心房颤动与炎症及慢性幽门螺旋杆菌感染相关性研究

目的探讨心房颤动(简称房颤)与炎症及慢性幽门螺旋杆菌(Hp)感染的关系。方法选取66例房颤患者为房颤组(其中阵发性房颤44例,慢性房颤22例),另取同期住院的阵发性室上性心动过速(简称室上速)患者67例作为对照组,用间接ELISA法测定血清Hp-IgG抗体,速率散射免疫比浊法测定C反应蛋白(CRP),比较两组Hp-IgG抗体,CRP的差异并分析HP抗体滴度与房颤及其它相关因素的关系。结果房颤组与对照组的Hp-IgG阳性率Hp-IgG对数值均无差异(P均>0.05)。房颤组CRP中位数较对照组高(1.17mg/dlvs0.65mg/dl,P<0.05)。结论房颤与慢性Hp感染不相关,与炎症相关。     

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。     

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。     

慢性风湿性心脏病C-反应蛋白浓度测定及其意义

目的通过对86例慢性风湿性心瓣膜病C-反应蛋白(CRP)含量测定,探讨炎症在慢性风心瓣膜病中的意义。方法选取我科住院慢性风心瓣膜病患者86例,其中瓣膜置换术后风心42例,非瓣膜置换风心患者44例,与同期44名正常健康人作对照,采用速率散射比浊法测定CRP水平。结果86例慢性风心瓣膜病患者的血清CRP水平显著高于健康对照组[(0.64±0.37)mg/dl比(0.21±0.20)mg/dl,P<0.05]。其中非瓣膜置换的风心瓣膜病患者的血清CRP水平显著高于瓣膜置换术后风心组和健康对照组[(0.89±0.42)mg/dl、(0.32±0.31)mg/dl和(0.21±0.20)mg/dl,分别P<0.05和P<0.01]。瓣膜置换术后的风心瓣膜病患者的血清CRP水平高于健康对照组[(0.32±0.31)mg/dl比(0.21±0.20)mg/dl,P>0.05],差异无统计学意义。联合瓣膜病变者(24例)的血清CRP水平显著高于单瓣膜病变者(20例)[(1.49±0.77)mg/dl比(0.50±0.48)mg/dl,P<0.05]。结论炎症在风湿性心瓣膜病慢性期仍然持续存在。风湿瓣膜病变的严重性可能使CRP浓度升高。     

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。     

心房颤动患者血栓前状态研究

目的 :研究心房颤动 (房颤 )患者血栓前状态相关指标 ,探讨其临床意义。方法 :在慢性房颤患者、具器质性心脏病无房颤患者和健康正常人中 ,测定血浆D 二聚体、血管性血友病因子(vWF)、纤维蛋白原 (Fg)、平均血小板体积 (MPV ) ,以及二磷酸腺苷、肾上腺素、胶原、花生四烯酸诱导的血小板最大聚集率。房颤患者根据是否服阿司匹林分为 2组 :房颤 1组为未服阿司匹林者 (17例 ) ,房颤 2组为服阿司匹林者 (18例 )。具器质性心脏病无房颤且未服用阿司匹林患者 (19例 )为窦性心律组 ,另选 17例正常健康者为对照组。结果 :房颤 1、2组血浆D 二聚体、vWF以及MPV明显高于窦性心律组和对照组 (P <0 0 5～ 0 0 1)。房颤 1、2组血浆Fg明显高于对照组 (P <0 0 5 )。以上指标在房颤 1组和房颤 2组之间的差异无显著性。与房颤 1组比 ,房颤 2组四种诱导剂的血小板最大聚集率均显著降低 ,有极显著性差异 (P <0 0 0 1)。vWF >15 0 %房颤患者Fg更高、左心房内径更大 ,与vWF≤ 15 0 %房颤患者比有显著性差异 (P <0 0 5 )。结论 :房颤患者存在着血栓前状态 ,且不受小剂量阿司匹林的影响 ,这些异常可能与房颤患者心房内血栓形成相关。     

吸烟对慢性阻塞性肺疾病急性加重期患者C-反应蛋白的影响

目的比较吸烟、戒烟及非吸烟慢性阻塞性肺疾病急性加重期(AECOPD)患者血中C-反应蛋白(CRP)的差异及其与血白细胞(WBC)计数的关系,探讨吸烟患者CRP的变化。方法回顾性分析广西医科大学第四附属医院呼吸内科2002年6月至2006年7月间568例AECOPD患者,分为吸烟组(n=156)、戒烟组(n=170)和非吸烟组(n=242),测定血清CRP质量浓度及血WBC计数。结果3组CRP质量浓度的中位数分别为5.7mg/L,5.6mg/L和5.8mg/L,组间比较差异无显著性意义,吸烟暴露对AECOPD患者血清CRP的升高无影响;3组WBC计数中位数分别为8.6×109/L,9.1×109/L和8.5×109/L,组间比较差异无显著性意义,CRP与WBC计数呈正相关(r=0.305,P<0.01)。结论吸烟、戒烟及非吸烟的AECOPD患者CRP均无差异,CRP与吸烟无关,与感染有一定的关系。     

心房颤动患者幽门螺旋杆菌感染的发生率及相关因素分析

目的探讨心房颤动(简称房颤)患者幽门螺旋杆菌(Hp)感染的情况及相关因素。分析超敏C反应蛋白(Hs-CRP)、白细胞介素-6(IL-6)、血脂(TC、TG、LDL-C、HDL-C)、胱抑素C(Cysc)以及左房内径(LAD)与房颤的相关性。方法选取房颤组患者69例,室上性心动过速(简称室上速)组患者50例,同时选取健康志愿者50例作为正常组,各组均行14C呼气试验,比较各组Hp阳性率。检测房颤组及室上速组两组Hs-CRP、IL-6、血脂、Cysc、LAD。结果房颤组Hp阳性率(56.5%,39/69)明显高于室上速组(34.0%,17/50)及正常组(30.0%,15/50)(P0.0167),室上速组与正常组比较Hp阳性率无显著差异(P0.05)。房颤组Hs-CRP(3.65 mg/L)、IL-6(6.66ng/L)、Cysc(1.33mg/L)中位数分别明显高于室上速组(1.06、2.77、0.97 mg/L)(P0.05),TC(3.69±0.97)、LDL-C(2.13±0.76)、HDL-C(中位数0.99mmol/L)均低于室上速组(4.31±0.96、2.43±0.73、1.09)(P0.05),LAD明显大于室上速组[(44.25±9.26)mm vs(28.87±4.85)mm,P0.05)],TG中位数与室上速组比较无显著差异(P0.05)。结论幽门螺旋杆菌感染、炎症、TC、LDL-C、HDL-C与房颤存在相关性。     

螺内酯对阵发性心房颤动的预防和治疗中的作用

目的:观察醛固酮受体拮抗剂螺内酯在阵发性心房颤动(房颤)复律后的治疗中,对血清醛固酮水平和左心房内径的影响,以及对窦性心律的维持作用。方法:选取阵发性房颤成功复律后的患者99例,随机分为治疗组(50例)和对照组(49例),对照组常规口服胺碘酮及福辛普利,治疗组在上述治疗的基础上再加服螺内酯20mg/d,随诊1年,观察治疗前后血清醛固酮浓度、左心房内径及窦性心律的维持情况。结果:两组患者治疗后血清醛固酮水平[对照组(82.1±27.6)ng/dl,治疗组(79.7±32.5)ng/dl]较治疗前[对照组(145.2±37.1)ng/dl,治疗组(142.9±35.7)ng/dl]均明显下降(P0.05),但两组间无显著差异(P0.05)。治疗后治疗组的左心房内径(36.6±9.7)mm明显小于对照组(41.2±7.4)mm(P0.05),且与治疗前相比[治疗组(45.5±9.2)mm,对照组(44.9±11.1)mm]均有显著缩小(P0.01)。治疗组患者房颤平均发作次数(4.68±2.51)次明显少于对照组(7.20±5.46)次,治疗组窦性心律的维持率(77.1%)显著高于对照组(52.2%)(P0.05)。结论:螺内酯对血清醛固酮水平无明显影响,但却可以在一定程度上延缓左心房的扩大,并能减少阵发性房颤的复发,提高窦性心律的维持率。     

92例心房颤动患者与C-反应蛋白及其-717A>G多态性关系的分析

目的:分析92例心房颤动(房颤)患者与C-反应蛋白(CRP)及其-717A>G多态性的关系.方法:采用免疫比浊法测定92例房颤患者(房颤组)和60例对照者(对照组)的血清CRP水平,同时应用聚合酶链反应检测CRP的-717A/G的基因多态性,结合其他临床资料分析.结果:Logistic回归分析显示自然对数转换CRP(InCRP)水平(0R=7 84,P<0 01)与房颤独立相关,房颤组的水平显著高于对照组.2组-717A/G基因型的分布趋势相同,差异无统计学意义;但等位基因频数分布2组间存在显著性差异(χ2=4 38,P<0 05),G等位基因在房颤组中表现为低频率.CRP水平与-717A/G基因型无关,但AA基因型个体TC水平显著高于GA+GG型个体(P<0 05),但这种关系仅限于房颤患者.结论:血清CRP水平升高可能是房颤的独立危险因子,AA基因型在房颤组中表现为高TC水平,可能代表更高的炎症状态.     

C-reactive protein and paroxysmal atrial fibrillation: evidence of the implication of an inflammatory process in paroxysmal atrial fibrillation.

BACKGROUND: Detection of inflammation is best achieved by measurements of C-reactive protein (CRP).We investigated whether inflammation might promote the development of paroxysmal atrial fibrillation (PAF), and whether high levels of CRP are associated with an increased risk of PAF. METHODS: We assessed the levels of CRP and other risk factors in patients with PAF of recent onset (<24 h), compared with age and sex matched controls with the same risk factors who had normal sinus rhythm. Patients with thyrotoxicosis, mitral stenosis, pulmonary emboli or pericarditis were excluded. Fifty patients with PAF and 50 control subjects were finally included. All patients received amiodarone (2.7 g over 24 hours). RESULTS: Conversion to normal sinus rhythm was achieved within 24 h in 40 patients. CRP levels were higher (P<0.001) in the PAF group (median = 0.80, min = 0.00, max = 5.90 mg/dl) compared with controls (median = 0.04, min = 0.00, max = 0.48 mg/dl). In the PAF group CRP levels were higher (P<0.001) for patients who failed to be cardioverted (median = 2.12, min = 0.80, max = 5.90 mg/dl) compared to cardiovertors. Nevertheless, CRP levels in patients who underwent successful cardioversion (median = 0.50, min = 0.00, max = 2.53 mg/dl) were higher compared with controls (P<0.001). Finally, CRP was higher in non-cardiovertors vs. control group, p<0.001. After multivariate adjustment left atrial size (OR, 4.4) and CRP levels (OR, 3.3) were significantly associated with successful cardioversion to sinus rhythm. CONCLUSION: These results suggest that CRP has a strong association with PAF and support the hypothesis that CRP is a potent determinant of successful cardioversion of PAF in sinus rhythm.     

Left atrial function in patients with a high C-reactive protein level and paroxysmal atrial fibrillation

OBJECTIVE: We evaluated left atrial dimensions and function in high C-reactive protein (CRP) patients with paroxysmal atrial fibrillation. BACKGROUND: In patients with increased plasma levels of CRP left atrial dysfunction may enhance the occurrence of arrhythmias. METHODS: Two-dimensional and pulsed Doppler echocardiography, were performed in 20 consecutive patients with high CRP levels and paroxysmal atrial fibrillation (group CRf) and in 20 patients with high CRP levels without this arrhythmia (group CR).Twenty normal subjects (group N) were also investigated. Groups were matched for age and gender. RESULTS: CRP was increased in the CRf (median = 1.03 mg/dl), CR (median = 0.84 mg/dl) and N groups (median = 0.23 mg/dl), (p < 0.001) for all comparisons. The CRf, CR and N groups had similar systolic and diastolic blood pressure, left ventricular mass index, left ventricular ejection fraction, isovolumic relaxation time and peak early and late transmitral Doppler flow velocities. Maximal left atrial volume was greater only in the CRf group (54.4 +/- 6.3 ml) compared with the N group (50.3 +/- 4.9 ml, p < 0.05). Left atrial volume preceding atrial contraction was similar in all groups, p=NS. Left atrial minimal volume decreased from 23.0 +/- 1.8 ml in the CRf group, to 19.8 +/- 1.8 ml in the CR group, p < 0.001 and to 18.1 +/- 2.1 ml in the N group, (p < 0.02). The passive emptying fraction of the CRf and CR groups was comparable to that of normal subjects. The CRf group had a decreased left atrial active emptying fraction (0.25 +/- 0.08) compared with the CR (0.36 +/- 0.09) and N groups (0.39 +/- 0.08), p < 0.001 for both comparisons.The reservoir fraction was decreased only in the CRf group compared to normal subjects (1.37 +/- 0.25 vs. 1.82 +/- 0.43, p < 0.001). CONCLUSIONS: These results suggest that the occurrence of paroxysmal atrial fibrillation in patients with a high CRP level is associated with enlargement of the left atrium, depression of its contractile function and is independent of left ventricular hypertrophy and function.The mechanisms linking these variables remain undefined.     

比索洛尔对持续性非瓣膜性心房颤动患者心房结构重构的影响

目的观察比索洛尔对持续性非瓣膜性心房颤动患者心房结构重构及C反应蛋白(CRP)的影响,并探讨其可能关系。方法将85例持续性非瓣膜性心房颤动患者,分为比索洛尔组(48例)和地高辛组(37例),随访观察(9.8±1.3)个月,治疗前后检测CRP和超声心动图观察左心房结构变化。结果比索洛尔组治疗后左心房内径(41.8±4.2)mmvs(39.7±5.3)mm,CRP 3.9 mg/Lvs3.5 mg/L,均较治疗前明显下降,差异有统计学意义(P<0.01),而地高辛组治疗前后左心房内径(41.8±4.6)mmvs(42.3±5.2)mm,CRP 3.8 mg/Lvs3.5 mg/L,差异无统计学意义(P>0.05)。比索洛尔组的左心房内径和CRP下降幅度与地高辛组比较,差异有统计学意义(P<0.01)。相关分析显示,左心房内径变化与CRP变化呈显著正相关(r=0.218,P=0.045)。结论比索洛尔可改善持续性非瓣膜性心房颤动患者的心房结构重构,并减轻炎性反应。     

C-reactive protein level and rate of detection of autoantibodies to beta(1)-adrenoreceptors in patients with supraventricular tachyarrhythmias

In order to assess concentration of C-reactive protein (CRP) and prevalence of autoantibodies against beta(1)-adrenoreceptors (abeta(1)-AR) in patients with cardiac supraventricular arrhythmias we studied 53 patients with arrhythmias and 20 healthy control subjects. Patients with idiopathic arrhythmias (atrial fibrillation or flutter and atrial tachycardia, n=35) comprised group I. Group II was formed of 15 patients with supraventricular arrhythmias and dilated cardiomyopathy (DCM) or chronic myocarditis. Patients of group III (n=23) had supraventricular arrhythmias and arterial hypertension (AH). CRP concentration was determined by recently developed well standardized high sensitivity method. abeta(1)-AR were detected in blood serum by direct immunoassay. Synthetic fragment containing 26 amino acids of abeta(1)-AR second loop was used as antigen. Patients with supraventricular arrhythmias and DCM or chronic myocarditis had higher median CRP (8.0 mg/1) than patients with idiopathic arrhythmias (0.78 mg/l), with supraventricular arrhythmias and AH (1.57 mg/l), or control group (0.6 mg/l). Groups I, II and III showed similar prevalence of ab1-AR (51.4, 40.0, 52.2%, respectively), that was significantly higher than in control subjects (10%) (p<0.005). These results provide evidence of the possible presence of autoimmune and/or inflammatory processes that may be involved in the genesis of supraventricular arrhythmias.     

Permanent atrial fibrillation in patients without structural heart disease is not associated with signs of infection by Chlamydia pneumoniae and Helicobacter pylori

OBJECTIVE: The objective of this study was to explore the role of Chlamydia pneumoniae and Helicobacter pylori infections in patients with idiopathic permanent atrial fibrillation. METHODS AND RESULTS: Sera from 72 patients with permanent atrial fibrillation without structural heart disease (mean age 69.6 years, 23 women) were analysed for IgG antibodies against Chlamydia pneumoniae and Helicobacter pylori and compared in a I:I age- and sex-matched case:control manner with those pooled from a healthy reference population of 72 individuals from the same geographical area. After excluding patients with other possible or definite factors known either to cause atrial fibrillation or to affect the prevalence of seropositivity to these agents, the frequency of seropositivity due to one or both of the infectious agents was compared. Serum C-reactive protein (CRP) level was assessed using immunoturbidimetry technique. Both agents were equally common in men and women. Neither seropositivity to Chlamydia pneumoniae (76% vs. 83%, patients vs. control subjests, ns) nor to Helicobacter pylori (57% contra 55%, patients vs. controls, ns) alone reached significance in the comparisons between patients with atrial fibrillation and control subjects. Serum CRP was higher in patients with AF (5.3 mg/L vs. 2.8 mg/L, P < 0.001). CONCLUSIONS: Though presence of permanent AF is associated with elevated CRP levels, this elevation is not the result of earlier infections with Chlamydia pneumoniae or Helicobacter pylori or their combination.     

Markers of inflammation before and after curative ablation of atrial flutter

BACKGROUND: Atrial arrhythmias are associated with inflammation. The cause and effect of the association are unknown. OBJECTIVE: The purpose of this study was to test the hypothesis that atrial tachyarrhythmias contribute to inflammation. METHODS: We performed a prospective observational study wherein C-reactive protein (CRP) and interleukin-6 (IL-6) levels from the femoral vein and coronary sinus (CS) were compared before curative ablation for atrial flutter (AFL; n = 59) and paroxysmal supraventricular tachycardia (SVT; n = 110). Follow-up levels were obtained at 1 and 6 months. RESULTS: Peripheral levels of both biomarkers were significantly higher in the AFL group. After multivariate adjustment, only those in the AFL group who presented in AFL or atrial fibrillation (AF) had significantly elevated CRP levels (odds ratio 1.26; P = .033). Levels of each marker were similar in the CS and peripheral blood in the SVT group; in the AFL group, both CRP and IL-6 were significantly lower in the CS than in the periphery (P = .0076 and P = .0021, respectively). CRP was significantly lower a median of 47 days after AFL ablation (from a median of 6.28 mg/L to a median of 2.92 mg/L; P = .028) and remained reduced at second follow-up. IL-6 decreased across three time points after AFL ablation (P = .002). No reduction in inflammatory biomarkers was observed after SVT ablation. CONCLUSIONS: CRP and IL-6 levels are elevated in patients presenting in AFL. Given the lower CS values in these patients, their origin appears to be systemic rather than cardiac. Because these levels significantly fall after ablation of AFL, the atrial tachyarrhythmia appears to be the cause (not the effect) of the inflammation.     

Relationship between inflammatory markers and clinical patterns of atrial fibrillation in patients with congestive heart failure

BACKGROUND: Occurence of atrial fibrillation (AF) adversely affects left atrial size and cardiac function. This arrhythmia is also associated with an increase of plasma CRP and fibrinogen concentration. It is not clear whether elevated levels of inflammatory markers in patients with congestive heart failure (CHF) are associated with AF, clinical symptoms or adverse cardiac remodelling. AIM: To investigate the association between levels of inflammatory markers and selected clinical and echocardiographic parameters as well as used treatment in the population of CHF patients with various forms of AF. METHODS: The cross-sectional study included 99 patients with CHF divided into 3 groups. Group I included patients with sinus rhythm. Group II consisted of patients admitted to hospital with AF and discharged with sinus rhythm (the category of paroxysmal and persistent AF). Group III comprised patients with permanent AF. In all patients plasma CRP and fibrinogen concentrations were measured and echocardiographic examination was carried out. Left atrial dimension (LA), ejection fraction (LVEF) and right ventricular systolic pressure (RVSP) were assessed. RESULTS: Mean CRP concentration in group III (5.83+/-5.36 mg/l) was significantly higher than in group I (p=0.001) and group II (p=0.033). In the group with permanent AF mean fibrinogen concentration was elevated to a higher level (391.0+/-77.3 mg/dl) than in group II (p=0.007) and group I (p=0.099). Mean LA and RV dimensions and RVSP in group III were significantly higher than in group I and group II. Multivariable analysis revealed that plasma CRP concentration was significantly associated with the presence of arterial hypertension (p <0.001) and LA enlargement (p=0.007). A significant association between fibrinogen level and CRP level (p=0.038), presence of permanent AF (p=0.045) and metabolic syndrome (p <0.05) was found. Values of ln CRP were significantly correlated with LA diameter (r=0.24; p=0.015). CONCLUSIONS: Increased plasma CRP level in patients with CHF were significantly associated with arterial hypertension and LA enlargement. Permanent form of AF and CRP level have been shown to be significantly associated with increased plasma fibrinogen concentration in the course of CHF.     

阵发性心房颤动患者C-反应蛋白、溶血磷脂酸变化及其临床意义

目的探讨阵发性心房颤动（房颤）患者血浆C-反应蛋白（CRP）、溶血磷脂酸（LPA）变化及其与冠状动脉粥样硬化的关系。方法对78例阵发性房颤患者（冠心病组32例、亚临床冠状动脉粥样硬化组24例、单纯房颤组22例）和30名健康人采用比浊散射法及有机溶剂抽提法，分别检测血浆CRP及LPA含量。结果冠心病组和亚临床冠状动脉粥样硬化组血浆CRP、LPA含量分别为（5．38±1．95）mg／L、（6．80±1．64）umol／L和（5．15±1．13）mg／L、（5．88±1．35）umol／L，两组比较差异无统计学意义（P均〉0．05），但均高于单纯房颤组[（1．65±0．45）mg／L、（2．18±0．33）umol／L]和正常组[（1．24±0．35）mg／L、（1．83±0．31）umol／L]（P均〈0．01）；后两组间比较差异无统计学意义（P〉0．05）。冠心病组、亚临床冠状动脉粥样硬化组CRP与LPA的相关系数分别为0．783、0．762，呈正相关（P〈0．01）。结论CRP及LPA对冠状动脉粥样硬化的发生、发展有促进作用，与阵发性房颤无明显关系。     

C-Reactive protein elevation predicts the occurrence of atrial structural remodeling in patients with paroxysmal atrial fibrillation

It has been poorly understood whether inflammation may contribute to atrial structural remodeling and increase the propensity for atrial fibrillation (AF) to persist. We investigated the relationship between C-reactive protein (CRP) elevation and the development of atrial remodeling in AF. The study population comprised 50 consecutive paroxysmal AF (PAF) patients and 50 control patients without AF. All patients underwent echocardiography, and high-sensitivity CRP was routinely measured. C-Reactive protein was significantly higher in the patients with PAF than control patients (0.231 ± 0.176mg/dl vs 0.055 ± 0.041mg/dl, P < 0.001). Other predictors of elevated CRP included left ventricular mass (P < 0.05), left ventricular end-systolic diameter (P < 0.05), and left atrial (LA) diameter (P < 0.001). In a multivariate analysis, only CRP and LA diameter were independent predictors of PAF. Elevated CRP levels correlated with LA diameter (r = 0.489, P < 0.001). Left atrial diameter was increased in PAF patients compared with control patients (P < 0.001). We found that a longer duration of AF is associated with higher CRP levels and a larger LA diameter (duration <30 days: CRP 0.166 ± 0.139mg/dl, LA diameter 38.4 ± 8.0mm; duration >30 days: CRP 0.345 ± 0.181mg/dl, LA diameter 45.6 ± 6.6mm; P < 0.001). In conclusion, longer AF duration is associated with CRP elevation and atrial structural remodeling, as approximated by larger LA diameter. However, CRP elevation, while correlating with LA diameter, was not an independent predictor of atrial structural remodeling. Thus, it remains unclear whether CRP and the inflammatory state are contributory to LA remodeling or whether LA remodeling or AF induces elevation in CRP and inflammation.