for TT, 1.80 mmol/L for CT and 2.27 mmol/L for CC subjects). In contrast, these differences were not observed in the non-smokers subgroup (1.57 mmol/L for TT, 1.46 mmol/L for CT and 1.49 mmol/L for CC subjects). In conclusion, the rs2516839 polymorphism may modulate serum triglyceride levels in response to cigarette smoking. Carriers of the C allele seem to be particularly at risk of CAD, when exposed to cigarette smoking.     

Fatty-Acid-Binding Protein 4 as a Novel Contributor to Mononuclear Cell Activation and Endothelial Cell Dysfunction in Atherosclerosis

Background—Elevated circulating fatty-acid-binding protein 4 (FABP4) levels may be linked with cardiovascular events. This study aimed to investigate the mechanistic role of FABP4 in atherosclerosis. Methods—We recruited 22 patients with angiographically proven coronary artery disease (CAD) and 40 control subjects. Mononuclear cells (MNCs) and human coronary endothelial cells (HCAECs) were used for in vitro study. Results—Patients with CAD were predominantly male with an enhanced prevalence of hypertension, diabetes, and smoking history. FABP4 concentrations were up-regulated in culture supernatants of MNCs from CAD patients, which were positively correlated with the patients’ age, waist–hip ratio, body mass index, serum creatinine, type 2 diabetes, and the presence of hypertension. The adhesiveness of HCAECs to monocytic cells can be activated by FABP4, which was reversed by an FABP4 antibody. FABP4 blockade attenuated the oxidized low-density lipoprotein (oxLDL)-induced expression of ICAM-1, VCAM-1, and P-selectin. FABP4 impaired the tube formation and migration via the ERK/JNK/STAT-1 signaling pathway. FABP4 suppressed phosphorylation of eNOS and expression of SDF-1 protein, both of which can be reversed by treatment with VEGF. Blockade of FABP4 also improved the oxLDL-impaired cell function. Conclusion—We discovered a novel pathogenic role of FABP4 in MNC activation and endothelial dysfunction in atherosclerosis. FABP4 may be a therapeutic target for modulating atherosclerosis.     

Correction to: Changes in dairy product consumption and subsequent type 2 diabetes among individuals with prediabetes: Tehran lipid and glucose study

Alterations in the gut microbiome (dysbiosis) has been associated with increased microbial translocation, leading to chronic inflammation in coronary artery disease (CAD). It has been proposed that modulation of gut microbiota by probiotic might modify metabolic endotoxemia. Therefore, the purpose of this study was to examine the effects of Lactobacillus rhamnosus GG (LGG) on endotoxin level, and biomarkers of inflammation in CAD participants. This study was a 12-weeks randomized, double-blind, and intervention on 44 patients with CAD. Patients were randomly allocated to receive either one LGG capsule 1.6 × 109 colony-forming unit (CFU) or the placebo capsules for 12 weeks. In addition, all the participants were also prescribed a calorie-restricted diet. Serum levels of interleukin-1β (IL-1β), Toll-like receptor 4 (TLR4), interleukin-10 (IL-10), and lipopolysaccharide (LPS), were assessed before and after the intervention. A significant decrease in IL1-Beta concentration (− 1.88 ± 2.25, vs. 0.50 ± 1.58 mmol/L, P = 0.027), and LPS levels (− 5.88 ± 2.70 vs. 2.96+ 5.27 mg/L, P = 0.016), was observed after the probiotic supplementation compared with the placebo. Participants who had ≥2.5 kg weight loss showed significantly improved cardiovascular-related factors, compared to patients with < 2.5 kg weight reduction, regardless of the supplement they took. These data provide preliminary evidence that probiotic supplementation has beneficial effects on metabolic endotoxemia, and mega inflammation in participants with CAD.     

Serum Small Dense Low-density Lipoprotein Concentrations are Elevated in Patients with Significant Coronary Artery Stenosis and are Related to Features of the Metabolic Syndrome

Serum small dense low-density lipoprotein (sd-LDL) concentrations were measured in patients with angiographically defined coronary artery disease (CAD) and compared to concentrations in healthy subjects. Five hundred and seventy patients with stable CAD were divided into CAD? and CAD+ based on angiography. Patients in whom stenosis was <50?% in diameter were classified as having a ??normal?? angiogram (CAD?), otherwise the patients were allocated to the CAD+ group. The CAD+ group was further subcategorized into single-, double- and triple-vessel disease (VD). Serum sd-LDL concentrations were significantly lower in controls compared with CAD+ and CAD? patients (P?<?0.001). Moreover, CAD+ patients had higher concentrations of sd-LDL than CAD? patients (P?<?0.01). sd-LDL levels were not significantly associated with severity of CAD defined by the number of stenosed coronary arteries (P?=?0.245). All participants were also categorized into subgroups with or without metabolic syndrome. Subjects with metabolic syndrome had higher levels of sd-LDL than subjects without metabolic syndrome (P?<?0.01). Multiple linear regressions showed that in CAD patients, triacylglycerol, total-cholesterol, body mass index, and waist circumferences were the most important determinants of serum sd-LDL concentrations. We found that sd-LDL levels were significantly higher in patients presenting with symptoms of CAD. Moreover, patients with significant stenosis of their coronary arteries (>50?% stenosis) had higher levels of sd-LDL compared to patients without significant lesions.     

益赛普治疗类风湿关节炎伴冠心病的临床疗效

目的观察TNFα拮抗剂益赛普治疗类风湿关节炎(Rheumatoid arthritis,RA)伴冠心病的临床疗效。方法选取60例确诊为活动期RA并发冠心病患者,随机分为慢作用药物组(30例,接受慢作用药物治疗,并在整个观察期内保持不变)和益赛普组(30例,在原慢作用药物治疗基础上皮下注射益赛普,每次25 mg,每周2次,持续3个月)。分别于治疗前及治疗12个月后采血,应用全自动荧光偏振免疫分析法测定血清同型半胱氨酸(Homocysteine,HCY)水平;评价临床疗效;经胸超声心动图测定冠状动脉血流储备(Coronary flow reserve,CFR);应用高分辨率B超对所有观察对象的肱动脉进行扫查,测定肱动脉内皮依赖性血管舒张率(Flow-mediated dilation rate,FMD);并记录12个月内发生的心血管疾病、不良反应以及肝肾功能的变化。结果益赛普组治疗后与治疗前比较,患者的血清HCY水平显著下降(P<0.05),CFR和FMD显著升高(P<0.05);慢作用药物组治疗后与治疗前比较,HCY、CFR和FMD均有所下降,但差异无统计学意义(P>0.05);与慢作用药物组比较,经益赛普治疗后,患者血清HCY水平显著下降(P<0.05),CFR和FMD显著升高(P<0.05);益赛普组临床症状缓解有效率明显高于慢作用药物组(P<0.05);12个月内,益赛普组主要心血管疾病发生率与慢作用药物组比较明显降低(P<0.05);两组不良反应发生率差异无统计学意义(P>0.05)。结论益赛普可以明显缓解RA患者的临床症状,延缓冠心病的进展,减少心血管危险疾病的发生。     

Differences in lipid parameters among statins treated patients with coronary arteriosclerosis – a pilot study

LDL, total cholesterol (TC), high‐density lipoprotein (HDL) are poor predictors of the cardiovascular risk among patients undergoing hypolipidaemic therapy with statins. Thus, in this pilot study we have attempted to determine, on the basis of routinely used assessments of lipid profiles, sensitive and inexpensive parameter which would associate with the severity of coronary artery disease in patients undergoing hypolipidaemic treatment who achieved LDL goal. Apolipoprotein (apo) B100, apoA1, LDL, triglycerides, HDL, lipoprotein (a) and TC levels were assessed in 140 patients referred for coronary angiography. The various ratios based on lipid parameters were calculated and compared to patients taking statins. Coronary arteriosclerosis was determined by the degree of single stenosis and quantitatively by applying the Gensini score. Uing multivariate analysis we have found that in the group with hypolipidaemic therapy and/or with treatment LDL target (70–100 mg/dL) the TC/apoB100 ratio was associated with coronary artery stenosis. Additionally, univariate analysis showed that the TC/apoB100 ratio (among treated subjects) was significantly lower in patients with haemodynamically significant stenosis of coronary arteries than in matched patients without coronary artery lesions.     

TLR4-Activated MAPK-IL-6 Axis Regulates Vascular Smooth Muscle Cell Function

Migration of vascular smooth muscle cells (VSMCs) into the intima is considered to be a vital event in the pathophysiology of atherosclerosis. Despite substantial evidence supporting the pathogenic role of Toll-like receptor 4 (TLR4) in the progression of atherogenesis, its function in the regulation of VSMC migration remains unclear. The goal of the present study was to elucidate the mechanism by which TLR4 regulates VSMC migration. Inhibitor experiments revealed that TLR4-induced IL-6 secretion and VSMC migration were mediated via the concerted actions of MyD88 and TRIF on the activation of p38 MAPK and ERK1/2 signaling. Neutralizing anti-IL-6 antibodies abrogated TLR4-driven VSMC migration and F-actin polymerization. Blockade of p38 MAPK or ERK1/2 signaling cascade inhibited TLR4 agonist-mediated activation of cAMP response element binding protein (CREB). Moreover, siRNA-mediated suppression of CREB production repressed TLR4-induced IL-6 production and VSMC migration. Rac-1 inhibitor suppressed TLR4-driven VSMC migration but not IL-6 production. Importantly, the serum level of IL-6 and TLR4 endogenous ligand HMGB1 was significantly higher in patients with coronary artery diseases (CAD) than in healthy subjects. Serum HMGB1 level was positively correlated with serum IL-6 level in CAD patients. The expression of both HMGB1 and IL-6 was clearly detected in the atherosclerotic tissue of the CAD patients. Additionally, there was a positive association between p-CREB and HMGB1 in mouse atherosclerotic tissue. Based on our findings, we concluded that, upon ligand binding, TLR4 activates p38 MAPK and ERK1/2 signaling through MyD88 and TRIF in VSMCs. These signaling pathways subsequently coordinate an additive augmentation of CREB-driven IL-6 production, which in turn triggers Rac-1-mediated actin cytoskeleton to promote VSMC migration.     

High Serum Apolipoprotein E Determines Hypertriglyceridemic Dyslipidemias, Coronary Disease and ApoA-I Dysfunctionality

The relevance of serum apolipoprotein E (apoE) levels to two hypertriglyceridemic dyslipidemias has not been clarified. We explored, in a cross-sectional (and short-term prospective) evaluation, the independent relationship of serum apoE to the atherogenic dyslipidemia, hypertriglyceridemia with elevated apoB (HtgB) and to apoA-I dysfunctionality, previously shown in Turkish adults to be independent of apoE genotype. Serum apoE concentrations were measured by immunonephelometry in 1,127 middle-aged adults. In multivariable regression analysis, apoE concentrations showed log-linear associations with apoB and apoA-I levels, waist circumference, independent of C-reactive protein (CRP), homeostatic model assessment (HOMA) index and other confounders. The likelihood of atherogenic dyslipidemia and of HtgB roughly tripled per 1-SD increment in apoE concentrations, additively to apoE genotype, HOMA, apoA-I, CRP concentrations and waist circumference; yet apoA-I, protective against atherogenic dyslipidemia, appeared to promote HtgB, a finding consistent with apoA-I dysfunctionality in this setting. Each 1-SD increment in the apoE level was moreover, associated in both genders with MetS (at OR 1.5), after adjustment for sex, age, apoB, apoA-I and CRP, or for apoE genotypes. Circulating apoE predicted in both genders age-adjusted prevalent and incident coronary heart disease (CHD), independent of apoE genotype and CRP (OR 1.32 [95 % CI 1.11; 1.58]). To conclude, in a general population prone to MetS, elevated apoE concentrations are strongly linked to HtgB and atherogenic dyslipidemia, irrespective of apoE genotype, are associated with MetS and CHD. Excess apoE reflects pro-inflammatory state and likely autoimmune activation.     

Changes in sialylation of low‐density lipoprotein in coronary artery disease

Reduction of LDL sialylation may correlate with coronary artery disease (CAD), but the details of this modification and its effect on CAD are not well studied. This study was aimed to show desialylation of LDL and to reveal more details of this modification. Blood samples were collected from 16 patients with CAD and 25 healthy individuals. Serum sialic acid was determined. LDL was extracted from all samples, and the interaction of the extracted materials with lectins (MAA, SNA, and DSA) was studied using the lectin blotting method. Serum total sialic acid (TSA) concentrations in CAD patients and healthy individuals were 71.9 ± 2.66 and 60.76 ± 2.34 mg/dL, respectively, and the difference between the two groups was statistically significant (p <0.001). The intensity of interaction of extracted LDL with SNA and MAA lectins was lower in CAD patients compared to that in normal subjects (p <0.001). The intensity of interaction of LDL with DSA was higher in CAD (p <0.001). There was a reverse correlation between TSA and intensity of LDL interaction with SNA and MAA in both groups, but in the case of DSA this correlation was direct and positive. These findings indicated an increase in desialylation of LDL in CAD. It was concluded that LDL was subjected to glycosylation changes in CAD and that there was a positive correlation between TSA and the desialylated form of LDL. This modification may contribute to the pathogenesis of CAD.