正常高值血压伴餐后高血糖患者血清内皮素与炎症因子水平变化及意义

目的探讨正常高值血压伴餐后高血糖患者血清内皮素与炎症因子水平变化及意义。方法采用放射免疫分析法测定血清内皮素（ET），采用胶乳免疫增强比浊法测定高敏C反应蛋白（hs-CRP），对54例正常高值血压伴餐后高血糖患者和60例正常高值血压不伴餐后高血糖患者（正常高值组）及45名健康对照者进行比较。结果正常高值血压伴餐后高血糖患者ET和hs—CRP水平分别为（93．15±8．05）pg／ml和（4．51±1．85）mg／L，正常高值组分别为（85．27±14．71）pg／ml和（3．35±1．41）mg／L，对照组分别为（73．02±18．35）pg／ml和（2．26±0．94）mg／L；正常高值血压伴餐后高血糖组高于对照组，也高于正常高值组（P〈0．01，P〈0．05）。结论在正常高值血压时血清内皮素与炎症因子水平已开始升高，血管内皮功能已经出现异常变化，当合并餐后高血糖时，这种异常变化更加明显，提示对此状态应予以早期干预，延缓病情进展。     

血糖控制达标2型糖尿病患者血清炎症指标与相关代谢指标关系分析

回顾性分析血糖控制达标的139例2型糖尿病患者一般临床资料及相关炎症指标;血清FKN采用双抗体夹心酶联免疫方法（ELISA）测定。根据体重指数（BMI）分为体重正常组（50例）、超重组（44例）及肥胖组（45例）,对相关指标进行统计分析。结果（1）三组血糖、糖化血红蛋白比较无差异（均P〉0．05）;与正常体重组比较,超重组及肥胖组FKN、hs—CRP水平显著升高,而HDL—C水平显著降低（均P〈0．05）。肥胖组收缩压和舒张压水平均高于正常体重组,肥胖组血清FKN、hs-CRP、ALT、TG水平显著高于超重组（均P〈0．05）。（2）Pearson相关性分析显示,血清FKN水平与BMI、腰围、TG呈正相关（P〈0．05）;血清hs—CRP与BMI、腰围、TG呈正相关（P〈0．01）,而与HDL—C呈负相关（P〈0．05）。（3）多元逐步回归分析显示,血清FKN与BMI具有显著相关性（β=0．32,P〈0．01,R2=0．40）;血清hs—CRP与BMI独立相关（β=0．30,P〈0．01,R2=0．37）。结论单纯血糖控制达标不能完全纠正2型糖尿病患者慢性炎症状态。     

高敏C反应蛋白与高血压左室肥厚及颈动脉粥样硬化的相关性研究

目的探讨高敏c反应蛋白（hs—CRP）与高血压左室肥厚（LVH）及颈动脉粥样硬化之间的关系。方法将入选的187例未经治疗的1～2级原发性高血压（EH）患者分为颈动脉正常组、颈总动脉IMT增厚组和颈动脉斑块组。采用胶乳免疫增强比浊法测定血清hs—CRP,行颈动脉超声检查测量颈总动脉内中膜厚度（IMT）,观察有无颈动脉斑块形成,从而判断有无颈动脉粥样硬化,分析血清hs—CRP与颈动脉粥样硬化、颈总动脉IMT、颈动脉斑块形成之间的关系。同时行心脏超声检查,根据左室质量指数（LVMI）将高血压患者分为LYH组与无LYH组。结果①颈动脉斑块组和颈动脉正常组血清hs—CRP分别为（6．34±1．35）mg／L和（2．34±0．53）mg／L,LVMl分别为（138．6±16．8）g／m。和（105．5±8．5）g／m2,颈动脉斑块组血清hs—CRP、LVMI均显著高于颈动脉正常组（P〈0．05）。②LVH组和NLVH组血清hs—CRP分别为（6．42±3．53）mg／L和（2．75±1．08）mg／L,IMT水平分别为（2．89±0．46）mm和（0．72±0．23）mm,LVH组血清hs—CRP、IMT均高于NLVH组（P〈0．01,P〈0．05）。相关分析表明,hs—CRP与LVMI及IMT均呈直线正相关（r=0．58,P〈0．05;r=0．53,P〈O．05）。结论血清hs—CRP与LVMI、IMT均密切相关,表明hs—CRP参与了高血压的发生发展,并且可能在高血压心血管重构过程中起到了至关重要的作用。     

高敏C反应蛋白、同型半胱氨酸与高血压颈动脉粥样硬化的相关性研究

目的探讨原发性高血压（EH）患者高敏C反应蛋白（hs—CRP）、同型半胱氨酸（Hcy）与颈动脉内膜-中层厚度（IMT）的相关性。方法选择初发未经降压治疗的EH患者128例作为高血压组,检测血压、身高、体重、体质量指数（BMI）及生化指标,采用胶乳免疫比浊定量法测hs—CRP,循环酶法测Hcy水平。按照中国高血压防治指南标准将EH患者分为高血压1级组（43例）、高血压2级组（46例）和高血压3级组（39例）,并对EH患者依据颈动脉超声结果将其分为无病变组（48例）、内膜增厚组（42例）和斑块组（38例）三个亚组。以40名健康人作为正常对照组。结果高血压组hs—CRP、Hcy水平均显著高于正常对照组,差异有统计学意义（P〈0．01）。高血压患者不同血压级别组间hs—CRP、Hcy水平比较,hs—CRP水平在各组间差异均有统计学意义（P〈0．01）,而Hey水平在各组间差异均无统计学意义（P〉O．05）;高血压合并不同程度颈动脉硬化组间hs—CRP、Hey水平比较,hs—CRP、Hcy水平斑块组和内膜增厚组高于无病变组,斑块组又明显高于内膜增厚组,差异均有统计学意义（P〈0．01）。进一步相关分析显示,IMT除与年龄、BMI、收缩压、舒张压、脉压、LDL呈正相关（P〈0．05或P〈0．01）外,同时与hs—CRP、Hcy呈正相关（r=0．610和r=0．571,P〈0．01）。结论ha—CRP、Hey与EH患者颈动脉粥样硬化（CAS）的发生发展有关,提示早期干预炎症反应及高Hcy血症可延缓动脉粥样硬化的进程。     

高敏C反应蛋白与高血压的关系

目的探讨血清高敏C反应蛋白（hs—CRP）浓度与高血压的关系。方法选择高血压患者128例,非高血压组102例为同期本院健康体检者,测定其血压、hs—CRP、血清胆固醇、甘油三酯、高密度脂蛋白、低密度脂蛋白、血糖、血尿酸等。结果高血压组和非高血压组血清hs—CRP浓度分别为（8．01±6．59）mg／L和（2．25±1．38）mg／L,P=0．000。血清hs—ClIP浓度随收缩压、舒张压及脉压水平的升高而增加。有合并症组和无合并症组的血清hs—CRP浓度分别为（7．24±7．30）mg／L和（3．54±2．17）mg／L,P=0．000。结论血清hs—CRP浓度与高血压密切相关,提示高血压患者血管壁存在炎症反应,炎症反应可能在高血压的发生、发展中起重要作用。     

超敏C-反应蛋白水平与心脑血管病的关系分析

目的：探讨心脑血管病患者血清超敏C-反应蛋白（hs—CRP）水平及临床意义。方法：选择住院治疗的脑卒中患者176例为脑卒中组,其中脑梗塞133例,脑溢血43例,又根据神经功能缺损评分分为1组（轻度,67例）,2组（中度,67例）,3组（重度,42例）;冠心病患者104例为冠心病组,其中,稳定型心绞痛（SAP,34例）,不稳定型心绞痛（UAP,34例）,急性心肌梗塞（AMI,36例）;正常人64例为正常对照组。采用免疫比浊法检测hs—CRP水平。结果：脑卒中组及冠心病组的血清hs—CRP水平显著高于正常对照组（P均〈0．01）。脑卒中组神经功能缺损越重,血清hs—CRP水平越高,组间比较差异显著（P〈0．05～〈0．01）。冠心病组AMI患者的血清hs—CRP水平较SAP、UAP显著升高（P〈0．01,〈0．05）。绪论：血清hs—CRP参与了心脑血管病后的炎症反应,且与病变严重程度有关。     

阿托伐他汀对高血压患者血压与炎症因子的影响

目的探讨阿托伐他汀对高血压患者血压与炎症因子的影响。方法82例高血压患者,随机分为阿托伐他汀治疗组和常规治疗组,另入选正常体检者60名为健康对照组,观察治疗前及治疗6周后血压、血脂及血清高敏C反应蛋白（hs—CRP）浓度和肝功能、肌酸激酶水平的变化。结果①高血压患者hs—CRP水平高于对照组（P〈0．05）;②阿托伐他汀治疗组血压、血脂、hs—CRP水平下降较常规治疗组更明显,差异有统计学意义（P〈0．05）。结论阿托伐他汀可降低高血压患者血压及hs—CRP水平。     

妊娠合并糖尿病患者血清pentraxin-3水平的临床分析

目的探讨血清正五聚蛋白3（pentraxin-3）和超敏C反应蛋白（hs-CRP）水平与妊娠合并糖尿病的关系及其临床意义。方法选取妊娠合并糖尿病患者39例（PCD组）,OGTY正常孕妇40例（NGT组）,健康的非妊娠妇女40例（NC组）,用酶联免疫吸附法检测血清pentraxin-3的水平,用免疫散射比浊法检测血清hs—CRP的水平,并检测BMI,糖脂代谢指标和HOMA-IR,并作相关分析。结果PCD组血清pentraxin-3和hs-CRP水平均显著高于NGT组和Nc组,差异有统计学意义（t=2．35—3．89,P均〈0．05）。PCD组患者血清pentraxin-3均与FBG、FINS、hs—CRP和HOMA—IR呈正相关（r=0．23、0．47、0．32、0．54,P均〈O．05）,HOMA-IR还是pentraxin-3水平的独立相关因素（B=0．36,P〈0．05）。结论血清pentraxin-3与妊娠合并糖尿病的发病有一定联系。     

超敏C-反应蛋白对急性冠状动脉综合征的近期预后意义

目的探讨急性冠状动脉综合征（ACS）患者超敏C-反应蛋白（hs—CRP）的表达及其近期预后意义。方法分别测定30例ACS患者入院时hs—CRP水平，并与30例稳定型心绞痛及30例健康成人hs—CRP作对照。以hs—CRP〉5mg／L为界，比较ACS患者阳性组及阴性组心脏事件发生率。血浆hs—CRP的测定采用微粒增强免疫透射比浊法。结果ACS组的hs—CRP水平（6．05±2．08）mg／L，较正常对照组（3．16±0.96）mg／L高（P〈0．01），也较稳定型心绞痛组（3．24±0．94）mg／L高（P〈0．01）。后两组hs—CRP无差异无统计学意义（P〉0．05）。hs-CRP水平高的ACS患者较hs—CRP水平低者预后更差。结论hs—CRP与ACS发生有关，可作为危险分层的指标之一。     

瑞舒伐他汀对急性冠脉综合征患者血清脂联素和高敏C反应蛋白的影响

目的探讨瑞舒伐他汀对急性冠脉综合征（ACS）患者血清脂联素（APN）、高敏C反应蛋白（hs—CRP）的影响。方法42例ACS患者,在常规治疗基础上加服瑞舒伐他汀10mg,睡前服用,1次／d。另选取年龄、性别等相匹配33例正常体检者为NC组。治疗时间12周。检测治疗前后2组研究对象血脂、APN、hs—CRP等因素的变化。结果治疗前ACS组的血清APN明显低于NC组（P〈0．05）,而血清hs—CRP明显高于NC组（P〈0．05）;瑞舒伐他汀治疗后血清APN明显升高,hs—CRP水平显著下降（P〈0．05）。结论瑞舒伐他汀可明显升高血清APN水平,明显降低ACS患者hs—CRP水平,从而可能改善ACS患者的炎症状态。     

高血压前期患者的代谢状态及高敏C反应蛋白、分泌型磷脂酶A_2的关系

目的探讨高血压前期患者的代谢状态及高敏C反应蛋白（hs-CRP）和分泌型磷脂酶A2（sPLA2）的关系。方法纳入300例体检部及心血管内科门诊初诊者,按照血压水平分为正常血压组（n=81）、高血压前期组（n=153）和高血压组（n=66）,分别检测炎症指标sPLA2和hs-CRP;同时观察体重指数（BMI）、空腹血糖（FBG）及血脂[包括总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）和高密度脂蛋白胆固醇（HDL-C）],并分析三组上述指标之间的差异。结果正常血压组、高血压前期组、高血压组hs-CRP和sPLA2水平呈升高趋势,差异均有统计学意义（P〈0.05）,高血压前期组和高血压组BMI、FBG、TC、TG、LDL-C和HDL-C与正常血压组相比差异有统计学意义（P〈0.05）。结论高血压前期及高血压均存在代谢紊乱,且hs-CRPs和sPLA2水平较正常人群升高。     

高血压前期与血尿酸、C-反应蛋白的相关性研究

目的探讨高血压前期与血尿酸（UA）、C-反应蛋白（CRP）水平的关系及临床意义。方法入选2010年门诊体检人群176例,按照血压水平分为血压正常组（n=56）、高血压前期组（n=66）、高血压组（n=54）三组,检测受试者血UA、CRP及总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白-胆固醇（HDL-C）、低密度脂蛋白-胆固醇（LDL-C）、体质指数（BMI）、空腹血糖（FBG）水平。采用多元线性逐步回归分析UA、CRP对血压的影响。结果①三组间TC、TG、LDL-C、HDL-C、BMI及FBG、收缩压（SBP）、舒张压（DBP）水平比较,差异均有统计学意义（P均〈0.01）;②高血压前期组血UA、CRP水平均显著高于正常血压组（P〈0.01）,同时低于高血压组（P〈0.01）;③多元线性回归分析显示血UA、CRP分别与SBP、DBP呈独立相关（P〈0.05～0.01）。结论高血压前期患者已有血UA、CRP水平的升高,血UA、CRP与血压独立相关。     

高血压前期合并糖耐量异常患者颈动脉内膜中膜厚度及心脏左室重构的研究

目的 探讨高血压前期合并糖耐量异常患者颈动脉内膜中膜厚度及心脏左心室结构、功能改变情况,并分别对两者危险因素进行分析.方法 300例患者分为正常对照组(NC组)61例、单纯高血压前期组(PH组)83例、单纯糖耐量异常组(IGT组)91例、高血压前期合并糖耐量异常组(PH+ IGT组)65例,超声测定颈动脉内膜中层厚度(IMT),心脏彩超计算左心室质量指数(LVMI)、室壁中层缩短率(mFS)、舒张早晚期充盈速度比值(E/A).结果 (1)IMT在PH组、IGT组、PH+IGT组均高于NC组[(0.7±0.1)mm、(0.7±0.1)mm和(1.0 ±0.1)mm比(0.6 ±0.1)mm,P均＜0.01],且PH+ IGT组较PH组、IGT组也表现出明显升高(P＜0.01),但在PH组与IGT组间比较差异无统计学意义(P＞0.05);血压血糖对其存在交互作用;回归分析示高敏C反应蛋白(hs-CRP)、餐后2h血糖(2 hPBG)、收缩压、舒张压与IMT正相关.(2)LVMI在PH组、PH+ IGT组高于NC组及IGT组[(97.0 ±3.3)g/m2、(97.1 ±2.8)g/m2比(87.0 ±2.0) g/m2、(87.9±1.5) g/m2,P均＜0.01],mFS在PH组、PH+ IGT组低于NC组及IGT组[(14.0±0.8)％、(14.0±0.8)％比(18.3±1.0)％、(18.2±0.5)％,P＜0.01],而LVMI、mFS在PH组与PH+ IGT组及NC组与IGT组间比较差异无统计学意义.回归分析LVMI与收缩压、舒张压呈正比,mFS则随收缩压、舒张压增加而减少.E/A值虽与收缩压呈反比,但4组间比较差异无统计表学意义(均P ＞0.05).结论 高血压前期即存在血管损害及心脏重构和收缩功能减退.合并糖耐量异常会加重动脉粥样硬化,但对心脏结构及功能影响不明显.     

Synergistic relationship between hyperglycaemia and inflammation with respect to clinical outcomes in non-ST-elevation acute coronary syndromes: analyses from OPUS-TIMI 16 and TACTICS-TIMI 18.

AIMS: To investigate the relationship between diabetes and inflammation and the potentially synergistic relationship between hyperglycaemia and inflammation on clinical outcomes in non ST-elevation ACS. METHODS AND RESULTS: The principal analysis was conducted in 2200 patients in OPUS-TIMI 16 with C-reactive protein data available and then validated in the invasive arm of TACTICS-TIMI 18 (n = 929). In addition, two further inflammatory markers [monocyte chemoattractant protein-1 (MCP-1) and von Willebrand factor (vWF)] were assessed in OPUS-TIMI 16. Diabetic patients had higher C-reactive protein and MCP-1 levels vs. non-diabetic patients in OPUS-TIMI 16 (9 vs. 7.8 mg/L, P = 0.002, and 190.6 vs. 170.8 pg/mL, P = 0.04, respectively), higher C-reactive protein levels in TACTICS-TIMI 18 (6.6 vs. 5.2 mg/L, P = 0.0005), and as expected higher glucose levels in both trials. Stratifying by the median C-reactive protein and diabetes in OPUS-TIMI 16, diabetic patients with C-reactive protein greater than or equal to the median were the highest risk group vs. non-diabetic patients with C-reactive protein less than the median (adjusted HR 1.63, 95% CI 1.20-2.23, P = 0.002). Directionally, similar findings were observed for MCP-1 and vWF in OPUS-TIMI 16 and for C-reactive protein in TACTICS-TIMI 18. After adjustment for diabetes, the risk associated with a 1 mmol/L increase in glucose was greater among those with a C-reactive protein greater than or equal to the median (HR 1.07, 95% CI 1.03-1.11) vs. those with a C-reactive protein less than the median (HR 1.02, 95% CI 0.97-1.06). After multivariable adjustment, the synergistic relationship between glucose and C-reactive protein and clinical outcomes remained statistically significant (P = 0.01). A similar pattern was observed in TACTICS-TIMI 18. CONCLUSION: Among ACS patients, diabetes was associated with both greater inflammation and higher glucose levels and patients with both hyperglycaemia and inflammation had worse outcomes. Better control of both inflammation and hyperglycaemia should be assessed in future ACS trials as a means to reduce the cardiovascular risk among diabetics.     

Predictive value of prehypertension for metabolic syndrome, diabetes, and coronary heart disease among Turks

BACKGROUND: Predictors of prehypertension and the latter's significance in predicting metabolic syndrome (MetS), type 2 diabetes (DM), and incident coronary heart disease (CHD) need further exploration. METHODS: Individuals with or without prehypertension (blood pressure (BP) 120-139 systolic or 80-89 mm Hg diastolic) were studied prospectively in a representative sample of Turkish adults. RESULTS: Mean age of 1,501 men and 1,533 women was 48 +/- 12 years at baseline. Prehypertension, identified in 32.8% of the sample, differed from the normotensive group mainly by age-adjusted obesity measures and C-reactive protein (CRP) and progressed to hypertension at more than twofold annual incidence as normotension did. In logistic regression analysis, adjusted for sex, age, heart rate, and smoking status, prehypertension was predictive for risk of MetS in both genders (relative risk (RR) 1.55 (95% confidence interval (CI) 1.21; 1.99)) compared with normotensives. However, DM and CHD were significantly predicted by prehypertension only in women (RR 2.06 and 1.98, respectively, for outcomes). Cardiometabolic risks in women were largely independent of obesity. Body mass index (BMI) at baseline predicted significantly subsequent development of new prehypertension in both genders (hazard ratio 1.39 (95% CI 1.17; 1.65)) and CRP tended to contribute to this risk. CONCLUSIONS: Prehypertension, compared with normotension, approximately doubles the risk for DM, MetS, and CHD in women without conferring substantial risk in Turkish men, except toward MetS. Excess cardiometabolic risk of prehypertension in women is independent of obesity. BMI is a determinant of prehypertension.     

Association between cardiac autonomic dysfunction and inflammation in type 1 diabetic patients: effect of beta-blockade.

AIMS: To assess the relationship between cardiac autonomic dysfunction and inflammation in patients with type 1 diabetes and whether beta-blocker therapy might improve both abnormalities in these patients. METHODS AND RESULTS: We studied 49 patients with type 1 diabetes (age 50.5 +/- 11 years, 33 men). Serum levels of high-sensitivity C-reactive protein, as a marker of inflammation, and frequency-domain heart rate variability (HRV) on 24 h Holter monitoring, as a measure of cardiac autonomic function, were assessed in all patients. Twenty-one patients with depressed HRV were subsequently randomized to receive atenolol (50 mg daily) or no-beta-blockade. HRV and C-reactive protein were re-assessed after 3-4 weeks from randomization. An inverse correlation was found between C-reactive protein levels and HRV parameters, with the highest r coefficient shown with low-frequency (LF) power (r = -0.38; P = 0.007). Furthermore, C-reactive protein serum levels were significantly higher in patients with bottom quartile values of LF power compared with patients with values in the three top quartiles (4.64 +/- 2.8 vs.1.79 +/- 1.6 mg/L, respectively; P = 0.003), also after adjustment for potential confounding variables (P = 0.013). HRV parameters improved significantly in patients treated with atenolol, but not in the no-atenolol group. Furthermore, C-reactive protein levels decreased in the beta-blockade group, but not in the no-beta-blockade group (P = 0.04 for changes between groups). CONCLUSION: In type 1 diabetic patients, serum C-reactive protein levels are significantly associated with depressed HRV; the favourable effects of beta-blockade on both HRV parameters and C-reactive protein serum levels suggest that autonomic nervous system may have significant modulator effects on inflammation.     

Serum total bilirubin concentration is associated with carotid atherosclerosis in patients with prehypertension

Objectives: Bilirubin has been demonstrated to be linked with anti-inflammatory and antioxidant progress. We aimed to evaluate the association between serum total bilirubin level and carotid intima-media thick-ness (cIMT) in patients with prehypertension. Methods: We consecutively enrolled pre-hypertensive patients from a community in Guangzhou between January 2017 and January 2018. All patients underwent carotid artery ultrasonography measurement. The correlation between serum total bilirubin and cIMT was assessed by using the Pearson’s correlation coefficient. Multiple logistic regression analysis was performed to assess the independent association between clinical parameters and carotid atherosclerosis. Results: A total of 691 subjects with prehypertension were included in this study. There were 101 patients with increased cIMT (mean age 52.69 ± 11.58 years; 50 male) and 590 subjects with normal cIMT (mean age50.28 ± 10.33 years; 332 male). We found that cIMT was significantly related with systolic blood pressure(r = 0.257, P < 0.001), C-reactive protein (r = 0.327, P < 0.001), total cholesterol (r = 0.218, P = 0.002) and total bilirubin (r =?0.489, P < 0.001). A multiple logistic regression analysis revealed that total bilirubin was an independent factor for atherosclerosis (OR = 0.476; 95%CI: 0.253, 0.764; P < 0.001). Conclusion: Our results suggested that serum total bilirubin was inversely related with cIMT, and might be an early clinical marker for predicting the occurrence of subclinical carotid atherosclerosis in patients with prehypertension.     

Lack of Correlation Between Activation of Hemostatic Mechanism and Inflammation in Unstable Angina Pectoris

In the acute phase of unstable angina, activation of the hemostatic mechanism is demonstrated by an increase in the plasma levels of markers of thrombin generation (prothrombin fragment 1+2) and thrombin activity (fibrinopeptide A). Increased concentrations of plasma C-reactive protein, an acute-phase reactant, have also been reported in patients with unstable angina. However, whether there is a correlation between the activation of the hemostatic mechanism and the acute-phase reaction of inflammation remains unclear. We measured the plasma levels of prothrombin fragment 1+2, fibrinopeptide A, and C-reactive protein in 91 patients consecutively hospitalized with recent-onset rest angina (Class IIIB Braunwald's classification), finding that they were above the normal limits in 48 (53%), 45 (49%), and 30 (33%) patients, respectively. There was no correlation between prothrombin fragment 1+2 and fibrinopeptide A (P = 0.34), prothrombin fragment 1+2 and C-reactive protein (P = 0.10), or fibrinopeptide A and C-reactive protein (P = 0.75). Plasma levels of prothrombin fragment 1+2 and fibrinopeptide A were both above normal levels in 32% of patients; 19% had both prothrombin fragment 1+2 and C-reactive protein, and 18% both fibrinopeptide A and C-reactive protein levels above the upper normal limits. All three markers were abnormally high in 11% of patients. According to the kappa cofficient test, the agreement between the elevation of the plasma concentrations of the markers was "random." In approximately half of the patients with acute unstable angina, there was an increase in the markers of the activation of the hemostatic mechanism and, in a smaller proportion, an increase in plasma C-reactive protein levels. The activation of the coagulation cascade and the acute-phase reaction of inflammation were infrequently associated in individual patients.     

Plasma levels of C-reactive protein after coronary stent implantation.

AIMS: This study was designed to investigate the role of inflammation on the occurrence of angiographic restenosis 6 months after coronary stent implantation and the influence of different kinds of antithrombotic and antiplatelet strategies on inflammation. METHODS AND RESULTS: In an open randomized trial, 40 consecutive patients were treated with aspirin (100 mg. day(-1)) and either ticlopidine (2x250 mg. day(-1)) (n=17), or phenprocoumon (INR 2.0-3.0) and dipyridamole (3x160 mg. day(-1)) (n=23) after successful elective coronary stent implantation. Plasma levels of C-reactive protein were determined one day before stent implantation and serially thereafter twice daily up to 120 h. C-reactive protein plasma levels increased significantly (P<0.0001) after stent implantation. Phenprocoumon and dipyridamole or ticlopidine had no effect on C-reactive protein plasma levels (P=0.51) or the occurrence of angiographic restenosis (P=0.48). C-reactive protein plasma levels were significantly higher in patients with lesion type C compared to types A or B (P=0.035), respectively. C-reactive protein plasma levels were significantly higher and mean shoulder levels occurred 48 h later in patients with restenosis compared to patients without restenosis after 6 months (P=0.038). CONCLUSIONS: Elevated C-reactive protein plasma levels still persisting 96 h after stent implantation might reflect a prolonged inflammatory reaction to coronary stent implantation which might causally be involved in pathophysiological mechanisms leading to restenosis.     

Arterial stiffness is related to systemic inflammation in essential hypertension

The acute phase-reactant high-sensitivity C-reactive protein, a marker of vascular inflammation and an atherosclerotic risk factor, is related to arterial stiffness in healthy subjects and in systemic vasculitis. To explore the relationship between markers of inflammation, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and high-sensitivity C-reactive protein with arterial stiffness, we studied untreated patients (n=78; 56% male; 47+/-1 years of age; mean+/-SEM) with essential hypertension. After overnight fast, augmentation index and pulse wave velocity were assessed noninvasively and related to plasma levels of inflammatory markers measured by ELISA. Pulse wave velocity was significantly related to plasma high-sensitivity C-reactive protein (r=0.31; P<0.001), TNF-alpha, (r=0.30; P<0.001) and IL-6 (r=0.21; P<0.05). There was also a relationship between heart rate-corrected augmentation index to high-sensitivity C-reactive protein (r=0.37; P<0.001), IL-6 (r=0.24; P<0.05), and TNF-alpha (r=0.19, P=0.06). High-sensitivity C-reactive protein was an independent predictor of pulse wave velocity and augmentation index in a multiple stepwise regression model. High-sensitivity C-reactive protein, a marker of systemic inflammation, is independently related to pulse wave velocity, a marker of aortic stiffness, and augmentation index, a manifestation of wave reflection, in essential hypertension.