高敏C反应蛋白与颈动脉粥样硬化的关系

目的 探讨高敏C反应蛋白和颈动脉粥样硬化的关系.方法 选取在神经内科住院的患者225例(其中脑梗塞患者133例),排除了应激、炎症、自身免疫性疾病等影响高敏C反应蛋白水平的疾病,全部患者行颈部血管彩超检测,观察颈动脉内膜-中膜厚度、斑块的检出情况及斑块评分、管腔的狭窄率,作为评价颈动脉粥样硬化的指标.根据血管彩超的检查结果分为颈动脉粥样硬化组和对照组.用微粒子透射增强免疫法(超敏)检测血浆高敏C反应蛋白的水平.分别比较颈动脉粥样硬化组与对照组高敏C反应蛋白水平的差别,分析高敏C反应蛋白和颈动脉内膜-中膜厚度、斑块评分之间的关系.结果 颈动脉粥样硬化组(130例)与对照组(95例)比较,二者之间的高敏C反应蛋白存在明显差异(P<0.05);偏相关分析显示,高敏C反应蛋白与颈动脉内膜-中膜厚度及斑块评分成正相关,相关系数分别为0.4807和0.3024.结论 颈动脉粥样硬化组较对照组高敏C反应蛋白水平高,高敏C反应蛋白与颈动脉粥样硬化的严重程度成正相关.     

老年高血压病患者颈动脉粥样硬化程度与血25-羟维生素D水平的相关性

目的　探讨老年高血压病患者颈动脉粥样硬化程度与血25-羟维生素D［25（OH）D］水平的相关性。方法　对2012年5月至12月间在宁波市第二医院就诊的老年高血压病患者经超声检测颈动脉内膜中膜厚度（IMT）,根据颈动脉IMT将患者分为颈动脉正常组（60例,对照组）、颈动脉内膜增厚组（60例）和颈动脉斑块组（60例）。采用ELISA法测定三组患者血清25（OH）D水平,分析25（OH）D水平与颈动脉IMT的关系。结果　颈动脉斑块组与颈动脉内膜增厚组血25（OH）D水平均低于颈动脉正常组（P<0.05）,颈动脉斑块组血25（OH）D水平低于颈动脉内膜增厚组（P<0.05）,差异均有统计学意义。结论　低血25（OH）D水平的老年高血压病患者具有颈动脉粥样硬化程度加重的危险,血25（OH）D水平测定有助于预测颈动脉粥样硬化程度。     

老年人颈动脉内膜-中层厚度增厚与斑块形成的相关危险因素分析

目的探讨老年人颈动脉内膜-中层厚度增厚(IMT)及斑块形成的相关危险因素。方法选择在我院行颈动脉超声检查的老年人共305例,根据超声检查结果分为对照组(41例)、内膜-中层厚度(IMT)增厚组(52例)和斑块组(212例),对各组的临床资料进行统计学分析,分析相关危险因素。结果单因素分析,3组间高血压、糖代谢异常、血尿酸、年龄差异有统计学意义(P<0.05)。多因素Logistic回归分析显示,年龄及血尿酸与颈动脉内中膜增厚有明显相关(P<0.05),高血压、年龄、血尿酸及体质指数与颈动脉粥样硬化斑块形成有明显相关(P<0.05)。结论年龄大及血尿酸升高为颈动脉内膜-中层厚度增厚与斑块形成的共同危险因素,高血压及体质指数为颈动脉斑块形成的危险因素。     

血管紧张素Ⅱ与2型糖尿病动脉粥样硬化的相关性

目的探讨血管紧张素Ⅱ(AngⅡ)与2型糖尿病(T2DM)颈动脉粥样硬化之间的关系。方法选取住院T2DM患者110例,其中颈动脉内膜正常组43例,颈动脉内膜增厚组35例,颈动脉硬化斑块组32例;性别、年龄相当的健康体检者30例作为对照组。检测血压、血浆AngⅡ、血糖、血脂。超声多普勒测定颈动脉内膜中层厚度(CIMT)。结果 T2DM患者中颈动脉硬化斑块组血浆AngⅡ水平明显高于颈动脉内膜增厚组和颈动脉内膜正常组(均P<0.01),颈动脉内膜增厚组血浆AngⅡ水平明显高于颈动脉内膜正常组(P<0.01);T2DM患者血浆AngⅡ和CIMT水平明显高于对照组(均P<0.01)。多元逐步线性回归分析显示高AngⅡ、糖化血红蛋白(Hb A1c)、低密度脂蛋白胆固醇(LDL-C)、体重指数(BMI)水平是T2DM患者CIMT增厚的危险因素(r=0.011,0.013,0.051,0.013,P<0.01或P<0.05)。T2DM患者血浆AngⅡ水平与CIMT、收缩压及舒张压呈正相关(r=0.529,0.232,0.248,P<0.01或P<0.05);校正收缩压和舒张压后,血AngⅡ水平仍与CIMT相关(r=0.532,P<0.01)。结论高血AngⅡ水平可能是T2DM合并颈动脉粥样硬化的危险因素之一。     

冠心病患者颈动脉硬化与高敏C反应蛋白水平的关系研究

目的探讨冠心病合并颈动脉粥样硬化与C反应蛋白(hs-CRP)水平增高及其危险因素的关系。方法对入选94例冠心病患者进行颈动脉超声测量观察颈动脉内膜厚度,粥样斑块的数量及部位。定量检测C反应蛋白水平。结果合并颈动脉粥硬化的冠心病患者血清C反应蛋白水平明显高于无颈动脉硬化患者(9.94±8.95mg)VS(4.12±2.85mg),P<0.05。颈动脉内有多个斑块的患者血清C反应蛋白明显高于颈动脉内膜中膜增厚的患者(12.68±8.34)VS(9.94±8.95)mg,P<0.05。结论血清C反应蛋白水平的高低与冠心病颈动脉粥样硬化程度,内膜厚度,斑块数量有一定相关性。合并颈动脉内膜增厚及斑块的患者血清C反应蛋白明显高于无颈动脉硬化患者。     

心血管疾病对高龄老年高血压病患者颈动脉内膜中膜厚度及心率变异性的影响

目的研究多种心血管疾病对高龄老年高血压病患者颈动脉内膜中膜厚度及心率变异性的影响。方法将高龄老年高血压病患者根据合并的其他心血管病分成单纯高血压病组(192例)、高血压病合并冠心病组(152例)、高血压病合并糖尿病组(145例)和高血压病合并冠心病及糖尿病组(184例),检测血脂及其他代谢指标含量,以颈部多普勒超声测定其颈动脉内膜中膜厚度,以动态心电图检测心律失常及心率变异性。结果高血压病合并冠心病及糖尿病组的空腹血糖水平和颈动脉斑块及狭窄的检出率、室性早搏、短阵房性心动过速及缺血性ST-T改变检出率,与前三组相比,差异均有统计学意义(P<0.05),总胆固醇水平与高血压病合并冠心病组及高血压病合并糖尿病组相比,差异有统计学意义(P<0.05)。四组患者的平均心率、夜间心率及心率变异性时域参数比较差异均有统计学意义(P<0.05)。结论高龄老年高血压病患者合并多种心血管疾病时的空腹血糖及血清总胆固醇水平偏高,易发生颈动脉粥样硬化斑块及狭窄,并且心率变异性减低明显。     

颈总动脉内膜-中膜厚度及粥样斑块与冠心病的关系

目的:研究颈总动脉内膜-中膜厚度(CIMT)及粥样斑块检出率与冠心病发病及冠脉病变严重程度的关系。方法:114例具有至少一项冠心病危险因素的患者,按冠状动脉造影结果分为冠心病组(70例)和对照组(44例),测定所有病例的双侧CIMT、颈总动脉内径和颈总动脉粥样斑块情况。结果:两组间各项冠心病危险因素均无显著差异。超声结果显示,冠心病组CIMT、粥样斑块检出率均显著增高(P<0.01),颈总动脉内径略增大,但差异不显著。CIMT≥0.8mm和检出粥样斑块为预测冠心病发病的独立指标(P<0.01)。CIMT和粥样斑块检出率均与冠脉病变严重程度呈正相关,在控制了多项影响因素后,相关性仍显著。结论:CIMT增厚、粥样斑块检出为冠心病发病的独立预测因素,并且与冠脉病变严重程度正相关。     

高龄糖尿病合并心房颤动患者高敏C反应蛋白和同型半胱氨酸与颈动脉硬化关系的研究

目的研究高龄糖尿病合并心房颤动(房颤)患者血清高敏C反应蛋白(hs-CRP)、同型半胱氨酸(Hcy)水平的变化及与颈动脉粥样硬化程度的相关性,探讨炎症、氧化应激在糖尿病合并房颤的发生、发展中的变化及意义。方法选择高龄糖尿病合并房颤患者(房颤组)115例,糖尿病窦性心律患者(窦律组)103例及窦性心律除外糖尿病者(对照组)98例。房颤组中阵发性房颤42例、持续性房颤37例及永久性房颤36例。检测各组hs-CRP和Hcy水平;颈动脉超声检测颈动脉内膜中层厚度(IMT)及斑块Crouse积分,评价颈动脉粥样硬化情况。结果与对照组比较,房颤组和窦律组hs-CRP、Hcy、IMT和斑块Crouse积分明显升高(P<0.05);与窦律组比较,房颤组上述指标明显升高(P<0.05)。房颤组患者hs-CRP、Hcy与房颤持续时间呈正相关(r=0.64、r=0.53,P<0.05),与IMT和斑块Crouse积分呈正相关(r=0.59、r=0.66,P<0.05)。结论炎症和氧化应激在高龄糖尿病合并房颤时颈动脉粥样硬化的发生、发展可能起重要作用,而且随着房颤的持续而加重,hs-CRP、Hcy水平与糖尿病合并房颤的发生、发展及颈动脉粥样硬化的严重程度密切相关。     

早发冠心病患者颈动脉内膜中膜厚度特点及其预测价值

探讨早发冠心病患者颈动脉内膜中膜厚度和斑块特征及其对早发冠心病的预测价值。应用B型超声检测早发冠心病患者颈动脉内膜中膜厚度和斑块情况 ,结合冠状动脉造影结果进行对比研究。结果发现 ,早发冠心病患者颈动脉内膜中膜厚度≥ 0 .8mm及斑块检出率明显高于对照组 (5 6 %比 11% ,P <0 .0 5 ) ;颈动脉超声阳性对预测早发冠心病的敏感性为 5 5 .7% ,特异性为 88.9% ,准确性为 87.2 % ;3支冠状动脉病变组平均内膜中膜厚度高于 1支冠状动脉病变组。多因素分析发现 ,颈动脉超声阳性是早发冠心病的独立危险因素 (OR =7.19,95 %CI:1.92～ 2 1.37,P =0 .0 0 7)。结果提示 ,早发冠心病患者颈动脉内膜中膜厚度增厚及斑块检出率升高 ,颈动脉超声阳性对诊断早发冠心病有着较高的特异性和准确性。     

血清铁蛋白与颈动脉粥样硬化和脑梗死的关系

目的探讨血清铁蛋白与脑梗死和颈动脉粥样硬化的关系。方法对133例脑梗死患者和92例对照者行颈动脉血管彩超检测,观察颈动脉内膜—中膜厚度、颈动脉有无斑块及斑块评分和管腔的狭窄率,作为评价颈动脉粥样硬化的指标。用酶联免疫吸附法检测血清铁蛋白的水平。比较脑梗死组和对照组血清铁蛋白水平的差异,及颈动脉内膜—中膜厚度、斑块评分与血清铁蛋白的关系。结果脑梗死组颈动脉粥样硬化的患病率(70.6%)较对照组(39.5%)明显增高,脑梗死组血清铁蛋白水平较对照组明显升高(248.5±107.4μg/L比197.6±94.8μg/L,P<0.05);对颈动脉粥样硬化的各主要危险因素行有序分类Logistic回归分析显示,血清铁蛋白、血压控制情况和年龄进入回归方程。血清铁蛋白水平与颈动脉内膜—中膜厚度及斑块评分之间呈正相关,偏相关系数分别为0.56和0.48(P<0.05);血清铁蛋白与低密度脂蛋白胆固醇水平呈正相关,Pearson积距相关系数为0.51(P<0.05)。结论脑梗死组血清铁蛋白水平较对照组高,血清铁蛋白与颈动脉粥样硬化的严重程度呈正相关。     

Thoracic aortic plaque enhances hypercoagulability in patients with nonrheumatic atrial fibrillation.

BACKGROUND: Patients with atrial fibrillation (AF) are at risk for thromboembolism, and coexistent cardiovascular diseases could affect their prothrombotic profiles. The relationship between plasma hemostatic markers and aortic atherosclerosis was determined in patients with AF or in sinus rhythm (SR). METHODS AND RESULTS: Sixty patients with nonrheumatic AF and 46 patients in SR who underwent transesophageal echocardiography and did not receive anticoagulant therapy constituted the study group. Markers for platelet activity (platelet factor 4 and beta-thromboglobulin), thrombotic status (thrombin-antithrombin III complex and prothrombin fragment 1+2 (F1+2)) and fibrinolytic status (plasmin-alpha2-plasmin inhibitor complex (PIC) and D-dimer) were determined. Levels of F1+2, PIC and D-dimer were higher in AF patients with severe atheroma than in those without severe atheroma (p<0.05). In patients in SR, hemostatic markers were not significantly increased even if they had severe aortic atherosclerosis. AF (Odds ratio (OR) 4.06, p=0.04) and age>or=75 years (OR 3.98, p=0.02) were independently predictive of elevated D-dimer levels and severe atheroma was predictive of elevated F1+2 levels (OR 5.52, p=0.04). CONCLUSIONS: Elderly patients with AF and severe aortic atherosclerosis might be in a prothrombotic state, and could benefit from intensive antithrombotic therapy.     

A transesophageal echocardiographic study on risk factors for stroke in elderly patients with atrial fibrillation: a comparison with younger patients

STUDY OBJECTIVES: Atrial fibrillation (AF) becomes an increasingly important cause of stroke as patients get older. The aim of the study was to determine whether risk factors of cerebral embolism among elderly patients with AF differed from those of younger patients by using transesophageal echocardiography (TEE). Design and setting: Cross-sectional study at a university hospital. METHODS: Cardiovascular lesions with the potential for thromboembolism in patients with AF were investigated using TEE. Left atrial spontaneous echocardiographic contrast (SEC), peak flow velocity in the left atrial appendage (LAA-flow), and aortic atherosclerosis of the thoracic aorta were assessed in 67 elderly (> or = 70 years old) and 135 younger (< 70 years old) patients. All patients underwent either brain CT (n = 54) or MRI (n = 148) to assess presence of cerebral infarction. RESULTS: Cerebral infarction due to embolism was noted in 113 patients with AF. There was a higher prevalence of cerebral embolism in elderly patients when compared with younger patients (78% vs 45%; p < 0.001). Cerebral embolism found in younger patients was associated with high grade of SEC and lower LAA-flow (p < 0.05). In addition to these TEE findings, aortic atherosclerosis was more severe in elderly patients with cerebral embolism than in those without cerebral embolism (p < 0.0001). By multivariate logistic analysis, LAA-flow was an independent predictor of cortical infarction in younger patients, but not in elderly patients, whereas aortic atherosclerosis was a useful marker in predicting embolic risk in elderly patients. CONCLUSIONS: TEE findings indicative of left atrial blood stasis were useful to identify the embolic risk of younger patients with AF, while atherosclerosis of the thoracic aorta appears to be an important marker for cerebral embolism in elderly patients.     

Role of homocysteine for thromboembolic complication in patients with non-valvular atrial fibrilation.

Thromboembolism is the most important complication in patients with atrial fibrilation (AF). Homocysteine is a toxic amino acid that has been recently accepted as a risk factor for atherosclerosis and stroke. The aim of the present study is to show whether there is a relation between hyperhomocysteinemia and thromboembolic complications in patients with non-valvular AF. We admitted 38 patients with non-valvular AF. The patients were divided into two groups: group A (n = 20; mean age, 75.7 +/- 10.4 years; three males/17 females), and group B (n = 18; mean age, 68.0 +/- 10.6 years; 11 males/seven females). While group A consisted of the patients with AF and stroke, group B was composed of the patients with AF but without stroke. The patients having sinus rhythm (15 subjects) were used as the reference group to obtain the cut-off value. Homocysteine was measured by the immunoassay method. The means of the homocysteine levels were 12.4 +/- 3.3 micromol/l in group A, 8.3 +/- 2.3 micromol/l in group B and 9.3 +/- 1.8 micromol/l in the reference group. The cut-off value was 10.6 micromol/l. Group A had a statistically higher homocysteine level than not only group B, but also the reference group (P < 0.05). While 60% of group A (n = 12) had the elevated homocysteine level, the rate was only 22% for group B (n = 4). In conclusion, hyperhomocysteinemia may be one of the explanations for the increased rate of thromboembolic complications in older patients with AF.     

C-Reactive protein in lone atrial fibrillation

An inflammatory cause of atrial fibrillation (AF) has been proposed on the basis of the presence of lymphocytic infiltrates in the biopsy results of patients with lone AF, alterations of C-reactive protein (CRP) and interleukin-6 levels in subjects with AF, and the time course of postoperative AF. Many previous studies exploring inflammatory factors in AF have been confounded by concomitant medical illnesses. Subjects with lone AF provide a unique opportunity to eliminate the effects of associated conditions. We therefore sought to determine CRP levels in homogenous cohorts of patients with lone AF or AF and hypertension. One hundred twenty-one subjects with lone AF, 52 subjects with AF and hypertension, and 75 control subjects were enrolled and studied. Plasma CRP levels were determined using a commercially available immunoassay. There was no significant difference in CRP levels between subjects with lone AF and controls (1.34 vs 1.21 mg/L, p = 0.18). CRP levels in subjects with AF and hypertension were elevated compared with those of controls and those of subjects with lone AF, although this difference was attributable to increased body mass indexes. CRP levels were not elevated in subjects with lone AF compared with controls. In conclusion, these findings clarify previous observations of elevations in CRP levels in subjects with AF and suggest that this marker of systemic inflammation is associated not with the arrhythmia per se, but rather with underlying cardiovascular disease.     

Elevated platelet microparticle levels in nonvalvular atrial fibrillation: relationship to p-selectin and antithrombotic therapy

BACKGROUND: Platelet microparticles (PMPs), are procoagulant membrane vesicles that are derived from activated platelets, the levels of which are elevated in patients with hypertension, coronary artery disease (CAD), diabetes, and stroke, all of which are conditions that lead to (and are associated with) atrial fibrillation (AF). We hypothesized the following: (1) PMP levels are elevated in patients with AF compared to levels in both healthy control subjects (ie, patients without cardiovascular diseases who are in sinus rhythm) and disease control subjects (ie, patients with hypertension, CAD, diabetes or stroke, but who are in sinus rhythm); (2) PMP levels correlate with levels of soluble P-selectin (sP-selectin) [a marker of platelet activation]; and (3) PMP levels are related to the underlying factors in patients with AF that contribute to the overall risk of stroke secondary to AF. METHODS: We performed a case-control study of 70 AF patients, 46 disease control subjects and 33 healthy control subjects. Peripheral venous levels of PMP and sP-selectin were analyzed by flow cytometry and enzyme-linked immunosorbent assay, respectively. RESULTS: Both AF patients and disease control subjects had significantly higher levels of PMPs (p < 0.001) and sP-selectin (p = 0.001) compared to healthy control subjects, but there was no difference between AF patients and disease control subjects. There was no difference in PMP levels between patients with paroxysmal and permanent AF (p = 0.581), and between those receiving therapy with aspirin and warfarin (p = 0.779). No significant correlation was observed between PMP and sP-selectin levels (p = 0.463), and the clinical characteristics that contribute to increased stroke risk in patients with AF. On stepwise multiple regression analysis in the combined cohort of AF patients plus disease control subjects, the presence/absence of AF was not an independent determinant of PMP and sP-selectin levels. CONCLUSION: There is evidence of platelet activation (ie, high PMP and sP-selectin levels) in AF patients, but this is likely to be due to underlying cardiovascular diseases rather than the arrhythmia per se.     

孤立性心房颤动患者血浆血小板α颗粒膜蛋白-140和血栓素B_2及6-酮-前列腺素F_(1α)浓度变化的研究

目的研究孤立性心房颤动(房颤)患者血小板功能改变,探讨房颤引起血栓前状态的原因。方法用放射免疫分析法对21例孤立性阵发性房颤(A组)、28例孤立性持续性房颤(B组)患者分别于房颤发作及终止后1周测定外周静脉血浆血小板а颗粒膜蛋白-140(GMP-140)、血栓素B2(TXB2)、6-酮-前列腺素F1α(6-K-PGF1α)浓度,并与27例风湿性心脏病二尖瓣狭窄伴持续性房颤(C组)、32例阵发性室上性心动过速患者(D组)及与20例健康体检者(对照组)相比较。结果A、B组患者房颤发作时及C组患者GMP-140、TXB2和TXB2/6-K-PGF1α比A组患者房颤终止后1周和D组及对照组明显上升。A组患者血浆GMP-140、TXB2浓度及TXB2/6-K-PGF1α与房颤发作时间呈正相关,而与患者年龄、性别及左心房内径等临床参数无关。结论无论是器质性心脏病房颤还是孤立性房颤,无论是阵发性房颤还是持续性房颤都存在血小板的激活和血管内皮细胞功能损伤。     

Platelet surface CD62P and CD63, mean platelet volume, and soluble/platelet P-selectin as indexes of platelet function in atrial fibrillation: a comparison of "healthy control subjects" and "disease control subjects" in sinus rhythm.

OBJECTIVES: The aim of this work was to comprehensively study the role of platelets in atrial fibrillation (AF), in relation to the underlying cardiovascular diseases and type of AF, and to analyze the effect of antithrombotic treatment on different aspects of platelet activation. BACKGROUND: Platelet activation is present in nonvalvular AF, but there is debate whether this is due to AF itself and/or to underlying cardiovascular diseases. METHODS: A total of 121 AF patients were compared with 65 "healthy control subjects" and 78 "disease control subjects" in sinus rhythm. Platelet activation was assessed using 4 different aspects of platelet pathophysiology: 1) platelet surface expression of CD62P (P-selectin) and CD63 (a lysosomal glycoprotein) (by flow cytometry); 2) mean platelet volume (MPV) (by flow cytometry); 3) plasma levels of soluble P-selectin (sP-selectin, enzyme-linked immunoadsorbent assay); and 4) total amount of P-selectin per platelet (pP-selectin) ("platelet lysis" assay). RESULTS: Both AF patients and "disease control subjects" had higher levels of CD62P (p < 0.001), CD63 (p < 0.001), and sP-selectin (p < 0.001) compared with "healthy control subjects," with no difference between AF patients and "disease control subjects." Patients with permanent AF had higher levels of sP-selectin (p = 0.014) and MPV (p = 0.025) compared with those with paroxysmal AF. The presence of AF independently affected the levels of CD62P expression, while "high-risk" AF patients (CHADS score > or =2) had higher levels of CD62P compared with those with "low risk." Introducing warfarin resulted in a reduction of pP-selectin (p = 0.013). CONCLUSIONS: There is a degree of excess of platelet activation in AF compared with "healthy control subjects," but no significant difference between AF patients and "disease control subjects" in sinus rhythm. Platelet activation may differ according to the subtype of AF, but this is not in excess of the underlying comorbidities that lead to AF. Platelet activation in AF may be due to underlying cardiovascular diseases, rather than due to AF per se.     

氨基酸末端脑钠素前体与心房颤动的相关性研究

目的探讨血清中氨基酸末端脑钠素前体（NT—pro BNP）水平与心房颤动（房颤）之间的关系。方法病例组心血管病患者136例，心功能I～Ⅱ级（NYHA分级），其中房颤患者90例，窦性心律患者46例；健康对照组30例。应用竞争性酶联免疫分析（ELISA）定量测定血清中NT—pro BNP水平，并进行统计学分析。结果房颤患者血清NT—pro BNP水平显著高于窦性心律患者和对照组（P〈0．01），窦性心律患者与对照组之间血清NT—pro BNP水平差异无统计学意义（P〉0．05）；房颤、年龄、右心房内径是血清NT—pro BNP水平升高的独立预测因素。结论房颤患者血清NT—pro BNP水平明显升高，监测血清NT—pro BNP水平的变化有助于房颤患者心功能的评价。     

Soluble E-selectin, von Willebrand factor, soluble thrombomodulin, and total body nitrate/nitrite product as indices of endothelial damage/dysfunction in paroxysmal, persistent, and permanent atrial fibrillation

BACKGROUND: Atrial fibrillation (AF) is associated with a prothrombotic state, which is related to endothelial damage/dysfunction. Plasma levels of soluble E-selectin (sE-sel), von Willebrand factor (vWf), and soluble thrombomodulin (sTM) have been used as indexes of endothelial activation, damage/dysfunction, and endothelial damage, respectively. Nitric oxide is also made by a healthy endothelium, and a total body nitrate/nitrite product (NOx) is used as a measure of endothelial nitric oxide production. We hypothesized that the levels of these markers of endothelial function would be abnormal in patients with paroxysmal, persistent, and permanent AF. METHODS: We studied 145 AF patients (paroxysmal AF, 35 patients; permanent AF, 50 patients; persistent AF, 60 patients) and 35 patients with "lone" AF. Plasma levels of sE-sel, vWf, and sTM (measured by enzyme-linked immunosorbent assay) and NOx (measured by a colorimetric assay based on the Griess reaction) were compared to 40 age-matched healthy control subjects in sinus rhythm. RESULTS: Patients with AF had significantly higher plasma levels of vWf (p < 0.001) and sE-sel (p = 0.005) compared with control subjects, but sTM and NOx levels were not significantly different. Levels did not differ significantly among the clinical subgroups of patients with paroxysmal, persistent, and permanent AF. Patients with lone AF had significantly higher vWF levels (p = 0.003) and significantly lower sTM levels (p = 0.0361) compared to control subjects, but sE-sel and NOx levels were not significantly different. There were no significant differences in the AF study population in vWF, sE-sel or sTM levels after 4 weeks of warfarin treatment. CONCLUSION: Endothelial perturbation exists in all clinical subgroups of patients with AF, including those with lone AF, which may contribute to the prothrombotic state seen in these patients.     

Levels of circulating procoagulant microparticles in nonvalvular atrial fibrillation

Circulating procoagulant microparticles (MPs) arising from cell activation or fragmentation during apoptosis retain procoagulant properties and are increased in severe thrombotic states. We investigated whether circulating procoagulant MP levels would be increased in nonvalvular atrial fibrillation (AF). Using a hospital case-control study design, circulating procoagulant MP levels were measured in 45 patients with permanent and/or persistent AF who were not receiving anticoagulant therapy and 90 age-matched control subjects (45 with cardiovascular risk factors and 45 without). Annexin V-positive MP levels (expressed as nanomoles per liter of phosphatidylserine equivalent) were higher in patients with AF (median 9.3, interquartile range 6.8 to 17.3 nmol/L) than in control subjects with cardiovascular risk factors (median 4.9, interquartile range 3.7 to 8.4 nmol/L) and control subjects without cardiovascular risk factors (median 3.2, interquantile range 2.3 to 4.6 nmol/L; p<0.001). Platelet-derived MPs (captured with antiglycoprotein Ib) and endothelial-derived MPs (captured with anti-CD31) were similar in patients with AF and control subjects with cardiovascular risk factors but were significantly higher than in control subjects without cardiovascular risk factors. On multiple regression analysis, the presence of AF was a strong predictor of annexin V-positive MP level (p<.001). In conclusion, circulating procoagulant MPs are increased in persistent and/or permanent AF and might reflect a hypercoagulable state that could contribute to atrial thrombosis and thromboembolism.