吸烟与颈动脉粥样硬化患者血清高敏C反应蛋白水平的相关性研究

目的观察颈动脉粥样硬化吸烟患者血清高敏C反应蛋白(hs-CRP)变化,并分析其在不同动脉粥样硬化亚型中的差异,探讨其临床意义。方法纳入颈动脉粥样硬化的吸烟患者298例为吸烟组,颈动脉粥样硬化的非吸烟患者120例为非吸烟组,无颈动脉粥样硬化的健康吸烟者50例和非吸烟者50例分别为对照1组和对照2组。采用胶体强化免疫比浊法检测各组血清hs-CRP水平。吸烟组再按斑块是否为稳定分为稳定性斑块及不稳定性斑块,分析吸烟对颈动脉粥样硬化患者hs-CRP水平的影响。结果吸烟组血清hs-CRP水平明显高于非吸烟组[(7.26±4.24)mg/L vs(3.56±2.28)mg/L],对照1组hs-CRP水平高于对照2组[(4.34±2.74)mg/L vs(3.17±1.68)mg/L],差异有统计学意义(P0.05)。吸烟指数与血清hs-CRP水平呈显著正相关(r=0.395,P0.01)。不稳定性斑块患者的每日吸烟量、吸烟时间及吸烟指数明显高于稳定性斑块患者(P0.05),高hs-CRP水平吸烟患者发生缺血及脑卒中复发事件比例显著高于低hs-CRP水平患者(11.36%vs 2.00%,P0.01)。结论吸烟可导致颈动脉粥样硬化患者血清hs-CRP水平增高,其可能与斑块的稳定性及缺血性脑卒中的复发密切相关。     

急性心肌梗死患者高敏C反应蛋白与梗死相关血管早期自发再通的相关性研究

目的探讨急性ST段抬高型心肌梗死(ST-segment elevation myocardial infarction,STEMI)患者入院时高敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)水平与梗死相关血管早期自发再通的直接相关性。方法收集2014年1月~2015年12月北京安贞医院诊断为急性STEMI患者268例,按照冠状动脉造影梗死相关血管TIMI血流分级分为血管未通组181例(TIMI 0~Ⅰ级),血管再通组87例(TIMIⅡ~Ⅲ级)。入院后立即采集外周静脉血,由中心化验室检测hs-CRP,常规行超声心动图检查,所有患者在症状发生12h内行冠状动脉造影。结果血管未通组与血管再通组梗死相关血管(左前降支、左回旋支和右冠状动脉)、病变血管(单支病变、双支病变和3支病变)比较,差异无统计学意义(P0.05)。血管再通组hs-CRP水平明显低于血管未通组,差异有统计学意义[(18.69±21.23)mg/L vs(25.17±24.36)mg/L,P0.05]。结论入院hs-CRP水平在急性STEMI患者早期血管再通中明显降低。     

高敏C反应蛋白与老年冠心病患者冠状动脉病变及对心脏事件的预测作用

目的评价高敏C反应蛋白(hs-CRP)与老年冠心病患者冠状动脉病变的关系以及对心脏事件的预测价值。方法对连续住院的237例老年冠心病患者测定hs-CRP(以3 mg/L为界值),分正常组(130例,hs-CRP≤3mg/L)和升高组(107例,hs-CRP>3 mg/L),所有患者均进行冠状动脉造影并随访8个月,统计主要心脏事件。结果升高组不稳定性心绞痛患者比例明显高于正常组(P<0.01),升高组冠心病患者冠状动脉多支病变、弥漫性病变、偏心病变、扩张重构、内膜不光滑的比例以及冠状动脉狭窄程度明显高于正常组(P<0.01)。随访分析显示,升高组患者的无心脏事件率明显低于正常组(P<0.01),多因素Cox回归分析显示,hs-CRP是心脏事件的独立预测因素(OR=3.16,P<0.05)。结论hs-CRP升高的老年冠心病患者冠状动脉易损斑块较多,狭窄程度重;hs-CRP升高是老年冠心病患者心脏事件的独立预测因素。     

高敏C反应蛋白和肌钙蛋白I在心力衰竭患者血清中的变化

目的探讨血清高敏C反应蛋白（hsCRP）及肌钙蛋白I（cTnI）在心力衰竭患者中的变化及意义。方法46例（NYHA分级Ⅲ-Ⅳ级）心力衰竭患者，Ⅲ级组26例，Ⅳ级组20例，分别于清晨空腹和心功能改善至Ⅰ-Ⅱ级后采血清，测定hsCRP和cTnI。选取45例体检健康者作为对照组。结果心衰组hsCRP和cTnI均较对照组升高（P〈0．01）；心衰组中心功能Ⅳ级组与Ⅲ级组比较cTnI值升高（P〈0．01），而hsCRP无明显差异。心衰组随着心功能的改善hsCRP和cTnI明显下降，与治疗前比较差异具有统计学意义（P〈0．01）。另外，不同病因心衰组hsCRP和cTnI差异均无统计学意义。结论心衰时hsCRP和cTnI均升高，且随着心功能损害加剧而增高明显，心衰患者存在明显的炎性活动和心肌细胞损害，并与病情严重程度相关。提示hsCRP和cTnI可能是反映心力衰竭病情变化的两项指标。     

无症状心肌缺血与高敏C反应蛋白和内皮功能失调

目的 探讨无症状心肌缺血（SMI）的发生是否与炎症因子和内皮功能失调有密切的关系。方法 对148例稳定性冠心病患者采用24h动态心电图监测,分为SMI组和非SMI组。并行血脂、血糖、高敏C反应蛋白（hsCRP）等测定,高分辨率超声评估肱动脉内皮功能。结果 60例患者（40．5％）动态心电图记录SMI,非SMI组与SMI组相比,hsCRP浓度明显降低（0．91±0．36：1．86±0．52,P〈0．05）,血流介导性舒张（FMD）功能有明显改善（3．02±1．46：6．36±3．79,P〈0．05）。多因素分析发现SMI仅与FMD（β=-0．452,P=0．046,OR=1．572）和hsCRP（β=1．233,P=0．036,OR=1．632）有独立相关性。结论 无症状冠心病患者仍有较高的SMI发生率;FMD、hsCRP与SMI之间有较强的相关性,提示炎症和内皮功能失调可能是SMI发生的机制之一,hsCRP和FMD有可能作为筛选SMI的替代指标。     

2型糖尿病患者亚临床动脉粥样硬化与高敏C反应蛋白水平的关系

目的探讨2型糖尿病(T2DM)患者亚临床动脉粥样硬化(SAS)与高敏C反应蛋白(hsCRP)的关系。方法 170例新确诊T2DM患者随访2年后,56例出现SAS,用免疫比浊法测定T2DM伴与不伴SAS患者及健康对照组hsCRP水平。结果伴SAS组hsCRP水平[0.64(0.50～7.07)mg/L]高于不伴SAS组[0.53(0.14～7.44)mg/L,P>0.05],2组均高于健康对照组[0.36(0.10-9.60)mg/L,均为P<0.05];将SAS为因变量,以各危险因素为自变量作Logistic回归分析显示:hsCRP、年龄、三酰甘油进入回归方程(P<0.05)。结论 hsCRP、年龄、三酰甘油可能是T2DM患者SAS发生的独立危险因素。     

冠状动脉病变与代谢综合征及高敏C反应蛋白关系的探讨

目的 探讨冠状动脉病变与代谢综合征、血清高敏C反应蛋白（hs—CRP）水平之间的关系。方法 对2003年4月至2004年4月期间北京协和医院就诊的227例临床怀疑冠心病的患者进行冠状动脉造影,将其中冠状动脉狭窄大于50％的170例患者按照中国代谢综合征诊断标准分为代谢综合征组和非代谢综合征组。对两组同时进行hs—CRP水平的测定。两组的冠状动脉造影和hs—CRP结果进行组内及组间统计学分析。结果 不同hs—CRP水平下冠状动脉病变类型的比较表明,随着hs—CRP水平的升高,代谢综合征组的冠状动脉病变严重程度加重,差异有统计学意义,特别是在hs-CRP〉3．5μg／ml时,这种差异尤其明显。结论 hs—CRP可以作为预测代谢综合征合并冠状动脉粥样硬化性心脏病患者冠状动脉病变严重程度的预测指标。     

C反应蛋白在终末期肾功能衰竭患者冠状动脉粥样硬化中的作用

近20余年来血液透析技术有了很大的发展,然而透析患者心血管合并症的死亡率仍居高不下,较普通人群高10～20倍,尤其是高龄、男性和糖尿病患者,其中主要原因是动脉粥样硬化性心脏病[1].     

高敏C反应蛋白与动脉粥样硬化

采用超敏感方法检测到的C反应蛋白被称为高敏C反应蛋白.高敏C反应蛋白在冠心病、中风、周围血管栓塞等疾病诊断和预测中发挥越来越重要的作用.越来越多的研究揭示了C反应蛋白直接参与了炎症与动脉粥样硬化等心血管疾病,并且是心血管疾病最强有力的预示因子与危险因子之一.各种炎症、组织感染损伤均会引起循环中多种血浆蛋白水平增加,其中C反应蛋白作为一种急性期反应蛋白,其水平增高是体内炎症的敏感指标.而炎症在动脉粥样硬化及心血管相关疾病的发生和发展过程中都起着重要的作用.本文将高敏C反应蛋白和动脉粥样硬化之间的关系及其机制进行综述.     

老年糖尿病伴动脉粥样硬化患者血浆高敏C反应蛋白变化的研究

目的探讨老年患者中高敏C反应蛋白(hS-CRP)变化与糖尿病伴动脉粥样硬化等大血管并发症的相关性。方法观察了2006年1月至2009年12月于我院住院老年2型糖尿病患者(年龄大于65岁)血中hS-CRP的水平,其中未合并双下肢动脉硬化患者18例,合并双下肢动脉硬化患者22例,另20例无糖尿病患者设为对照组。结果 (1)hS-CRP(mg/L)在对照组、2型糖尿病组及糖尿病合并下肢动脉硬化组分别为2.46±0.38、10.06±1.07、29.38±1.60,组间比较有显著差异(P<0.01);各组高密度脂蛋白(HDL)(mmol/L)分别为1.59±0.05、1.25±0.03、1.10±0.03,组间比较有显著差异(P<0.05);(2)40例2型糖尿病患者中合并高血压、冠心病及脑梗死的患病率分别为65.0%、42.5%、27.5%,其中22例合并动脉粥样硬化患者中同时合并高血压、冠心病及脑梗死的患病率分别为72.7%、54.5%、31.8%。结论 hS-CRP在糖尿病合并双下肢动脉硬化老年患者人群中更加显著升高,与高密度脂蛋白呈负相关,提示其与糖尿病、脂代谢紊乱共同促进动脉粥样硬化等大血管并发症的发生与发...     

Improvement by oral metoprolol of exercise-induced ischemic dysfunction in patients with coronary heart disease

The effect of metoprolol on global left ventricular function during exercise was analyzed with nuclear ventriculography in 17 patients with ischemic heart disease. All had stable angina pectoris and ST-segment depression of more than 0.1 mV during treadmill exercise when not taking metoprolol. Each patient was stressed with supine bicycle exercise to the same load on a maintenance dose of metoprolol (100 mg X 2/day) and on a second occasion without the drug, the two being separated by 7 days. The mean heart rate and systolic blood pressure were significantly reduced both at rest and exercise with metoprolol. There was no significant difference of rest left ventricular ejection fraction with or without metoprolol. At exercise, however, every patient showed improvement of left ventricular function, the average left ventricular ejection fraction increasing by 14% (+/- 6) relative to the same exercise without metoprolol (p less than 0.001). We conclude that chronic metoprolol treatment in patients with ischemic heart disease can ameliorate left ventricular dysfunction induced by exercise and may thereby reduce myocardial ischemia.     

SYNTAX积分预测冠心病复杂病变患者经皮冠状动脉介入治疗预后的作用

目的评价SYNTAX积分对冠心病3支病变和(或)左主干病变患者PCI预后的作用。方法经冠状动脉造影证实的3支病变和(或)左主干病变并接受PCI的患者1 90例。对每例患者造影结果进行SYNTAX评分,SYNTAX评分按三分位数分为:低分组、中分组和高分组,通过门诊或电话随访患者主要不良心脑血管事件(MACCE)。结果经PCI的冠心病3支病变和(或)左主干病变190例患者中,29例出现MACCE,发生率为15.3%。SYNTAX积分低分组、中分组及高分组的MACCE发生率分别为9.1%、1 6.2%及30.9%。Cox多因素分析显示,SYNTAX积分HR=2.07,95%CI:1.25～3.44,差异有统计学意义(P=0.005)。结论 SYNTAX积分是预测PCI预后的较理想工具,该积分系统也适用于我国冠心病3支病变和(或)左主干病变患者PCI术后预后的预测。     

Angiographic coronary morphology in patients with ischemic heart disease

OBJECTIVES: To determine whether ischemia- or infarct-related arteries (IRAs) are accompanied by certain findings specific to clinical settings, coronary cineangiography was reviewed of 71 patients with stable effort angina pectoris (SAP), 72 with unstable angina pectoris (UAP), 118 with acute myocardial infarction (AMI) and 137 with old myocardial infarction (OMI). METHODS: The morphology of identifiable ischemia- or infarct-related lesions (IRLs) was classified as totally occlusive, and simple (Type I lesion) or complex (Type II lesion). Complex lesions were subdivided into Type IIa lesions (narrowing with irregular, poorly defined or hazy borders, sharp leading or trailing edges that overhang or are perpendicular to vessel walls, and globular endoluminal negative images), Type IIb (2 or more serial, closely spaced narrowings together with multiple irregularities), Type IIc (luminal narrowing with extraluminal contrast pooling, single or paired short thin linear radiolucencies with or without a variable degree of outpouching, and narrowing with definite outpouching with or without radiolucency), and Type IId (narrowing with morphology not included in Types IIa-IIc). RESULTS: Total occlusive lesions among identifiable IRLs occurred at 17 sites (23.9%) in patients with SAP, 7 (9.7%) with UAP, 48 (40.7%) with AMI and 30 (21.9%) with OMI. The mean diameter stenosis of identifiable IRLs was 89.4% in patients with SAP, 92.0% with UAP, 93.1% with AMI, and 87.4% with OMI. Patent identifiable IRLs in patients with SAP had a significantly higher frequency of Type I lesions (29 sites, 40.8%) compared with those with UAP, AMI and OMI (p < 0.01), followed by a relatively lower occurrence of Types IIa 12 (16.9%), IIb 8 (11.3%), IIc 3 (4.2%) and IId 2 (2.9%) lesions. Patients with UAP were characterized by a higher occurrence of Type IIa (34 sites, 47.2%, p < 0.01) and IIc (13 sites, 18.1%, p < 0.01) lesions compared with those with SAP. Patients with AMI had total occlusion (48 sites, 40.7%, p < 0.05) and Type IIa lesion (38 sites, 32.2%, p < 0.05) more frequently than those with SAP. Patients with OMI showed fewer total occlusions (30 sites, 21.9%), same occurrence of Type IIa lesion (39 sites, 28.5%), and higher occurrence of IIb (23 sites, 16.8%) and IIc (20 sites, 14.6%) than those with AMI. CONCLUSIONS: This analysis of coronary cineangiographies from patients with UAP, AMI and OMI, which share a common pathogenesis, shows that IRAs, especially IRLs, are associated with certain morphology specific to clinical settings, and that the morphology and severity of stenosis could change in a short period. The present results may improve coronary cineangiography interpretation about pathophysiological issues in vivo affecting coronary circulation.     

Percutaneous coronary angioscopy in patients with ischemic heart disease

Percutaneous transluminal coronary angioscopy was performed during routine coronary angiography in seven patients and during PTCA in one patient with ischemic heart disease. A flexible fiberscope with an external diameter of 1.4 mm was introduced through an 8F or 9F guiding catheter used for PTCA into the coronary arteries. Warmed saline solution (15 to 20 ml) was injected through the guiding catheter into the coronary arteries for replacement of blood. Twenty-one of the 31 coronary segments were visualized and photographed on color cinefilms. The lumen of the atherosclerotic segment showed narrowing with smooth surface or with spiral folds. PTCA caused dilatation of the stenosed segment with scattered thin thrombi. These findings indicate the usefulness of angioscopy to observe luminal changes in the coronary arteries of patients with ischemic heart disease.     

冠心病患者血清中纳米细菌与高敏C反应蛋白的关系

目的:检测冠心病患者血清中纳米细菌感染率与高敏C反应蛋白(hs-CRP)的浓度,并探讨其临床意义。方法:采用酶联免疫吸附试验(ELISA)检测冠心病组与对照组血清中的纳米细菌抗原,同时用免疫比浊法测定其血清中的hs-CRP,并进行相关性分析。结果:冠心病组血清纳米细菌感染率为27.08%(13/48),与对照组6.25%(3/48)比较,差异有统计学意义(P<0.05)。冠心病组hs-CRP浓度(4.81±7.12)mg/L显著高于对照组(0.73±0.80)mg/L,差异有统计学意义(P<0.05)。冠心病组血清hs-CRP与纳米细菌血清检测结果呈正相关(r=0.489,P<0.05)。结论:冠心病患者血清中的纳米细菌感染率与hs-CRP浓度均升高,二者具有正相关关系。     

超敏C反应蛋白和胱抑素C与冠心病的关联性研究

目的分析超敏C反应蛋白(hs-CRP)和胱抑素C(Cys-C)与冠心病的关联性。方法选取2017-08~2018-01收治的冠心病患者218例作为冠心病组,再根据Gensini评分结果分为三组:≤30分为轻度病变组77例,30~48分为中度病变组69例,≥48分为重度病变组72例,另外选取同时期健康体检者48名作为对照组。hs-CRP浓度和Cys-C浓度均采用免疫透射比浊法测定。结果冠心病组hs-CRP和Cys-C均高于对照组(P0.05)。与轻度病变和中度病变组比较,重度病变组hs-CRP和Cys-C均显著升高(P0.05)。与轻度病变组比较,中度病变组hs-CRP和Cys-C均显著升高(P0.05)。结论 hs-CRP和Cys-C与冠心病的严重程度存在关联性。     

Role of coronary artery spasm in ischemic heart disease. Therapeutic implications

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)     

Elevated C-reactive protein levels and coronary microvascular dysfunction in patients with coronary artery disease.

AIMS: It is still unknown whether elevated C-reactive protein levels are responsible for coronary microcirculatory dysfunction in patients with coronary artery disease (CAD). This study was aimed at evaluating the association between C-reactive protein levels and endothelium-dependent and endothelium-independent coronary blood flow (CBF) responses in non-culprit arteries of patients with CAD. METHODS AND RESULTS: We studied 28 patients (14 with normal and 14 with elevated C-reactive protein levels, >5 mg/L) with single-vessel disease and otherwise angiographically normal coronary arteries undergoing percutaneous transluminal coronary angioplasty (PTCA). CBF was measured in the non-PTCA vessel using an intracoronary Doppler guide wire and quantitative coronary angiography at baseline, after intracoronary infusion of substance P and of adenosine, and expressed as per cent change from baseline. The increases in CBF during infusion of substance P and of adenosine were lesser in patients with elevated than in those with normal C-reactive protein levels (34+/-22 vs. 61+/-34%, P=0.04 and 131+/-53 vs. 189+/-89%, P=0.03, respectively). Multivariable analysis identified elevated C-reactive protein level as the only independent predictor of reduced response to substance P (P=0.01) and adenosine (P=0.02). CONCLUSION: In patients with CAD, evidence of systemic inflammation is independently associated with endothelium-dependent and endothelium-independent coronary microvascular dysfunction, which, in turn, may be critical to precipitate myocardial ischaemia, in particular, in unstable patients.     

Systemic inflammation is related to coronary microvascular dysfunction in obese patients without obstructive coronary disease

Background and AimsObesity, systemic inflammation and changes in the heart functions are associated with increased cardiovascular risk. This study aimed to investigate coronary microvascular dysfunction as an early marker of atherosclerosis in obese patients without any evidence of cardiovascular disease.Methods and results86 obese subjects (aged 44 ± 12 years, body mass index (BMI) 41 ± 8 kg m⁻²), without evidence of heart disease, and 48 lean controls were studied using transthoracic Doppler echocardiography for detecting coronary flow reserve (CFR). A value of CFR ≤ 2.5 was considered abnormal. We measured interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and adiponectin in all patients. Patients with abnormal CFR underwent coronary multislice computed tomography (MSCT) in order to exclude an epicardial stenosis. CFR in obese subjects was lower than in lean subjects (3.2 ± 0.8 vs. 3.7 ± 0.7, p = 0.02) and was abnormal in 27 (31%) obese patients and in one (2%) control (p < 0.0001). All subjects with abnormal CFR showed no coronary stenosis at MSCT. At multivariable analysis, IL-6 and TNF-α were the only determinants of CFR (p < 0.02 and p < 0.02, respectively). At multivariable logistic regression analysis, IL-6 and TNF-α were the only determinants of CFR ≤ 2.5 (p < 0.03 and p < 0.03, respectively).ConclusionsCFR is often reduced in obese subjects without clinical evidence of heart disease, suggesting a coronary microvascular impairment. This microvascular dysfunction seems to be related to a chronic inflammation mediated by adipocytokines. Our findings may explain the increased cardiovascular risk in obesity, independently of BMI.