通心络对急性冠状动脉综合征病人血管细胞黏附分子-1水平影响的研究

目的观察通心络治疗急性冠状动脉综合征病人2周后血清血管细胞黏附分子-1(VCAM-1)等水平的变化,以了解短期通心络治疗对斑块稳定性的影响.方法 32例急性冠状动脉综合征病人随机分为常规治疗组(未服用通心络及任何调脂药物,19例)和通心络组(760 mg,每天3次,13例)治疗,测定治疗前后病人血清VCAM-1和血脂水平的变化.结果两组间治疗前后血脂各组成分的变化差异均无统计学意义.通心络组治疗后血清VCAM-1水平降低13.5%,与治疗前比较有统计学意义(P＜0.05).结论急性冠状动脉综合征早期予通心络短期治疗,可明显降低血清VCAM-1的水平,可能具有一定的增加斑块稳定性的作用.     

冠心病病人血清CXCL4和CXCL12水平与冠状动脉粥样斑块稳定性的关系

目的探讨冠心病病人血清血小板趋化因子4(CXCL4)和血小板趋化因子12(CXCL12)水平与冠状动脉粥样斑块稳定性的关系。方法选取2016年3月—2018年3月在焦作市人民医院住院治疗的冠心病病人152例,根据临床症状和冠状动脉造影检查结果,将病人分为稳定型心绞痛组(SAP组,67例)和急性冠脉综合征组(ACS组,85例),另选取同期行冠状动脉造影检查且排除冠心病的病人45例作为对照组,所有研究对象行冠状动脉造影和血管内超声检查,酶联免疫吸附试验(ELISA法)检测血清CXCL4和CXCL12水平。结果 SAP组和ACS组高血压、高脂血症和吸烟史比例高于对照组,差异有统计学意义(P0.05);SAP组和ACS组病人血清CXCL4和CXCL12水平均高于对照组,且ACS组高于SAP组,差异有统计学意义(P0.05);软斑块病人血清CXCL4和CXCL12水平均高于硬斑块病人,差异有统计学意义(P0.05);ACS组病人斑块负荷和偏心指数高于SAP组,而管腔面积低于SAP组,差异有统计学意义(P0.05);Pearson相关分析结果显示,冠心病病人血清CXCL4水平与管腔面积呈正相关(r=0.171,P=0.035),而与斑块面积、斑块负荷和偏心指数呈负相关(r值分别为-0.171,-0.230,-0.279,均P0.05);冠心病病人血清CXCL12水平与管腔面积呈正相关(r=0.167,P=0.040),而与斑块面积、斑块负荷和偏心指数呈负相关(r值分别为-0.183,-0.180,-0.179,均P0.05)。结论血清CXCL4和CXCL12与冠心病斑块稳定性有关,斑块稳定性越差,血清CXCL4和CXCL12水平越高。     

辛伐他汀对急性冠脉综合征患者炎症因子水平影响的研究

目的 观察辛伐他汀治疗75例急性冠脉综合征患者2周后血清血管内皮生长因子(VEGF)和血管细胞黏附分子-1(VCAM-1)等炎症因子水平的变化,以了解短期辛伐他汀治疗对斑块稳定性的影响.方法 75例急性冠脉综合征患者随机分为常规治疗组(未服用辛伐他汀及任何调脂药物,30例)和辛伐他汀组(20 n.g/d,15例)治疗,测定治疗前后患者血清VEGF、VCAM-1和血脂水平的变化.结果 辛伐他汀组治疗后血清VEGF和VCAM-1水平分别降低29.7%和21.7%,与治疗前比较差异有统计学意义(P<0.05或P<0.01).两组治疗后血浆总胆固醇(TC)浓度均有显著下降(P<0.01),但两组间下降程度比较差异无统计学意义;辛伐他汀组治疗后血浆LDL-C浓度显著下降21.0%(P<0.01).辛伐他汀组VEGF的下降百分数与VCAM-1的下降百分数之间有相关性(r=0.25,P<0.05),与TC(r=0.12,P=0.33)、低密度脂蛋白(LDL-C)(r=0.08,P=0.52)的下降百分数之间无相关性.结论 在急性冠状动脉综合征的早期予以2周辛伐他汀治疗,可明显降低血清炎症因子的水平,具有一定的增加斑块稳定性的作用.     

血清PDGF、Ang-2与冠状动脉粥样硬化斑块性质的关系

目的探讨血小板源性生长因子(PDGF)、血管生成素2(Ang-2)与冠状动脉粥样硬化斑块性质的相关性。方法选取在我院治疗的冠心病患者110例,其中急性冠状动脉综合征(ACS)患者45例(ACS组),稳定型心绞痛(SAP)患者65例(SAP组),同时选取健康志愿者60例作为对照组,检测各组血清PDGF和Ang-2水平,同时采用血管内超声(IVUS)和冠状动脉造影检测ACS组和SAP组。结果 SAP组PDGF和Ang-2分别为(3. 67±0. 56) ng/L和(354. 22±30. 20) pg/m L,明显高于ACS组和对照组(P 0. 05); SAP组偏心指数和Gensini积分分别为(0. 63±0. 21)和(46. 59±7. 22)分,明显高于ACS组(P 0. 05); SAP组以稳定斑块、混合斑块为主,ACS组以易损斑块为主比较差异有统计学意义(P 0. 05); PDGF、Ang-2与偏心指数呈正相关(r=0. 30和0. 30,P 0. 05); PDGF、Ang-2与Gensini积分呈正相关(r=0. 51和0. 51,P 0. 05)。结论血清PDGF、Ang-2水平与冠状动脉粥样硬化斑块性质以及冠状动脉病变程度有一定相关性。     

血清sVCAM-1和sICAM-1与冠状动脉病变相关性研究

目的 探讨血清血管细胞黏附分子—1(sVCAM—11)和细胞间黏附分子—1(sICAM—1)水平与冠状动脉病变程度及稳定性之间的相关关系。方法 采用ELISA方法测定52例急性冠脉综合征(ACS)、20例稳定型心绞痛(SAP)患者和对照组24例血清sVCAM—1和sICAM—1浓度，用Censini积分系统评价其冠状动脉照影结果，进行统计学分析。结果 SAP组和ACS组的sVCAM—1、sICAM—1水平和Censini积分均显著高于对照组(P＜0．01)，ACS组的sVCAM—1水平显著高于SAP组(P＜0．01)；SAP组和ACS组之间的sICAM—1水平和Censini积分无显著性差别(P＞0．05)。sVCAM—1、sICAM—1与Censini积分均有高度相关性(相关系数分别为0．694，P=0.000；0．412，P＝0．000)。结论 血清sVCAM—1和sICAM—1水平与冠状动脉病变程度有一定相关性，ACS组的血清sVCAM—1水平高于SAP组。     

高敏C-反应蛋白与白介素-6在急性冠状动脉综合征意义

目的 探讨急性冠状动脉综合征(acute coronary symptom,ACS)病人血清高敏C反应蛋白(high sensitivity-C reactive protein,hs-CRP)和白介素-6(interleukin-6,IL-6)浓度的变化及临床意义.方法 ACS组ACS病人60例,稳定型心绞痛(stable angina pectoris,SAP)组病人40例,对照组为40名健康人,检测血清IL-6、hs-CRP水平.结果 ACS组血清IL-6、hs-CRP水平明显高于SAP组和对照组(P＜0.01);ACS组中,急性心肌梗死病人又高于不稳定型心绞痛病人(P＜0.05);SAP组与对照组差异无统计学意义(P＜0.05);血清IL-6和hs-CRP水平呈正相关(r=0.5942,P＜0.01).结论 ACS病人血清IL-6和hs-CRP升高,其水平变化反映ACS的严重程度.     

冠心病患者血清降钙素原、超敏C反应蛋白水平变化及其与冠状动脉斑块的相关性研究

目的观察冠心病患者血清降钙素原(PCT)、超敏C反应蛋白(hs-CRP)水平变化,探讨其与冠状动脉斑块的相关性。方法选取2012年2月—2015年8月梅州市人民医院收治的冠心病患者200例,根据冠状动脉造影结果将患者分为稳定型心绞痛(SAP)组121例和急性冠脉综合征(ACS)组79例。采用虚拟组织学血管内超声(VH-IVUS)检查斑块面积、面积狭窄率、血管平均径、管腔平均径、血管重塑指数、斑块偏心指数、斑块负荷、坏死核心(NC)面积、钙化部分(DC)面积、纤维脂质成分(FF)面积等冠状动脉斑块指标。比较两组患者实验室检查指标、冠状动脉斑块指标,并分析冠心病患者血清PCT、hs-CRP水平与冠状动脉斑块指标的相关性。结果两组患者空腹血糖及血清总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平比较,差异无统计学意义(P0.05);ACS组患者血清PCT、hs-CRP水平高于SAP组(P0.05)。两组患者斑块面积、面积狭窄率、血管平均径、管腔平均径、斑块负荷、DC面积比较,差异无统计学意义(P0.05);ACS组患者血管重塑指数、斑块偏心指数、NC面积、FF面积大于SAP组(P0.05)。Pearson相关性分析结果显示,冠心病患者血清PCT水平与血管重塑指数(r=0.612)、斑块偏心指数(r=0.658)、NC面积(r=0.688)呈正相关,与FF面积(r=-0.695)呈负相关(P0.05);血清hs-CRP水平与血管重塑指数(r=0.456)、斑块偏心指数(r=0.724)、NC面积(r=0.487)呈正相关,与FF面积(r=-0.616)呈负相关(P0.05)。结论与SAP患者相比,ACS患者血清PCT、hs-CRP水平升高,血管重塑指数、斑块偏心指数、NC面积、FF面积增大,且冠心病患者血清PCT、hs-CRP水平与冠状动脉斑块形成有一定相关性。     

急性冠状动脉综合征血管内超声斑块显像特征与血浆同型半胱氨酸水平的相关性研究

目的:探讨急性冠状动脉综合征(ACS)斑块稳定性与血浆同型半胱氨酸(Hcy)水平的相关性,寻找不稳定斑块的危险因素.方法:对49例 ACS 患者和35例稳定型心绞痛(SAP)患者"罪犯"冠状动脉进行血管内超声( IVUS)检查,同时测定外周血浆Hcy水平.结果:ACS组Hcy水平明显高于SAP组(P<0.05);ACS组患者冠状动脉病变处以软斑块为主69.4% (34/49) , SAP患者冠状动脉病变处以硬斑块为主77.1% ( 27/35) ,差异有统计学意义(P<0.05).与SAP比较,ACS组不稳定斑块和内膜破裂,血栓形成病变占比例明显增高(P<0.01);ACS组病变处斑块面积大(P<0.01),斑块负荷重(P<0.01),以偏心斑块(P=0.000)和正性重构为(P=0.002)主.Hcy水平、斑块面积、狭窄率、斑块负荷、偏心指数均可影响斑块的稳定性.Logistic回归分析显示Hcy与斑块不稳定相关.结论:Hcy可能是ACS斑块不稳定的相关因素,可作为预测斑块不稳定的指标.     

64排螺旋CT联合血清IL-6、Hcy水平检测对冠状动脉斑块稳定性的预测价值

目的探讨64排螺旋CT冠状动脉成像联合血清白细胞介素-6(IL-6)、同型半胱氨酸(Hcy)水平检测对冠状动脉斑块稳定性的预测价值。方法选择2015年8月—2017年6月我院收治的可疑冠心病病人137例为研究对象,均行冠状动脉造影(CAG)和冠状动脉CT造影检查,采用双抗体夹心-酶联免疫吸附法测定血清IL-6水平,采用循环酶法测定Hcy水平;选取冠状动脉CT未见粥样硬化的33例病人作为对照组,其余104例冠心病病人根据冠状动脉CT检查的Ct值分为易损斑块组(37例)、混合斑块组(32例)和硬质斑块组(35例),根据病史及CAG诊断结果分为急性冠脉综合征组(ACS组,53例)和稳定型心绞痛组(SAP组,51例),比较各组IL-6和Hcy水平。结果 ACS组易损斑块病人多于SAP组,硬质斑块病人少于SAP组,差异均有统计学意义(P0.05);ACS组血清IL-6、Hcy水平高于SAP组和对照组,SAP组高于对照组,差异均有统计学意义(P0.05);易损斑块组血清IL-6、Hcy水平高于混合斑块组、硬质斑块组和对照组,混合斑块组高于硬质斑块组和对照组,硬质斑块组高于对照组,差异均有统计学意义(P0.05);冠心病病人冠状动脉斑块的Ct值与血清IL-6、Hcy水平均呈负相关(P0.05)。结论冠状动脉CT可显示冠状动脉斑块的性质,不同稳定性斑块病人的血清IL-6、Hcy水平差异明显,64排螺旋CT结合IL-6、Hcy水平检测能够预测冠状动脉斑块的稳定性。     

血清总胆红素预测冠状动脉斑块稳定性的临床研究

目的:探讨血清总胆红素浓度在预测冠状动脉斑块稳定性中的临床作用。方法:入选冠心病患者75例,依据疾病程度分为急性冠状动脉综合征(acute coronary syndrome,ACS)组40例,稳定型心绞痛(stable angina pectoris,SAP)组35例,另随机纳入非冠心病患者40例为正常对照(normal control,NC)组,行冠状动脉造影检查,进一步对冠心病患者行血管内超声(intravascular ultrasound,IVUS)检查,术前测定各组患者血清胆红素浓度,分析ACS组和SAP组冠状动脉斑块稳定性差异,比较3组患者血清胆红素水平及其与斑块性质关联性。结果:ACS组血清总胆红素、直接胆红素和间接胆红素水平均显著低于SAP组和NC组(P0.05);IVUS显像特征显示ACS组管腔面积、纤维帽厚度显著低于SAP组,而斑块负荷、脂核大小、偏心指数、重构指数均显著高于SAP组(P0.01);血清总胆红素水平与纤维帽厚度呈显著正相关(r=0.306,P0.01),与脂核大小、偏心指数、重构指数呈显著负相关(r=-0.315、-0.324、-0.310,P0.01)。结论:血清总胆红素与冠状动脉斑块稳定性呈显著正相关,可以作为临床预测冠心病患者斑块稳定性的血液学指标。     

Enhanced platelet/endothelial activation in depressed patients with acute coronary syndromes: evidence from recent clinical trials.

Platelets play a key role in the progression of acute coronary syndromes (ACS). Clinical depression alone is also associated with enhanced platelet activation. The purpose of this study was to compare concentrations of established biomarkers of enhanced platelet/endothelial activation in clinically depressed versus non-depressed patients enrolled in recent clinical trials for ACS. Two hundred and eighty-one baseline plasma samples from patients with acute myocardial infarction (ASSENT-2; n = 41), with ACS (PRONTO; n = 126) and with clinical depression plus previous acute coronary syndrome within 6 months (SADHART; n = 64), and from normal healthy controls (n = 50) were analyzed. Blood was drawn before applying any therapeutic strategies including interventions, thrombolytics, infusions, and selective serotonin re-uptake inhibitors. Platelet factor 4, beta-thromboglobulin, platelet/endothelial cell adhesion molecule-1, P-selectin, thromboxane, prostacyclin, vascular cell adhesion molecule-1, and E-selectin were measured by enzyme-linked immunosorbent assay by a single core laboratory. Patients with ACS exhibited a higher degree of platelet activation than controls independently of the presence of depression. Plasma levels of P-selectin, thromboxane, prostacyclin, and vascular cell adhesion molecule-1 were the highest in the acute myocardial infarction group when compared with ACS despite the presence or absence of clinical depression. Surprisingly, patients with ACS and depression exhibited the highest levels of platelet factor 4, beta-thromboglobulin, and platelet/endothelial cell adhesion molecule-1 when compared with myocardial infarction or angina patients without clinical depression. E-selectin plasma level was constantly elevated compared with controls but did not differ among the groups dependent on the incidence of depression. The depressed plus ACS group had higher plasma levels of all biomarkers compared with the non-depressed patients. Retrospective analysis of the data from several clinical trials reveals that clinical depression is associated with enhanced activation of platelet/endothelial biomarkers even above the level expected in ACS. These findings may contribute to the unfavorable outcome associated with clinical depression in patients with ACS.     

Changes of serum hepatocyte growth factor in coronary artery disease

Hepatocyte growth factor (HGF) is an endothelial cell specific growth factor involved in the repair of endothelial cells and collateral formation, however, the role for coronary artery disease is still unknown. We measured serum HGF level in various coronary artery diseases to examine the clinical significance. Serum HGF level was measured using the enzyme-linked immunosorbent assay method in patients with stable effort angina pectoris (n = 26), old myocardial infarction (n = 18), unstable angina pectoris (UAP; n = 10) and acute myocardial infarction (AMI; n = 21). As a control group, we selected 11 patients with neurocirculatory asthenia. Blood samples from peripheral veins were collected at cardiac catheterization before heparin administration. In the AMI group, blood samples were also collected at 48, 72 hr, 1, 2, 3 and 4 weeks from the peripheral veins and 48 and 72 hr after reperfusion from the coronary sinus. Serum HGF level was significantly higher in the UAP (0.41 +/- 0.12 ng/ml, p < 0.001) and AMI groups (0.38 +/- 0.26 ng/ml, p < 0.05) compared to the control group (0.19 +/- 0.09 ng/ml). Serum HGF level peaked 48 hr after reperfusion in both the peripheral veins (0.42 +/- 0.16 ng/ml) and coronary sinus (0.58 +/- 0.23 ng/ml) in the AMI group, with a significantly higher level in the coronary sinus than the peripheral veins (p < 0.05). No significant correlation between peak HGF level in the peripheral veins and peak creatine kinase (CK), CK-MB, ejection fraction and cardiac index was observed. Serum HGF was elevated in acute coronary syndrome, indicating advanced endothelial cell damage. HGF is produced, at least partially, in the heart in patients with AMI. Serum HGF level may be useful to detect endothelial cell damage rather than myocardial cell damage.     

急性冠状动脉综合征患者冠状动脉循环粘附分子的变化

目的探讨急性冠状动脉综合征患者冠状动脉循环血浆细胞间粘附分子1和血管细胞粘附分子1水平变化的临床意义.方法应用酶联免疫吸附法检测65例冠心病患者(30例急性冠状动脉综合征,35例稳定型心绞痛)及27例对照者冠状动脉循环(冠状静脉窦-主动脉根部)血浆细胞间粘附分子1和血管细胞粘附分子1水平,比较其水平变化与不同冠心病类型之间的关系.结果急性冠状动脉综合征组冠状静脉窦和主动脉根部血浆细胞间粘附分子l和血管细胞粘附分子1水平明显高于稳定型心绞痛组和对照组(P＜0.05);急性冠状动脉综合征组冠状动脉循环(冠状静脉窦与主动脉根部的差值)血浆细胞间粘附分子1和血管细胞粘附分子1水平明显高于稳定型心绞痛组和对照组(P＜0.01).稳定型心绞痛组和对照组冠状静脉窦、主动脉根部和冠状动脉循环血浆细胞间粘附分子1和血管细胞粘附分子1水平无明显差别(P＞0.05).血浆细胞间粘附分子1和血管细胞粘附分子1水平与冠状动脉病变受累支数无关.结论急性冠状动脉综合征时血浆细胞间粘附分子1和血管细胞粘附分子1浓度显著升高,冠状动脉循环血浆细胞间粘附分子1和血管细胞粘附分子1变化反映冠状动脉炎症活动程度,细胞粘附分子参与斑块的不稳定.     

Soluble adhesion molecules and unstable coronary artery disease

Leukocyte adhesion and transendothelial migration, prerequisites in the development of atherosclerosis, are largely mediated by adhesion molecules. In addition, unstable coronary syndromes usually involve platelet activation and thrombus formation at the site of atherosclerotic plaque. Therefore, we compared plasma levels of soluble P-selectin, a measurement of platelet activation, as well as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in patients with atherosclerosis undergoing coronary angiography (n=76). Soluble P-selectin levels, as measured by ELISA, were significantly elevated in patients with unstable (n=44) vs stable (n=32) atherosclerotic disease (73.0 +/- 2.5 ng/ml vs 52.3 +/- 3.0 ng/ml, respectively, P<0.01). By logistic regression analysis, plasma level of soluble P-selectin was an independent predictor of an unstable coronary syndrome (OR 4.2, CI 1.4-12.9, P<0.01). Soluble E-selectin level, a marker of endothelial activation, was associated with extent of atherosclerosis but did not correlate with disease stability. Interestingly, soluble P-selectin was inversely correlated with plasma levels of the antioxidant alpha-tocopherol (R=-0.443, P<0.001), a known inhibitor of platelet function. In summary, amongst the soluble adhesion molecules, only P-selectin is significantly increased in patients with unstable coronary syndromes. This study suggests that platelet activation persists in patients with unstable coronary syndromes despite concurrent aspirin therapy. In addition, the beneficial effects of alpha-tocopherol in patients with cardiovascular disease may be related to inhibition of platelet function.     

Adhesion Molecules as Markers of Clinical Severity in Stable Angina

The relationship between coronary artery disease and adhesion molecules has been investigated, but the clinical significance of adhesion markers is not clear. The aim of this study was to clarify the relationship between soluble adhesion molecules and clinical severity of stable angina. Fifty-six patients with stable angina with confirmed coronary artery disease, by coronary angiography and electrocardiography during their episodes of chest pain, were enrolled. Vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and E-selectin were measured, and the relationship between adhesion molecule levels and cardiac events during the follow-up period (6 months) was evaluated. Cardiac events included non-fatal myocardial infarction, coronary revascularization (coronary artery bypass grafting or coronary angioplasty), and death of any cause. Serum levels of vascular cell adhesion molecule-1 (623 ± 131 ng/ml), and E-selectin (65 ± 26 ng/ml) were higher in the 8 patients with cardiac events than the 48 patients without cardiac events (551 ± 137, and 44 ± 21 ng/ml, respectively). There was no difference in intercellular adhesion molecule-1 levels between patients with cardiac events and those without (307 ± 133, and 246 ± 123 ng/ml). In conclusion, the risk of cardiac events is increased in patients with stable angina who have increased levels of vascular cell adhesion molecule-1 and E-selectin.     

Serum levels of angiogenic factors indicate a pro-angiogenic state in adults with sickle cell disease

Hypoxia-induced angiogenesis may play an important role in the pathophysiology of sickle cell disease (SCD). Serum levels of angiopoietin (Ang)-1, Ang-2, vascular endothelial growth factor, placenta growth factor (PlGF), soluble tunica intima endothelial kinase 2 (sTIE2), erythropoietin (EPO) and endothelial activation markers (soluble vascular adhesion molecule-1, soluble intercellular adhesion molecule-1) were determined in controls, HbSS (n = 35) and HbSC (n = 23) patients. In the asymptomatic phase, serum Ang-2 (P < 0.001), EPO (P < 0.001) and sTIE2 (P = 0.03) were elevated in patients. During painful crises, increased Ang-2 (P < 0.001) and PlGF (P = 0.04) occurred in HbSS and Ang-2 (P = 0.05) in HbSC patients. These results indicate a pro-angiogenic state in SCD, mainly because of elevated Ang-2 levels.     

Association of soluble fms-like tyrosine kinase-1 with pulmonary hypertension and haemolysis in sickle cell disease

The pathophysiology of pulmonary hypertension (PHT) in sickle cell disease (SCD) is probably multifactorial. Soluble fms-like tyrosine kinase-1 (sFLT-1) is a member of the vascular endothelial growth factor receptor (VEGFR) family. By adhering to and inhibiting VEGF and placenta growth factor, it induces endothelial dysfunction. We sought to evaluate the association of sFLT-1 with clinical complications of SCD. We confirmed that sFLT-1 was significantly elevated in SCD patients compared to healthy, race-matched control subjects. The level of sFLT-1 was significantly higher in patients with PHT, but no association was observed between sFLT-1 and the frequency of acute pain episodes or history of acute chest syndrome. sFLT-1 was correlated with various measures of haemolysis, erythropoietin and soluble vascular cell adhesion molecule-1. By inducing endothelial dysfunction, sFLT-1 may contribute to the pathogenesis of SCD-associated PHT, although this effect does not appear to be independent of haemolysis.     

冠心病患者血清缺氧诱导因子-1α与血管内皮生长因子水平的变化

目的:研究冠心病(CHD)患者血清血管内皮生长因子(vascular endothelial growth factor,VEGF)和低氧诱导因子-1α(hypoxia inducible factor1α,HIF-1α)水平的变化意义。方法:CHD患者79例,分为急性冠脉综合征(ACS)组42例,稳定型心绞痛(SAP)组37例,另选35例作为对照组,所有患者清晨空腹抽血应用ELISA法测定VEGF和HIF-1α水平。结果:ACS组VEGF和HIF-1α水平显著高于SAP组和对照组(P0.05);SAP组VEGF和HIF-1α水平与对照组比较差异无统计学意义。结论:VEGF和HIF-1α水平升高可能是冠状动脉粥样硬化斑块的不稳定的标志。     

细胞间粘附分子-1和C反应蛋白在急性冠脉综合征患者中的表达及临床意义

目的观察不稳定性心绞痛(UAP)和急性心肌梗死(AMI)患者血清可溶性细胞间粘附分子-1(sICAM-1)和超敏C反应蛋白(hs-CRP)水平的变化,探讨炎症标志物与急性冠脉综合征发病的关系及临床意义.方法选择急性冠脉综合征患者56例(包括AMI组26例、UAP组30例),以同期住院的冠状动脉造影检查正常的30例患者作为对照组,进行对比研究.采用酶联免疫吸附测定法测定血清sICAM-1和hs-CRP水平,并记录每例患者狭窄程度＞50%的冠状动脉病变数.结果血清sICAM-1浓度在AMI组明显高于UAP组及对照组,在UAP组明显高于对照组;血清hs-CRP浓度在AMI组明显高于UAP组及对照组,但UAP组与对照组比较无显著差异;直线相关分析显示,血清sICAM-1水平与受累冠状动脉血管病变数相关,而hs-CRP水平与受累冠状动脉血管病变数无相关关系.结论炎症参与了急性冠脉综合征的发病,炎症因子sICAM-1血清水平升高与急性冠脉综合征的发生密切相关,还与动脉粥样硬化的范围和程度相关,可以作为监测急性冠脉综合征病情的指标,而hs-CRP水平升高主要与其稳定性有关.     

Extent of coronary atherosclerosis and homocysteine affect endothelial markers

The aim of the study was to evaluate the effects of the presence, extent, and clinical stability of coronary artery disease on endothelial function parameters, C-reactive protein and homocysteine levels. Fifty-eight patients with angiographically documented coronary artery disease and 25 patients with normal coronary arteries were evaluated for risk factors, plasma homocysteine, C-reactive protein, and soluble adhesion molecule levels. Vascular cell adhesion molecule-1 and sE-selectin were significantly higher in the group with coronary artery disease than in healthy subjects (p = 0.005 and p = 0.031, respectively). Patients with unstable angina had significantly higher C-reactive protein (p < 0.001), troponin I (p < 0.01), and leukocyte counts (p < 0.05) than those with stable angina. sE-selectin levels were correlated with the extent of coronary atherosclerosis (r = 0.444, p < 0.05), and plasma homocysteine levels were associated with vascular cell adhesion molecule-1 (r = 0.479, p < 0.05) in unstable cases. These results suggest that vascular cell adhesion molecule-1 and sE-selectin are useful for determining the presence of coronary atherosclerosis, whereas C-reactive protein, troponin 1, and leukocyte count are predictors of clinical stability.