C反应蛋白与心房颤动的关系

目的探讨C反应蛋白(CRP)作为系统炎症因子在心房颤动发生和发展中的作用。方法入选98例患者将其分为正常对照组(n=34)、阵发性房颤组(n=31)和持续房颤组(n=33),比较各组C反应蛋白水平。结果心房颤动组CRP水平[(1.85±0.44)mg/d]比正常对照组的水平[(0.41±0.13)mg/d]高,P<0.01;在心房颤动组中持续房颤组血清中CRP[(2.02±0.54)mg/d]高于阵发性房颤组[(1.55±0.40)mg/d],P<0.01,阵发性房颤组[(2.02±0.54)mg/d]高于正常对照组(0.41±0.13)mg/dl,P<0.01。并且不同原因引起的房颤CRP不同,冠心病最高,其次为高血压,心肌病最低。结论CRP在心房颤动患者中明显升高,说明炎症状态在心房颤动的发生和持续中起一定作用。     

C反应蛋白增高在心房颤动中的意义

目的 :探讨C反应蛋白 (CRP)增高在心房颤动 (房颤 )发病中的意义。方法 :应用免疫比浊法测定 96例诊断为房颤患者血清CRP水平 ,与对照组比较 ,并对房颤按持续时间、病因不同分设亚组 ,进行统计学分析。结果 :房颤组、对照组血清CRP水平分别为 (4 .30± 2 .87)、(1.15± 0 .90 )mg L ,两组相比P <0 .0 5。器质性、孤立性房颤者CRP水平分别为 (5 .0 6± 1.92 )、(4 .37± 1.32 )mg L ,均高于对照组 ,P <0 .0 5。持续性、永久性房颤者CRP水平分别为 (5 .6 0± 1.80 )、(5 .0 0± 1.6 0 )mg L ,均高于阵发性房颤 [(3.30± 1.2 0 )mg L],P <0 .0 5。结论 :CRP增高反映的炎症状态可能促进房颤发生 ,以及呈持续性发作。     

C反应蛋白与心房颤动的关系

目的探讨C反应蛋白(CRP)作为系统炎症因子在心房颤动发生和发展中的作用。方法入选98例患者将其分为正常对照组(n=34),阵发性心房颤动组(n=31)和持续性心房颤动组(n=33),比较各组CRP水平。结果心房颤动组CRP水平(18.5±4.4)mg/L比正常对照组(4.1±1.3)mg/L高,P<0.01;在心房颤动组中持续性心房颤动组血清中CRP(20.2±5.4)mg/L高于阵发性心房颤动组(15.5±4.0)mg/L,P<0.01;阵发性心房颤动组(20.2±5.4)mg/L高于正常对照组(4.1±1.3)mg/L,P<0.01。不同原因引起的心房颤动CRP不同,冠心病最高,其次为高血压,心肌病最低。结论CRP在心房颤动患者明显升高,其代表的炎症状态在心房颤动的发生和持续中起一定作用。     

超敏C-反应蛋白和C-反应蛋白的测定对SARS的诊断价值

目的　研究血清超敏C -反应蛋白 (hs -CRP )和C -反应蛋白 (CRP)对严重急性呼吸综合征 (SARS)的诊断价值。方法　SARS病人 2 0例、细菌性肺炎病人 2 0例、健康对照 2 0例 ,血清hs -CRP和CRP采用胶乳免疫比浊法全自动定量测定。结果　hs -CRP和CRP测定结果分别为 :健康对照组 (0 6 9± 0 6 2 )mg/L和 (4 4± 0 9)mg/L、细菌性肺炎组 (10 79± 1 36 )mg/L和 (98 0± 2 8 9)mg/L、SARS组 (3 16± 3 72 )mg/L和 (11 0± 9 6 )mg/L。三组间差异均有显著意义 (P <0 0 1)。结论　SARS病人和细菌性肺炎病人早期血清hs -CRP和CRP均升高 ,但细菌性肺炎病人升高更加显著 ,比SARS组分别增加 2 4倍和 7 9倍 ,对SARS与细菌性性肺炎的鉴别诊断有重要意义     

非瓣膜性心房颤动患者血清C-反应蛋白变化及其临床意义

目的测定非瓣膜性心房颤动(简称房颤)患者血清C-反应蛋白及外周血白细胞的变化,以探讨炎症机制在非瓣膜性房颤的发生发展中的作用。方法对135例房颤患者(房颤组)和120例非房颤患者(对照组),采用免疫比浊法测定其血清中CRP水平,用库尔特JT血球仪测定外周血白细胞数(WBC)、中性粒细胞百分率(N%)、中性粒细胞绝对值(N)、淋巴细胞百分率(L%)、淋巴细胞绝对值(L)。应用超声心动图诊断左室肥厚(LVH)及左房内径(LAD)。观察CRP及白细胞变化与房颤关系。结果房颤组血中CRP水平显著高于非房颤组(6.41±2.73mg/Lvs3.66±1.18mg/L;P<0.05)。其中房颤合并LVH较不合并LVH组CRP显著增高(7.51±3.32mg/Lvs5.76±2.92mg/L;,P<0.05)。四分位法研究表明房颤组血清CRP水平位于最高四分位者显著多于对照组;房颤组血清CRP水平位于最高四分位者较同组最低四分位者显著增加(P<0.05)。CRP位于最高四分位者LAD较位于最低四分位者显著增加(P<0.05)。两组WBC、N%、N、L%、L无显著性差异。结论慢性炎症反应在非瓣膜性房颤的发生发展中可能起到重要的作用。     

热休克蛋白在风湿性心脏病并发心房颤动患者中的表达

目的比较多种热休克蛋白(HSP)在风湿性心脏病(RHD)并发心房颤动(简称房颤)患者和窦性心律(简称窦律)患者中的表达。方法 73例RHD患者,其中伴慢性房颤患者(A组)38例和不伴房颤患者(B组)35例。测定两组患者血沉、血清超敏C反应蛋白水平。经开胸手术获取右心耳组织标本,进行免疫组织化学染色,测量HSP27、HSP60、HSP70和HSP90的分布密度。结果与B组比较,A组HSP27分布密度均显著降低(255±117μm2/mm2vs 558±133μm2/mm2,P<0.05),而HSP60、HSP70和HSP90的分布密度在两组间无显著差异。在A组,HSP27分布密度与左房直径呈负相关(r=-0.58,P<0.05),与性别、年龄、体重指数、射血分数、血沉和超敏C反应蛋白水平等无关。结论 HSP27的表达水平与RHD并发的房颤相关。     

普罗布可对兔动脉粥样硬化模型中斑块稳定性及热休克蛋白60表达的影响

目的观察动脉粥样硬化(AS)兔模型中热休克蛋白60(HSP60)的表达及其与斑块稳定性之间的关系和普罗布可对HSP60表达的影响。方法20只新西兰大白兔随机分正常对照组(n=6)、高脂饮食组(n=8)、普罗布可组(n=6)。对照组予以普食喂养,高脂饮食组和普罗布可组予高脂喂养。4周后高脂饮食组和普罗布可组行髂动脉内膜球囊损伤术。术后普罗布可组每只兔子加用普罗布可1000mg/d口服,10周末处死动物。采用HE染色观察动脉病理形态学变化,免疫组化染色检测动脉中HSP60的表达,酶联免疫吸附法测血清中的C反应蛋白(CRP)、白细胞介素(IL)-6、氧化低密度脂蛋白(ox-LDL)、HSP60的水平。结果高脂饮食组动脉可见典型的动脉粥样硬化斑块,普罗布可组无典型斑块形成,内膜增厚较为明显;与高脂饮食组相比较,普罗布可组血清CRP、IL-6、ox-LDL、HSP60水平降低;普罗布可组内膜和中膜HSP60的表达较高脂饮食组明显减少。血清HSP60水平与CRP、IL-6、ox-LDL水平正相关。结论HSP60在兔AS模型中的表达水平明显增加,与斑块的不稳定性有关,普罗布可可抑制兔AS模型血清和斑块中HSP60的表达。     

阿托伐他汀对急性冠脉综合征患者血清高敏C反应蛋白和妊娠相关血浆蛋白-A水平的影响

目的探讨阿托伐他汀干预对急性冠脉综合征(ACS)患者血清高敏C反应蛋白(hs-CRP)和妊娠相关血浆蛋白-A(PAPP-A)水平的影响。方法采用酶联免疫吸附法测定不稳定型心绞痛患者(UAP,n=37)、急性心肌梗死患者(AMI,n=24)、稳定型心绞痛患者(SAP,n=29)和健康体检者(n=32)的hs-CRP和PAPP-A水平。同时将ACS患者(包括UAP和AMI组,n=61)随机分为常规治疗组(n=30)和阿托伐他汀干预组(阿托伐他汀10mg/d,n=31),并于治疗前后分别测定血清hs-CRP和PAPP-A水平。结果(1)hs-CRP和PAPP-A水平在UAP组[(16.7±1.24)mg/L,(63.88±1.82)μg/L]、AMI组[(18.52±1.96)mg/L,(66.41±1.24)μg/L]比SAP组[(4.6±1.16)mg/L,(47.56±0.72)μg/L]、正常对照组[(3.2±0.88)mg/L,(45.17±1.28)μg/L]显著升高(P<0.05)。(2)2周后,阿托伐他汀干预组血清hs-CRP和PAPP-A水平较治疗前明显降低[hs-CRP(18.52±2.37)mg/Lvs.(3.58±1.33)mg/L;PAPP-A(67.83±2.15)μg/Lvs.(45.62±1.58)μg/L,P<0.05],且较常规治疗组治疗2周后亦有显著降低[hs-CRP(3.58±1.33)mg/Lvs.(5.23±1.98)mg/L;PAPP-A(45.62±1.58)μg/Lvs.(51.35±2.15)μg/L,P<0.05]。结论阿托伐他汀干预可以减少急性冠脉综合征患者动脉粥样硬化斑块的炎症反应,具有稳定斑块的作用。     

风湿性心脏瓣膜病房颤肺静脉组织学及pgp9.5蛋白分布研究

目的:探讨风湿性心脏瓣膜病合并房颤病人肺静脉组织学及pgp9.5(product gene protein 9.5)蛋白表达的变化特点。方法:选取风湿性心脏瓣膜病行瓣膜置换术病人26例,术中收集右上肺静脉标本。将病人分为房颤心律组(n=14),窦性心律组(n=12),对肺静脉标本行HE染色及pgp9.5蛋白Envension免疫组织化学染色。结果:与窦性心律组相比,房颤组心肌袖部心肌细胞肥大,肌束间间隙较大,排列更紊乱;脂肪垫及心肌组织有大量表达pgp9.5蛋白的细胞。结论:风湿性心脏病合并房颤致肺静脉心肌袖部心肌细胞肥大,间隙增宽;免疫组化染色表明肺静脉组织有大量表达pgp9.5蛋白的细胞存在。     

风湿性心脏瓣膜病房颤肺静脉组织学及pgp9．5蛋白分布研究

目的:探讨风湿性心脏瓣膜病合并房颤病人肺静脉组织学及pgp9.5(product gene protein 9.5)蛋白表达的变化特点.方法:选取风湿性心脏瓣膜病行瓣膜置换术病人26例,术中收集右上肺静脉标本.将病人分为房颤心律组(n=14),窦性心律组(n=12),对肺静脉标本行HE染色及pgp9.5蛋白Envension免疫组织化学染色.结果:与窦性心律组相比,房颤组心肌袖部心肌细胞肥大,肌束间间隙较大,排列更紊乱;脂肪垫及心肌组织有大量表达pgp9.5蛋白的细胞.结论:风湿性心脏病合并房颤致肺静脉心肌袖部心肌细胞肥大,间隙增宽;免疫组化染色表明肺静脉组织有大量表达pgp9.5蛋白的细胞存在.     

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.     

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。     

Electrophysiological properties in chronic lone atrial fibrillation

BACKGROUND. Although the electrophysiological mechanisms underlying self-sustaining atrial fibrillation (AF) are unclear, recent studies suggest that one requirement for reentry, slow conduction, is frequently present in patients with AF. However, these observations limited to paroxysmal AF may not necessarily apply to chronic AF. Therefore, electrophysiological properties of the atrium and sinus nodal function in chronic lone AF were evaluated. METHODS AND RESULTS. Electrophysiological studies were performed after electrocardioversion in 12 patients with chronic lone AF. Atrial enlargement was absent in the patients with AF. Twelve patients without atrial arrhythmias served as the control group. The patients with AF had a higher incidence of sinus nodal dysfunction, a shorter atrial effective refractory period (215 +/- 19 msec versus 238 +/- 23 msec, p less than 0.02), and a longer P wave duration than control patients (115 +/- 16 msec versus 86 +/- 16 msec, p less than 0.01). The conduction delay zone was significantly greater in patients with AF (60 +/- 12 msec) than that in the control patients (8 +/- 13 msec, p less than 0.01), and the maximal conduction delay was also greater in the study patients than those in the control group, both to the His bundle region (31 +/- 12 msec versus 10 +/- 15 msec, p less than 0.01) and to the coronary sinus (41 +/- 15 msec versus 15 +/- 11 msec, p less than 0.01). The fragmented atrial activity zone was wider in the study group (23 +/- 25 msec) than in control subjects (1.7 +/- 4 msec, p less than 0.02). Repetitive atrial firing was observed in four patients with AF but it was not seen in the control group. CONCLUSIONS. These electrophysiological features, which are manifestations of the abnormal atrial electrophysiology, would favor production of atrial reentry in chronic lone AF.     

Effect of disopyramide on initiation of atrial fibrillation and relation to effective refractory period

Electrophysiologic studies were performed before and after intravenous administration of disopyramide (2 mg/kg) to 40 patients with either documented or suspected atrial fibrillation (AF). In control studies, sustained AF (greater than 1 minute), nonsustained AF (1 to 60 seconds) and no AF were found in 14, 18 and 8 patients, respectively. After disopyramide, the ability to initiate AF was totally lost in 18 patients (group A), while 22 patients (group B) showed sustained AF (11 patients) or nonsustained AF (11 patients). The effective refractory period of the atrium was 232 +/- 41 ms in the control study and 266 +/- 49 ms after disopyramide. Atrial functional refractory periods before and after disopyramide were 282 +/- 43 and 317 +/- 48 ms, respectively. The differences and ratios of the refractory periods after and before disopyramide were higher in group A than in group B (p less than 0.001). The prolongation of atrial refractoriness after disopyramide was important to suppress the initiation of AF in group A. In some group B patients, on the other hand, the initiation of AF was promoted after disopyramide. Disopyramide may alter the atrial electrophysiologic substrate required for AF initiation.     

MinK gene polymorphism in the pathogenesis of lone atrial fibrillation

INTRODUCTION: Atrial fibrillation (AF) is the most common type of complex arrhythmia found in everyday clinical practice. Lone AF is a particular form occurring in 2% to 31% of patients with confirmed AF. Genetic factors may underline this arrhythmia. AIM: To determine the relationship between G38S polymorphism in the MinK gene and the incidence of lone AF, and to evaluate this polymorphism as a genetic marker of susceptibility to AF. METHODS: The study involved 69 patients with lone AF and 60 control healthy subjects. Both groups included patients aged up to 65 years without cardiovascular or thyroid disease. MinK genotype was determined with PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism). The MinK gene was present in two allelic forms: G and S. RESULTS: The MinK G allele was found significantly more often in patients with AF (62.32%) compared to control subjects (41.80%) (p=0.009). In the AF group GS occurred more frequently (55.07%) than GG (34.78%) and SS genotypes (10.14%). In a logistic regression model the presence of G variant was associated with increase of AF risk in the study population (OR 2.39; 95% CI 0.88-6.54; p=0.084). Presence of GG genotype was associated with significant, over 10-fold, increase of AF risk. Presence of S allele of the MinK gene met criteria of protective factor against AF in the study population. CONCLUSIONS: 1. G38S polymorphism in the MinK gene seems to be associated with incidence of lone AF in the study population. 2. GG genotype carrier state may significantly relate to increased risk of AF in the study group. 3. G38S polymorphism in the MinK gene could be used as a genetic marker of risk of lone AF.     

Atrial fibrillation and atrial vulnerability in patients with Brugada syndrome

OBJECTIVES: We sought to study atrial vulnerability in patients with Brugada syndrome. BACKGROUND: Atrial fibrillation (AF) often occurs in patients with Brugada syndrome, but atrial vulnerability in Brugada syndrome has not been evaluated. METHODS: The patient group consisted of 18 patients with Brugada syndrome. The control group consisted of 12 age- and gender-matched subjects who had neither organic heart disease nor AF episodes. The incidence and clinical characteristics of AF were evaluated in all 18 patients with Brugada syndrome, and an electrophysiologic study was performed in all 12 control subjects and in 14 of the 18 patients with Brugada syndrome. The atrial effective refractory period of the right atrium (RA-ERP), intra-atrial conduction time (conduction time from the stimulus at the right atrium to atrial deflection at the distal portion of the coronary sinus), duration of local atrial potential, and repetitive atrial firing (occurrence of two or more premature atrial complexes after atrial stimulation) were studied. RESULTS: Spontaneous AF occurred in 7 of the 18 patients with Brugada syndrome but in none of the control subjects. The RA-ERP was not different between the two groups. The intra-atrial conduction time was increased in the Brugada syndrome group versus the control group (168.4 +/- 17.5 vs. 131.8 +/- 13.0 ms, p < 0.001). The duration of atrial potential at the RA-ERP was prolonged in the Brugada syndrome group versus the control group (80.3 +/- 18.0 vs. 59.3 +/- 9.2 ms, p < 0.001). Repetitive atrial firing was induced in nine patients with Brugada syndrome and in six control subjects. Atrial fibrillation was induced in eight patients with Brugada syndrome but in none of the control subjects. In patients with Brugada syndrome without spontaneous AF, the intra-atrial conduction time and duration of atrial potential were also increased. CONCLUSIONS: Atrial vulnerability is increased in patients with Brugada syndrome. Abnormal atrial conduction may be an electrophysiologic basis for induction of AF in patients with Brugada syndrome.     

Comparison of amiodarone versus ibutilide for the prevention of immediate recurrences of atrial fibrillation during pulmonary vein isolation

During segmental ostial ablation for pulmonary vein isolation, pulmonary vein potentials are easily identified during sinus rhythm or left atrial pacing. Therefore, maintenance of atrial fibrillation (AF) during the procedure is desirable. However, cardioversion is occasionally followed by an immediate recurrence of AF. This study compared the efficacy of ibutilide and amiodarone in preventing immediate recurrences of AF in patients who underwent pulmonary vein isolation. The subjects of this study were 25 patients (mean age 56 +/- 10 years) who underwent pulmonary vein isolation for AF who had an immediate recurrence of AF within 60 seconds after 2 transthoracic cardioversions. The patients were randomized to receive an infusion of either 300 mg of amiodarone over 10 minutes or 1 mg of ibutilide over 5 minutes. Cardioversion was repeated 15 minutes after the drug infusion. If immediate recurrences of AF occurred 2 more times, the alternative study drug was administered, and cardioversion was repeated. Immediate recurrences of AF were suppressed by amiodarone in 8 of 10 patients (80%), and by ibutilide in 9 of 15 patients (60%, p = 0.4). After crossover, immediate recurrence of AF was suppressed in 2 of 6 patients (33%) by amiodarone, and in 1 of 2 patients (50%) by ibutilide (p = 0.6). Ibutilide and amiodarone, when used alone or in combination, prevented immediate recurrences of AF in 20 of 25 patients (80%). There were no adverse drug effects. Ibutilide and amiodarone were equally effective in suppressing immediate recurrences of AF. Overall, immediate recurrences of AF can be prevented by amiodarone and/or ibutilide in 80% of patients.     

Optimal β-blocker for prevention of atrial fibrillation after on-pump coronary artery bypass graft surgery: Carvedilol versus metoprolol

BACKGROUND: Atrial fibrillation (AF) is the most common arrhythmia after coronary artery bypass graft (CABG) surgery. It has been shown that prophylactic oral beta-blocker administration reduces the incidence of post-CABG AF. However, the optimal beta-blocker has not been identified. OBJECTIVE: This study sought to determine whether oral carvedilol (with its unique anti-inflammatory and antioxidant properties) is more effective than oral metoprolol for prevention of AF after CABG surgery. METHODS: Between April 2006 and December 2006, 120 patients (63 men, mean age 61 +/- 9.4 years) who were scheduled to undergo their first on-pump CABG were enrolled in this study. The patients were randomized in a prospective 1:1 manner to receive either oral carvedilol (n = 60) or oral metoprolol (n = 60). The end point of the study was the occurrence of the new-onset AF during the first 5 days after CABG. RESULTS: AF occurred in 29 of 120 patients (24.0%). The incidence of postoperative AF was 15.0% (9 of 60) in the carvedilol group and 33% (20 of 60) in the metoprolol group (P = .022). The carvedilol group was treated with mean daily dose of 46 +/- 9 mg and metoprolol group with mean daily dose of 93 +/- 11 mg. There were no differences between the study groups regarding any known preoperative, perioperative, or postoperative characteristics (all values were P >.05). No significant adverse effect was observed in either group. CONCLUSION: This prospective study suggested that oral carvedilol is more effective than oral metoprolol in the prevention of AF after on-pump CABG. It is well tolerated when started before and continued after the surgery. However, further prospective studies are needed to clarify this issue.     

几丁质酶-3样蛋白-1在心房颤动发病机制中的作用

目的探讨几丁质酶-3样蛋白-1（ehitinase-3．1ike-1protein,YKL-40）在心房颤动（房颤）发病机制中的作用。方法选择在广州市番禺区何贤纪念医院心内科住院的房颤患者71例（其中阵发性房颤组22例,持续性房颤组30例．永久性房颤组19例）为研究对象。另外,选择同期年龄匹配的健康体检者20名为对照组。采用酶联免疫吸附试验（ELISA）方法检测各组血浆YKL-40浓度并进行比较。结果各组间基线资料比较,差异无统计学意义（P〉0。05）。永久性房颤组、持续性房颤组及阵发性房颤组血浆YKL-40浓度均显著高于对照组,差异有统计学意义[（4．21±0．62）μg／L、（3．72±0．63）μg／L、（3．29＋0．75）μg／Lus（2．79±0．56）μg／L,P〈0．05];持续性及永久性房颤组血浆YKL-40浓度高于阵发性房颤组,差异有统计学意义（P〈0．05）;永久性房颤组YKL-40浓度高于持续性房颤组．差异有统计学意义（P〈0．05）。结论YKL-40可能参与房颤的发生、发展。     

Prevalence of inducible paroxysmal supraventricular tachycardia during esophageal electrophysiologic study in patients with unexplained stroke

BACKGROUND: The relationships between stroke and atrial tachycardia or atrial fibrillation were previously reported. Electrophysiological study is one of the means, used to detect and evaluate these atrial tachyarrhythmias. But, some other arrhythmias as paroxysmal supraventricular tachycardia, can be induced during electrophysiologic study and their significance in stroke is unknown. The aim of the study was to assess the significance of inducible paroxysmal supraventricular tachycardia (PSVT) in stroke. METHODS: One hundred thirty seven patients, aged 61+/-12 years had unexplained stroke (group I) and were compared to 60 subjects aged 45+/-18.5 years without stroke and history of tachycardia (group II); Holter monitoring (HM), echocardiogram and esophageal electrophysiologic study (EPS) in basal state and after isoproterenol were performed. RESULTS: Heart disease was noted in 19 group I patients (14%) and 10 group II patients (17%). In group I, atrial fibrillation or tachycardia (AF-AT) was induced in 20 patients (15%) and PSVT was induced in 19 patients (14%) aged 66+/-12 years. In group II, AF/AT was induced in 3 patients (5%); no group II patient had induced PSVT. After 3+/-1 years, in group I, one of 98 patients without induced arrhythmias had new strokes and 2 had AF; 5 patients with induced AT/AF developed AF; 5 patients with induced PSVT had PSVT's, requiring ablation in 4 of them; 1 died from a new stroke; one had a second non-fatal stroke and 3 patients developed AF (16%). In group II, there were no events. CONCLUSION: In 14% of patients with unexplained stroke, PSVT was inducible during esophageal electrophysiologic study. Further studies are warranted to assess the significance of this finding in patients with unexplained stroke.