脂蛋白(a)在慢性心房颤动患者左心房血栓形成中的作用

许多研究表明 ,高水平的脂蛋白 (a) [Lp(a) ]是冠心病形成的独立危险因子 ,但其在慢性心房颤动(房颤 )患者左心房 (LA)血栓形成中的作用目前研究较少。我们通过经食管超声心动图 (TEE)检查或在心脏瓣膜置换手术时进行探查以证实慢性房颤患者有无LA血栓 ,并检测其血清Lp(a)浓度 ,探讨Lp(a)在LA血栓形成中的作用 ,为筛选评估房颤患者栓塞危险性的有效指标、合理应用抗凝剂、减少栓塞并发症提供依据。资料与方法　　 1.研究对象 :自 1999年 10月至 2 0 0 1年 5月共收集我院慢性房颤患者 98例 ,其中男 4 2例 ,女 5 6例 ,年龄 2 3～ 70岁 ,…     

心房颤动患者血栓形成与抗凝血酶Ⅲ关系的探讨

本文对术前部分心房颤动患者血浆抗凝血酶Ⅲ(AT-Ⅲ)的含量及功能活性进行测定。随意选其中有血栓和无血栓者各25例进行比较发现,血栓组AT-Ⅲ含量及功能活性均明显低于无血栓组(P<0.001),同时发现左房内径和二尖瓣口径血栓组也明显小于无血栓组(P<0.05)。     

炎症与非瓣膜性心房颤动血栓形成的关系

目的:通过观察非瓣膜性心房颤动患者血浆C反应蛋白(CRP)、D-二聚体的浓度及左心房直径、射血分数的水平,研究CRP与其左心房内血栓形成的关系.方法:将经食管超声心动图(TEE)检查的非瓣膜性心房颤动患者(107例)分为:左心房血栓形成组31例(血栓组)、无左心房血栓形成组76例(非血栓组).检测血浆中CRP、D-二聚体的浓度及经胸超声心动图检测左心房直径、缩短分数、射血分数.结果:血栓组与非血栓组CRP浓度(中位数1.65 mg/L:0.80 mg/L,P＜0.01)、D-二聚体浓度(中位数188.00 μg/L:92.00 μg/L,P＜0.01)、左心房直径[(54.68±12.44):(46.77±12.31)mm,P＜0.05]、射血分数[(58.20±9.42):(62.81±8.67)%,P＜0.05]、缩短分数[(30.46±5.75):(35.24±5.41)%,P＜0.01].Logistic回归发现CRP、左心房直径与非瓣膜性心房颤动并发血栓形成独立相关(P＜0.05),而D-二聚体、射血分数、缩短分数与非瓣膜性心房颤动并发血栓形成无显著相关.结论:CRP增高、左心房直径扩大是非瓣膜性心房颤动并发血栓形成的高危因素,炎症反应可能参与了心房内血栓形成.     

心房颤动患者血栓形成机制的研究进展

心房颤动是临床上最常见的心律失常,与卒中和血栓栓塞关系密切。心房颤动通过破坏生理止血机制而增加血栓形成风险,这一机制可通过魏尔啸(Virchow)的“血液成分异常”“血管壁异常”和“血液流动异常”三联征来解释。左心耳因其复杂的形态结构和特殊的功能特点,成为心房颤动患者血栓形成的主要部位。提高对心房颤动血栓形成的各种因素的认识,有助于更好地对心房颤动血栓形成风险进行危险分层,并提供及时有效的治疗。     

非瓣膜性心房颤动血栓形成的相关因素分析

目的通过观察非瓣膜性心房颤动患者血浆C反应蛋白、D-二聚体的浓度及左心房直径、射血分数的水平,研究C反应蛋白与非瓣膜性心房颤动患者左心房内血栓形成的关系。方法按照经食管超声心动图（TEE）检查结果将非瓣膜性心房颤动患者98名分为：左心房血栓形成组（血栓组）22例、无左心房血栓形成组（非血栓组）76例。检测血浆中C反应蛋白、D-二聚体的浓度及经胸超声心动图检测左心房直径、射血分数。结果血栓组在C反应蛋白浓度、D-二聚体浓度、左心房直径、射血分数、缩短分数方面与非血栓组差异有统计学意义,分别为C反应蛋白浓度（中位数1.60mg/L比0.80 mg/L,P=0.003）、D-二聚体浓度（中位数170.50μg/L比92.00μg/L,P=0.004）、左心房直径（55.20±12.94 mm比46.77±12.31 mm,P=0.002）、射血分数（57.46%±9.10%比62.81%±8.67%,P=0.006）、缩短分数（29.82%±5.26%比35.24%±5.41%,P〈0.001）。Logistic回归,发现C反应蛋白、左心房直径与非瓣膜性心房颤动合并血栓形成独立相关（P〈0.05）,而D-二聚体、射血分数、缩短分数与非瓣膜性心房颤动合并血栓形成无显著相关。结论CRP增高、左心房直径扩大是非瓣膜性心房颤动合并血栓形成的高危因素,炎症反应可能参与了心房内血栓的形成。     

慢性心房颤动患者左心房扩大与左心房血栓形成的相关性

目的:探讨慢性心房颤动患者左心房扩大与左心房血栓形成的相关性。方法:选择我院确诊的80例慢性心房颤动伴左心房扩大患者为左心房扩大组,80例慢性心房颤动左心房无扩大患者为心房无扩大组,应用经食管超声检测左心房大小及观察有无血栓。根据食管超声检查结果分为血栓形成组(22例)和无血栓组(138例),通过单因素及多元逐步Logistic回归分析,分析左心房血栓形成的危险因素。结果:超声心动图显示左心房扩大组心房内血栓形成率明显高于左心房无扩大组(17.5%比10.0%,P<0.05)。多因素Logistic回归分析显示,与心房内血栓形成的相关的危险因素有:左心房直径(OR=4.514,95%CI:1.243～14.206,P=0.01)、病程(OR=1.106,95%CI:0.898～1.071,P=0.035)。结论:心房颤动患者的左心房扩大,可导致心肌收缩力下降,增加左心房内血栓形成的危险性,是左心房内血栓形成的有意义的预测因子。     

心房颤动患者血栓形成与腺苷、血小板P选择素表达的关系

目的　研究慢性心房颤动 (房颤 )患者血栓形成与血浆腺苷水平、血小板活化的关系。方法　应用反相高效液相色谱及流式细胞仪 ,分析窦性心律及房颤患者血浆腺苷水平、血小板P选择素、GPⅡb/Ⅲa表达量 ,同时放免法测定血浆TXB2 、6 keto PGF1α含量 ,计算TXB2 / 6 keto PGF1α。并应用不同浓度的 8 苯基茶碱阻断腺苷受体 ,流式细胞仪分析其对血小板P选择素表达量的影响。结果　房颤组血浆腺苷水平明显低于窦性心律组 ,分别为 (5 5 6± 2 7 3) μg/L与 (77 5± 30 2 ) μg/L ,(P <0 0 1)。血小板P选择素表达量明显高于窦性心律组 ,分别为 (6 5 3± 3 37) %与 (4 72± 1 97) % ,P <0 0 5。血小板GPⅡb/Ⅲa有增高趋势 ,但无统计学意义 (18 7± 8 6 ) %与 (15 6± 8 3) % ,P >0 0 5。血浆TXB2 及TXB2 / 6 keto PGF1α含量均显著增高 [(15 0 3± 5 8 0 )ng/L与 (10 2 4± 36 5 )ng/L ,P <0 0 1;1 43± 0 5 9与 0 74± 0 2 9,P <0 0 0 1];而血浆 6 keto PGF1α的含量无显著变化 (P >0 0 5 )。血小板P选择素表达量房颤血栓形成组明显高于窦性心律无血栓组 [(7 34± 2 74) %与 (4 72± 1 97) % ,P <0 0 1];房颤血栓形成组与房颤无血栓组无显著差异 [(7 34± 2 74) %与 (6 17± 2 76 ) %     

老年慢性心房颤动患者左心房内血栓形成的危险因素与预测

目的　研究老年慢性非瓣膜病心房颤动患者中左心房内血栓形成的危险因素与预测 ,并探讨其可能的原因。方法　 6 4例老年慢性心房颤动患者 ,通过单因素及多元逐步logistic回归分析 ,首次将轻度二尖瓣反流作为一项待选变量 ,结合超声影像学和其他临床指标 ,对左心房内血栓形成的危险因素进行分析。结果　与左心房内血栓相关的因素有 :轻度二尖瓣反流、心房颤动持续时间、血小板表面P 选择素表达、血浆 β 血小板球蛋白 (P <0 .0 5 )。轻度二尖瓣反流与心房颤动持续时间是左心房内血栓形成的独立危险因素。结论　轻度二尖瓣反流增加而非降低心房颤动患者左心房内血栓形成 ,其原因可能与轻度二尖瓣反流激活血小板有关。持续的心房颤动可能通过心房肌的结构重构导致心肌收缩力进一步下降 ,增加血栓形成的危险性     

吸附式采样器采集尿液有形成分对泌尿内科疾病诊断效果分析

目的研究吸附式小便采样器采集尿液分析其有形成分变化对泌尿内科疾病诊断及预后判断的影响情况。方法98例泌尿内科住院病人分别用吸附式小便采样器与目前临床检验常用的尿杯采集尿样，在同等条件下进行有形成分检测、比较。结果采样器组有形成分95．5％以上在可控范围内，其余少数可通过“修饰”而接近真值。结论吸附式小便采样器取样与传统的尿杯采样，其检测结果符合率高，可取代尿杯用于临床采样。     

溶血磷脂酸与心房颤动患者血栓形成相关性研究

心房内血栓形成以及体动脉尤其是脑动脉栓塞是心房颤动(AF)患者严重的并发症.近年来,溶血磷脂酸(LPA)预测血栓形成的作用受到重视.我们分析LPA与AF患者血栓形成的相关性,从而进一步探讨LPA在预测AF患者血栓形成中的价值.     

Increased markers of thrombogenesis in chronic atrial fibrillation: effects of warfarin treatment.

OBJECTIVE--To determine whether chronic atrial fibrillation is associated with abnormalities in plasma fibrinogen, von Willebrand factor (vWF) (a marker of endothelial disturbance), or fibrin D- dimer (a measure of fibrin turnover); and if so, whether such levels are related to haemodynamic disturbance (enlarged left atrium, poor left ventricular function) or existing treatment with warfarin or aspirin. To investigate the effects of introducing warfarin in patients with atrial fibrillation on fibrinogen and D- dimer levels. DESIGN--Cross sectional population sample controlled study and longitudinal study of patients undergoing anticoagulation. SETTING--District general hospital. SUBJECTS--87 patients (44 men and 43 women of mean (SEM) age 63.0 (1.0)) with chronic atrial fibrillation. At the time of the study, 37 were taking no antithrombotic medication (group 1), 31 were taking warfarin (including two on warfarin and aspirin) (group 2) and 19 were taking aspirin alone (group 3). They were compared with 158 population controls from a random population sample (the second Glasgow monitoring trends and determinants in cardiovascular disease study). As part of clinical treatment warfarin was introduced in 20 patients with chronic atrial fibrillation (14 men and six women of mean (SEM) (range) age 63.9 (2.35 (32-74) years). RESULTS--Plasma fibrinogen remained significantly increased in patients of group 1 (no antithrombotic medication) compared with that of the population controls (median difference 1.23 g/l; 95% confidence interval (CI) 0.88 to 1.62, P < 0.0001). There was also a significant increase in plasma D-dimer levels (median difference 77 ng/ml; 95% CI 38 to 122, P < 0.01) and vWF (median difference 63 IU/dl; 95% CI 38 to 89, P < 0.0001). There was no significant difference in plasma fibrinogen (median difference 0.14 g/l; 95% CI -0.44 to 0.77, P = 0.65) or vWF (median difference 3.5 IU/dl; 95% CI - 41 to 41, P = not significant in patients of group 2 (warfarin treatment) compared with that of patients in group 1. Levels of D-dimer were significantly lower in group 2 (median difference 90 ng/ml, 95% CI 39 to 150, P < 0.0001) than in group 1. There were no significant differences in plasma fibrinogen (median difference 0.08 g/l; 95% CI - 0.52 to 0.77, P = 0.73), D-dimer (median difference - 34 ng/ml; 95% CI - 114 to 21.0, P = 0.25), or vWF (median difference 2%; 95% CI - 35 to 41, P = not significant) levels between patients of groups 1 and 3. There were no significant correlations between the coagulation indices and left atrial volume or ventricular function. There was a significant positive correlation between plasma fibrin D-dimer and vWF levels in patients of groups 1 and 3 (r = 0.52, P < 0.001). There was a significant reduction in median plasma fibrin D-dimer levels at 2 months after the introduction of warfarin (181 ng/ml v 80 ng/ml, P < 0.001), but no effect on plasma fibrinogen. CONCLUSIONS--Increased median plasma fibrinogen and vWF levels were found in patients with chronic atrial fibrillation. Plasma D-dimer levels were also increased in patients with chronic atrial fibrillation not receiving warfarin, suggesting increased intravascular thrombogenesis in such patients. Introduction of warfarin normalised circulating fibrin D- dimer levels, suggesting that warfarin treatment was effective in preventing excessive fibrin turnover, consistent with the antithrombotic effects of warfarin. These results suggest three possible thrombotic markers to assess patients with atrial fibrillation who are at high risk of thrombogenesis; D-dimer also merits assessment as a measure of reduction in thrombotic risk in patients receiving warfarin.     

The effects of atrial fibrillation on regional blood flow in the awake dog

To determine the acute effects of atrial fibrillation on regional blood flow, measurements were made in awake dogs with this arrhythmia induced and sustained by rapid atrial stimulation. Atrial fibrillation reduced cardiac output (from 3.7 +/- 0.3 to 3.0 +/- 0.2 L/min, P less than 0.05), but mean aortic and left atrial pressures were not changed. Although average ventricular myocardial blood flow remained the same, dogs with an average basal myocardial blood flow less than 106 mL/min/100g showed an immediate increase (from 85 +/- 5 to 120 +/- 9 mL/min/100g, P less than 0.05), whereas those with a higher basal value showed a decrease (from 144 +/- 14 to 110 +/- 18 mL/min/100g, P less than 0.05). Moreover, change in myocardial blood flow with atrial pacing, at a rate equal to the average ventricular rate of atrial fibrillation, was directionally similar to that found during atrial fibrillation. However, left atrial myocardial blood flow increased significantly both during atrial fibrillation and pacing. Sustained atrial fibrillation resulted in a fall in splanchnic and renal cortical flow. Brain blood flow also decreased during atrial fibrillation. While the fall in cerebral blood flow was immediately evident, in the cerebellum and brain stem, this decrease was not statistically significant until the 15 min measurement. Also, presence of a ligated common carotid artery did not influence cerebral regional blood flow either under basal conditions or with atrial fibrillation. Thus, in awake dogs the fall in cardiac output that occurs with atrial fibrillation may be accompanied by diverse effects on regional circulations.     

Interleukin-6, endothelial activation and thrombogenesis in chronic atrial fibrillation.

BACKGROUND: A prothrombotic or hypercoagulable state has been described in AF, which could increase the risk of thromboembolism. As inflammation has been related to thrombogenesis and endothelial activation, we hypothesised that the prothrombotic state in AF (as assessed by an index of thrombogenesis, prothrombin fragment 1+2 [F1+2]) and endothelial activation (soluble E-selectin (sEsel)) could be related to an index of inflammation (interleukin-6 (IL-6)). PATIENTS AND METHODS: We studied 191 consecutive patients (98 male; mean age 72.3+/-9.2 years) with chronic non-rheumatic AF who were not on anticoagulant therapy. Plasma IL-6, sEsel and F1+2 were measured by ELISA. Research indices were compared to 74 controls in sinus rhythm matched for age and sex. In 43 patients with AF, the effects of introducing anticoagulation (INR 2.0-3.0) were also studied. RESULTS: Patients with AF had elevated levels of F1+2 (p<0.001) and IL-6 (p=0.045), but not sEsel. There was no significant correlation between F1+2 and IL-6. In multivariate analysis, only F1+2 levels were independently associated with the presence of AF (p=0.001). After oral anticoagulation, plasma levels of F1+2 and sEsel were significantly decreased (both p<0.01). CONCLUSION: High levels of IL-6 in AF suggest an inflammatory state, which appears to be more related to clinical variables of the patients, rather than to the presence of AF per se. There was no association of inflammation with endothelial activation (sEsel) or the presence of abnormal thrombogenesis (high F1+2 levels) in AF. Moreover, no changes in IL-6 levels were found despite the reduction of the other markers by oral anticoagulant therapy.     

细胞凋亡在慢性风湿性心房颤动左房结构重构中的作用

目的探讨细胞调亡在心房颤动(AF)患者心房结构重构中的作用;检测风湿性心脏病患者左房中caspase-3和Bc l-2的蛋白含量及其细胞凋亡的发生率。方法选择风湿性心脏病患者43例,其中窦性心律(SNR)组15例,阵发性AF(PAF)组8例,慢性AF(CAF)组20例。在外科手术前行超声心动图检查,手术中取左房组织,应用免疫印迹法测定患者的caspase-3和Bc l-2的蛋白含量;应用TUNEL法检测心房肌细胞凋亡,计算其凋亡指数(AI)。结果①与SNR组比较,CAF组caspase-3的蛋白含量增加到394%±99.4%(P<0.001);Bcl-2蛋白含量则降低到32.8%±15.9%(P<0.001),而PAF组的各蛋白含量则无明显变化;②CAF组左房心肌细胞AI为24.6%±9.1%,明显高于SNR组和PAF组(P<0.01)。③CAF组caspase-3的蛋白含量及AI分别与左房内径、AF持续时间呈明显正相关;Bc l-2的蛋白含量与左房内径和AF持续时间呈明显负相关(P均<0.05)。④AI与caspase-3、Bc l-2的蛋白含量分别呈正、负相关;P均<0.05。Caspase-3的蛋白含量与BCL-2的呈负相关,P<0.05。结论CAF时,caspase-3蛋白表达增加和Bc l-2蛋白表达降低导致的细胞凋亡可能是AF发病的重要机制之一。     

The effects of radio-frequency ablation on blood pressure control in patients with atrial fibrillation and hypertension

Purpose

The effects of radio-frequency ablation (RFA) on blood pressure (BP) regulation in patients with atrial fibrillation (AF) and hypertension remain unknown. We hypothesized that patients with successful ablation had a lower BP and/or lesser utilization of antihypertensive drug therapy during follow-up when compared to patients with failed ablation.

Methods and results

This was a retrospective evaluation of patients with AF and hypertension treated with ablation at the University of Utah between July 2006 and June 2010. BP and use of antihypertensive medications were assessed at baseline and 1?year follow-up. A total of 167 patients were identified. Eight patients were excluded due to the need for AAD therapy beyond the blanking period thus leaving 80 patients in the success group and 79 patients in the failure group. The mean BP and HR at baseline were not significant between the groups. In the success group, the mean systolic BP decreased from a baseline value of 129?±?17 to 125?±?14?mmHg at 1?year (p?=?0.075). In contrast, in the failure group, the mean systolic BP increased from a baseline value of 124?±?16 to 127?±?14?mmHg at 1?year (p?=?0.176). Between-group comparison revealed a p value of 0.026. Minimal changes in diastolic BP were noted in both groups. No significant changes in antihypertensive therapy were noted.

Conclusion

We have shown that successful catheter ablation in patients with AF and hypertension is associated with a decrease in systolic BP when compared to an increase in patients with failed ablation. Our findings suggest that restoring sinus rhythm could have an antihypertensive effect in patients with AF and hypertension.     

Effect of atrial fibrillation on atrial blood flow in conscious dogs

This study was undertaken to examine the independent effects of atrial tachycardia, ventricular tachycardia, and atrial fibrillation (AF) on atrial and ventricular blood flow in conscious, heart-blocked dogs using radioactive microspheres. Atrial blood flow averaged 0.54 ± 0.08 ml/min/g during the control period at an atrial rate of 124 beats/min and a ventricular rate of 90 beats/min. Atrial flow increased to 0.72 ± 0.12 ml/min/g during atrial pacing at 236 beats/min, but was not significantly altered by ventricular pacing at 200 beats/min. AF at a ventricular rate of 90 beats/min resulted in atrial flow values of 0.91 ± 0.08 ml/min/g. The ratio of atrial flow to left ventricular flow during AF averaged 1.18 ± 0.08. Administration of a maximal vasodilating dose of adenosine during AF further increased atrial flow to 2.18 ± 0.16 ml/min/g. Atrial tachycardia or AF did not significantly affect ventricular blood flow. These data indicate (1) that atrial blood flow increases significantly during AF, reaching flow values per gram of tissue comparable to those of the left ventricle, and (2) that this flow is regulated by the metabolic needs of the atrial tissue and does not represent maximal vasodilation.     

A cross-sectional and diurnal study of thrombogenesis among patients with chronic atrial fibrillation

OBJECTIVES

First, we sought to determine whether there is diurnal variation in hemostatic factors related to thrombogenesis and hypercoagulability among patients with chronic atrial fibrillation (AF). Second, we sought to determine whether levels of soluble thrombomodulin (sTM), a marker of endothelial function, or soluble P-selectin (sP-sel), an index of platelet activation, are altered in patients with AF as compared with subjects in sinus rhythm.

BACKGROUND

Atrial fibrillation is associated with an increased risk of stroke and thromboembolism and is known to confer a hypercoagulable state, with abnormalities of thrombosis, platelet activation and endothelial cell function. Many cardiovascular events, such as acute myocardial infarction, have thrombosis as an underlying process, and they undergo diurnal variation.

METHODS

Fifty-two patients (45 men, mean [±SD] age 66 ± 6 years) with chronic AF, none of whom received antithrombotic therapy, were studied. Baseline levels of fibrinogen, sP-sel, sTM and von Willebrand factor (vWF) were compared to those levels in matched healthy control subjects in sinus rhythm. In a subgroup of 20 patients, five venous blood samples were collected through an indwelling cannula at 6-h intervals from 12 to 12 the following day and were analyzed for the same markers.

RESULTS

Patients with chronic AF had higher plasma sP-sel, sTM, vWF and fibrinogen levels as compared with control subjects in sinus rhythm. Significant correlations were found between fibrinogen and sP-sel in patients with AF (r = 0.567 [Spearman], p < 0.001) and in control subjects (r = 0.334, p = 0.016). There was no significant diurnal variation in plasma levels of sP-sel, sTM, vWF or fibrinogen over the 24-h study period (repeated measures analysis of variance, p = NS).

CONCLUSIONS

There is no circadian or diurnal variation in the hypercoagulable state seen in AF, as assessed by plasma fibrinogen and markers of platelet (sP-sel) and endothelial function (vWF and sTM). The persistent hypercoagulable state, together with the loss of diurnal variation in various hemostatic markers, in chronic AF may contribute to the high risk of stroke and thromboembolic complications in these patients.