房颤患者中suPAR、MMP-2、hsCRP水平及射频消融手术预后探讨
|
摘要
研究背景
心房纤颤是临床最常见的心律失常类型,随着人口老龄化,其患病率逐年增高。心房纤颤引起患者卒中风险增加,增加总死亡率,并严重降低生活质量。近年来,射频消融手术逐渐成为治疗房颤的重要手段,由于其费用相对较高,且存在一定的风险,寻找术后复发的预测因素具有重要意义。炎症因子在房颤以及射频消融手术预后的意义也成为临床研究的热点之一。近期有研究发现高敏C反应蛋白(hsCRP)、基质金属蛋白酶-2(MMP-2)在预测术后复发方面可能具有一定意义,但也存在不一致的结果。可溶型纤维酶原激活物受体(suPAR)是近年来发现的另一种炎症因子,为纤维酶原激活物受体(uPAR)的剪切形式,有研究显示发现suPAR水平与心血管病的发病风险相关,但目前尚无研究证明其在房颤中的水平及与预后的关系。
研究目的
1.研究房颤患者与对照组之间基线水平suPAR、MMP-2、hsCRP的差异及相关因素。
2.探讨射频消融手术后炎症因子水平的变化及其意义。
3.研究房颤患者射频消融术后的复发状况及其临床因素,并探讨房颤患者中suPAR、MMP-2、hsCRP水平及其与房颤射频消融术后预后的关系。
研究方法
1.收集2011年7月至2012年2月间,于北京协和医院心内科行射频消融手术治疗的房颤患者的血液样本及临床资料,并对术后复发情况进行随访。
2.收集2012年5月间至北京协和医院体检中心体检的无心律失常人群的血样及体检资料,并在性别、年龄、高血压、糖尿病、冠心病等患病情况与房颤组相匹配。
3.酶联免疫吸附法(ELISA)测定基线血浆MMP-2及suPAR水平,放射免疫透射比浊法检测基线hsCRP水平,并研究其与房颤的相关性及影响因素。
4.研究射频消融治疗后炎症因子水平的变化。
5.探讨炎症因子与房颤射频消融治疗后复发的相关性与意义.
结果
1.持续性房颤患者中基线血浆MMP-2水平显著高于对照组,阵发性房颤患者中基线血浆suPAR水平显著低于对照组。
2.房颤患者中基线血浆suPAR水平与年龄、血清肌酐水平、基线hsCRP水平以及MMP-2水平正相关。
3. hsCRP在射频消融手术后1-4天出现显著上升,射频消融手术一周内出现早期发作的患者,其hsCRP增加程度显著高于无发作的患者,但早期发作与手术3个月之后的复发无明显相关性。
4.射频消融术后复发患者与非复发患者其基线血浆MMP-2及suPAR水平、基线血清hsCRP水平无显著差别。
5.复发患者与非复发患者比较,左房前后径、左房体积无显著差异,而左心房体积指数显著高于非复发患者。
结论
1.在本研究中,基线水平MMP-2、suPAR及hsCRP水平不能预测房颤射频消融手术治疗后的复发。
2.射频消融手术一周内出现的早期发作与炎症水平升高相关。
3.与左房前后径以及左房体积相比,左房体积指数增加与房颤复发的相关性更加密切。
Background
Atrial fibrillation (AF) is the most common arrhythmia in clinical work. And its prevalence is increasing as the population ages. AF confers higher risk of stroke, increases the total mortality, and decreases the quality of life significantly. In recent years, radiofrequency ablation procedure has become an important means for the treatment of AF. Because of the relative higher expense and risk of the procedure, it is important to find the predictors of recurrence after the procedure. The impact of inflammation factors in AF and its value in the prediction of recurrence after RFCA have become the focus of recent clinical research. Recently it is reported that high sensitivity C-reactive protein (hsCRP) and matrix metalloproteinases are valuable in the recurrence prediction, but controversy still exists. Soluble urokinase-type plasminogen activator receptor (suPAR) is another inflammation factor that is the cleavage form of the urokinase-type plasminogen activator receptor (uPAR). Recent research shows that suPAR is related to the risk of cardiovascular disease, but the level of suPAR in AF patients and its relationship with AF recurrence are still unknown.
Objectives
1. To research the difference of the baseline suPAR, MMP-2, hsCRP levels between AF patients and the control group.
2. To research the change of the inflammation factor levels after the RFCA procedure.
3. To research the recurrence of AF after RFCA and the relative clinical factors, and to research the relationship between the levels of suPAR, MMP-2and hsCRP and the recurrence.
Methods
1. The AF patients that underwent RFCA in the cardiology department of Peking Union medical college hospital between July,2011and February,2012were included in this research. The clinical data and blood samples at baseline were collected. The recurrence in the follow-up was recorded.
2. The subjects of the control group are selected from the people that underwent phisycal examination at the PUMCH physical examination center in May,2012. The age, gender, and history of hypertension, diabetes mellitus, CVD and smoking were matched with the AF group. Anyone with AF history or other kinds of arrhythmia was concluded.
3. The plasma levels of MMP-2and suPAR were determined with double-antibody sandwich enzyme-linked immunosorbent assay (ELISA). The serum levels of hsCRP were determined with immune transmission turbidity method. The baseline levels of inflammation factors were detected and the relationships with AF were analyzed.
4. The levels of inflammation factors at baseline and after the RFCA procedure were determined.
5. The relativity and value of inflammation factors in the recurrence of AF after RFCA were analyzed.
Result
1. The baseline level of plasma MMP-2in the persistent AF patients is significantly higher than the control group, and the baseline level of plasma suPAR in the paroxysmal AF patients is lower than the control group.
2. The plasma level of suPAR in AF patients is positively related to age and the levels of serum creatine (SCr), hsCRP and MMP-2.
3. The level of hsCRP increases greatly at1-4days after ablation. The amplitude in the patients with early recurrence of AF in one week after ablation is significantly higher than the patients without recurrence. However the early recurrence shows no relationship with the recurrence during follow-up.
4. There are no significant differences between the levels of baseline MMP-2, suPAR and hsCRP in the recurrence gtoup and non-recurrence group.
5. There are no significant differences between the left atrial dimensions and left atrial volumes of the recurrence group and non-recurrence group, the left atrial volume index (LAVI) of the recurrence group is significantly higher than the non-recurrence group.
Conclusions
1. In this research the baseline MMP-2, suPAR and hsCRP levels cannot predict the AF recurrence after RFCA.
2. The early AF recurrence in one week after RFCA is related the increase of inflammation level.
3. The increase of LAVI is better related to the risk of AF recurrence after RFCA than left atrial dimension and volume.
心房纤颤是临床最常见的心律失常类型,随着人口老龄化,其患病率逐年增高。心房纤颤引起患者卒中风险增加,增加总死亡率,并严重降低生活质量。近年来,射频消融手术逐渐成为治疗房颤的重要手段,由于其费用相对较高,且存在一定的风险,寻找术后复发的预测因素具有重要意义。炎症因子在房颤以及射频消融手术预后的意义也成为临床研究的热点之一。近期有研究发现高敏C反应蛋白(hsCRP)、基质金属蛋白酶-2(MMP-2)在预测术后复发方面可能具有一定意义,但也存在不一致的结果。可溶型纤维酶原激活物受体(suPAR)是近年来发现的另一种炎症因子,为纤维酶原激活物受体(uPAR)的剪切形式,有研究显示发现suPAR水平与心血管病的发病风险相关,但目前尚无研究证明其在房颤中的水平及与预后的关系。
研究目的
1.研究房颤患者与对照组之间基线水平suPAR、MMP-2、hsCRP的差异及相关因素。
2.探讨射频消融手术后炎症因子水平的变化及其意义。
3.研究房颤患者射频消融术后的复发状况及其临床因素,并探讨房颤患者中suPAR、MMP-2、hsCRP水平及其与房颤射频消融术后预后的关系。
研究方法
1.收集2011年7月至2012年2月间,于北京协和医院心内科行射频消融手术治疗的房颤患者的血液样本及临床资料,并对术后复发情况进行随访。
2.收集2012年5月间至北京协和医院体检中心体检的无心律失常人群的血样及体检资料,并在性别、年龄、高血压、糖尿病、冠心病等患病情况与房颤组相匹配。
3.酶联免疫吸附法(ELISA)测定基线血浆MMP-2及suPAR水平,放射免疫透射比浊法检测基线hsCRP水平,并研究其与房颤的相关性及影响因素。
4.研究射频消融治疗后炎症因子水平的变化。
5.探讨炎症因子与房颤射频消融治疗后复发的相关性与意义.
结果
1.持续性房颤患者中基线血浆MMP-2水平显著高于对照组,阵发性房颤患者中基线血浆suPAR水平显著低于对照组。
2.房颤患者中基线血浆suPAR水平与年龄、血清肌酐水平、基线hsCRP水平以及MMP-2水平正相关。
3. hsCRP在射频消融手术后1-4天出现显著上升,射频消融手术一周内出现早期发作的患者,其hsCRP增加程度显著高于无发作的患者,但早期发作与手术3个月之后的复发无明显相关性。
4.射频消融术后复发患者与非复发患者其基线血浆MMP-2及suPAR水平、基线血清hsCRP水平无显著差别。
5.复发患者与非复发患者比较,左房前后径、左房体积无显著差异,而左心房体积指数显著高于非复发患者。
结论
1.在本研究中,基线水平MMP-2、suPAR及hsCRP水平不能预测房颤射频消融手术治疗后的复发。
2.射频消融手术一周内出现的早期发作与炎症水平升高相关。
3.与左房前后径以及左房体积相比,左房体积指数增加与房颤复发的相关性更加密切。
Background
Atrial fibrillation (AF) is the most common arrhythmia in clinical work. And its prevalence is increasing as the population ages. AF confers higher risk of stroke, increases the total mortality, and decreases the quality of life significantly. In recent years, radiofrequency ablation procedure has become an important means for the treatment of AF. Because of the relative higher expense and risk of the procedure, it is important to find the predictors of recurrence after the procedure. The impact of inflammation factors in AF and its value in the prediction of recurrence after RFCA have become the focus of recent clinical research. Recently it is reported that high sensitivity C-reactive protein (hsCRP) and matrix metalloproteinases are valuable in the recurrence prediction, but controversy still exists. Soluble urokinase-type plasminogen activator receptor (suPAR) is another inflammation factor that is the cleavage form of the urokinase-type plasminogen activator receptor (uPAR). Recent research shows that suPAR is related to the risk of cardiovascular disease, but the level of suPAR in AF patients and its relationship with AF recurrence are still unknown.
Objectives
1. To research the difference of the baseline suPAR, MMP-2, hsCRP levels between AF patients and the control group.
2. To research the change of the inflammation factor levels after the RFCA procedure.
3. To research the recurrence of AF after RFCA and the relative clinical factors, and to research the relationship between the levels of suPAR, MMP-2and hsCRP and the recurrence.
Methods
1. The AF patients that underwent RFCA in the cardiology department of Peking Union medical college hospital between July,2011and February,2012were included in this research. The clinical data and blood samples at baseline were collected. The recurrence in the follow-up was recorded.
2. The subjects of the control group are selected from the people that underwent phisycal examination at the PUMCH physical examination center in May,2012. The age, gender, and history of hypertension, diabetes mellitus, CVD and smoking were matched with the AF group. Anyone with AF history or other kinds of arrhythmia was concluded.
3. The plasma levels of MMP-2and suPAR were determined with double-antibody sandwich enzyme-linked immunosorbent assay (ELISA). The serum levels of hsCRP were determined with immune transmission turbidity method. The baseline levels of inflammation factors were detected and the relationships with AF were analyzed.
4. The levels of inflammation factors at baseline and after the RFCA procedure were determined.
5. The relativity and value of inflammation factors in the recurrence of AF after RFCA were analyzed.
Result
1. The baseline level of plasma MMP-2in the persistent AF patients is significantly higher than the control group, and the baseline level of plasma suPAR in the paroxysmal AF patients is lower than the control group.
2. The plasma level of suPAR in AF patients is positively related to age and the levels of serum creatine (SCr), hsCRP and MMP-2.
3. The level of hsCRP increases greatly at1-4days after ablation. The amplitude in the patients with early recurrence of AF in one week after ablation is significantly higher than the patients without recurrence. However the early recurrence shows no relationship with the recurrence during follow-up.
4. There are no significant differences between the levels of baseline MMP-2, suPAR and hsCRP in the recurrence gtoup and non-recurrence group.
5. There are no significant differences between the left atrial dimensions and left atrial volumes of the recurrence group and non-recurrence group, the left atrial volume index (LAVI) of the recurrence group is significantly higher than the non-recurrence group.
Conclusions
1. In this research the baseline MMP-2, suPAR and hsCRP levels cannot predict the AF recurrence after RFCA.
2. The early AF recurrence in one week after RFCA is related the increase of inflammation level.
3. The increase of LAVI is better related to the risk of AF recurrence after RFCA than left atrial dimension and volume.
引文
[1]. Zhang, S., Atrial fibrillation in mainland China:epidemiology and current management. Heart,2009. 95(13):p.1052-5.
[2].Camm, A.J., et al., Guidelines for the management of atrial fibrillation:the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Europace,2010.12(10):p. 1360-420.
[3].Haissaguerre, M., et al., Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med,1998.339(10):p.659-66.
[4]. Cox, J.L., et al., The surgical treatment of atrial fibrillation. II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg,1991.101(3):p.406-26.
[5]. Wijffels, M.C., et al., Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation,1995.92(7):p.1954-68.
[6]. Chung, M.K., et al., C-reactive protein elevation in patients with atrial arrhythmias:inflammatory mechanisms and persistence of atrial fibrillation. Circulation,2001.104(24):p.2886-91.
[7]. Rizos, I., et al., Interleukin-2 serum levels variations in recent onset atrial fibrillation are related with cardioversion outcome. Cytokine,2007.40(3):p.157-64.
[8].Luan, Y., et al., Interleukin-18 among atrial fibrillation patients in the absence of structural heart disease. Europace,2010.12(12):p.1713-8.
[9]. Conway, D.S., et al., Relationship of interleukin-6 and C-reactive protein to the prothrombotic state in chronic atrial fibrillation. J Am Coll Cardiol,2004.43(11):p.2075-82.
[10]. Kallergis, E.M., et al., Extracellular matrix alterations in patients with paroxysmal and persistent atrial fibrillation:biochemical assessment of collagen type-I turnover. J Am Coll Cardiol,2008.52(3):p.211-5.
[11].Kalogeropoulos, A.S., et al., Novel association patterns of cardiac remodeling markers in patients with essential hypertension and atrial fibrillation. BMC Cardiovasc Disord,2011.11:p.77.
[12]. Spinale, F.G., Myocardial matrix remodeling and the matrix metalloproteinases:influence on cardiac form and function. Physiol Rev,2007.87(4):p.1285-342.
[13]. Chen, C.L., et al., Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metalloproteinases in rapid atrial pacing-induced atrial fibrillation. J Mol Cell Cardiol,2008.45(6):p. 742-53.
[14].Stockand, J.D. and J.G. Meszaros, Aldosterone stimulates proliferation of cardiac fibroblasts by activating Ki-RasA and MAPK1/2 signaling. Am J Physiol Heart Circ Physiol,2003.284(1):p. H176-84.
[15]. Alfonso-Jaume, M.A., et al., Cardiac ischemia-reperfusion injury induces matrix metalloproteinase-2 expression through the AP-1 components FosB and JunB. Am J Physiol Heart Circ Physiol,2006.291(4): p. H1838-46.
[16]. Mountain, D.J., et al., Interleukin-1beta increases expression and activity of matrix metalloproteinase-2 in cardiac microvascular endothelial cells:role of PKCalpha/betal and MAPKs. Am J Physiol Cell Physiol,2007.292(2):p. C867-75.
[17]. Bergman, M.R., et al., A functional activating protein 1 (AP-1) site regulates matrix metalloproteinase-2 (MMP-2) transcription by cardiac cells through interactions with JunB-Fral and JunB-FosB heterodimers. Biochem J,2003.369(Pt 3):p.485-96.
[18]. Wary, K.K., et al., A requirement for caveolin-1 and associated kinase Fyn in integrin signaling and anchorage-dependent cell growth. Cell,1998.94(5):p.625-34.
[19].Ossowski, L. and J.A. Aguirre-Ghiso, Urokinase receptor and integrin partnership:coordination of signaling for cell adhesion, migration and growth. Curr Opin Cell Biol,2000.12(5):p.613-20.
[20]. He, Y., et al., Interaction between cancer cells and stromal fibroblasts is required for activation of the uPAR-uPA-MMP-2 cascade in pancreatic cancer metastasis. Clin Cancer Res,2007.13(11):p.3115-24.
[21], Pliyev, B.K., Activated human neutrophils rapidly release the chemotactically active D2D3 form of the urokinase-type plasminogen activator receptor (uPAR/CD87). Mol Cell Biochem,2009.321(1-2):p. 111-22.
[22]. Donadello, K., et al., suPAR as a prognostic biomarker in sepsis. BMC Med,2012.10:p.2.
[23]. Persson, M., et al., Soluble urokinase plasminogen activator receptor in plasma is associated with incidence of CVD. Results from the Malmo Diet and Cancer Study. Atherosclerosis,2012.220(2):p. 502-5.
[24]. Liu, J., et al., High-sensitivity C-reactive protein as a predictor of atrial fibrillation recurrence after primary circumferential pulmonary vein isolation. Pacing Clin Electrophysiol,2011.34(4):p.398-406.
[25].Okumura, Y., et al., Impact of biomarkers of inflammation and extracellular matrix turnover on the outcome of atrial fibrillation ablation:importance of matrix metalloproteinase-2 as a predictor of atrial fibrillation recurrence. J Cardiovasc Electrophysiol,2011.22(9):p.987-93.
[1]. Nabauer, M., et al., The Registry of the German Competence NETwork on Atrial Fibrillation:patient characteristics and initial management. Europace,2009.11(4):p.423-34.
[2]. Guglin, M., et al., Relation of Obesity to Recurrence Rate and Burden of Atrial Fibrillation. The American Journal of Cardiology,2011.107(4):p.579-582.
[3]. Wijffels, M.C., et al., Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation,1995.92(7):p.1954-68.
[1]. Kalogeropoulos, A.S., et al., Novel association patterns of cardiac remodeling markers in patients with essential hypertension and atrial fibrillation. BMC Cardiovasc Disord,2011.11:p.77.
[2]. Xu, J., et al., Atrial extracellular matrix remodeling and the maintenance of atrial fibrillation. Circulation,2004.109(3):p.363-8.
[3]. Spinale, F.G., Myocardial matrix remodeling and the matrix metalloproteinases:influence on cardiac form and function. Physiol Rev,2007.87(4):p.1285-342.
[4]. Frustaci, A., et al., Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation,1997.96(4):p.1180-4.
[5]. Corradi, D., et al., Myocyte changes and their left atrial distribution in patients with chronic atrial fibrillation related to mitral valve disease. Hum Pathol,2005.36(10):p.1080-9.
[6]. Ossowski, L. and J.A. Aguirre-Ghiso, Urokinase receptor and integrin partnership:coordination of signaling for cell adhesion, migration and growth. Curr Opin Cell Biol,2000.12(5):p.613-20.
[7]. Pliyev, B.K. and M.Y. Menshikov, Release of the soluble urokinase-type plasminogen activator receptor (suPAR) by activated neutrophils in rheumatoid arthritis. Inflammation,2010.33(1):p.1-9.
[8]. Andersen, O., et al., Soluble urokinase plasminogen activator receptor is a marker of dysmetabolism in HIV-infected patients receiving highly active antiretroviral therapy. J Med Virol,2008.80(2):p. 209-16.
[9]. Slot, O., et al., Soluble urokinase plasminogen activator receptor in plasma of patients with inflammatory rheumatic disorders:increased concentrations in rheumatoid arthritis. Ann Rheum Dis,1999. 58(8):p.488-92.
[10].Fazioli, F., et al., A urokinase-sensitive region of the human urokinase receptor is responsible for its chemotactic activity. EMBO J,1997.16(24):p.7279-86.
[11]. Huttunen, R., et al., Plasma level of soluble urokinase-type plasminogen activator receptor as a predictor of disease severity and case fatality in patients with bacteraemia:a prospective cohort study. J Intern Med,2011.270(1):p.32-40.
[12].Persson, M., et al., Soluble urokinase plasminogen activator receptor in plasma is associated with incidence of CVD. Results from the Malmo Diet and Cancer Study. Atherosclerosis,2012.220(2):p. 502-5.
[13]. Pliyev, B.K., Activated human neutrophils rapidly release the chemotactically active D2D3 form of the urokinase-type plasminogen activator receptor (uPAR/CD87). Mol Cell Biochem,2009.321(1-2):p. 111-22.
[14]. Ostrowski, S.R., et al., Interleukin-6 infusion during human endotoxaemia inhibits in vitro release of the urokinase receptor from peripheral blood mononuclear cells. Scand J Immunol,2005.61(2):p. 197-206.
[15].Lyngbaek, S., et al., CRP and suPAR are differently related to anthropometry and subclinical organ damage. Int J Cardiol,2012.
[16].Sehestedt, T., et al., Soluble urokinase plasminogen activator receptor is associated with subclinical organ damage and cardiovascular events. Atherosclerosis,2011.216(1):p.237-43.
[17].Eugen-Olsen, J., et al., Circulating soluble urokinase plasminogen activator receptor predicts cancer, cardiovascular disease, diabetes and mortality in the general population. J Intern Med,2010.268(3):p. 296-308.
[18].Pawlak, K., D. Pawlak and M. Mysliwiec, Urokinase-type plasminogen activator and metalloproteinase-2 are independently related to the carotid atherosclerosis in haemodialysis patients. Thromb Res,2008.121(4):p.543-8.
[1]. Stein, A., et al., Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization. Europace,2008.10(4):p.444-9.
[2]. Hsieh, M.H., et al., Alterations of heart rate variability after radiofrequency catheter ablation of focal atrial fibrillation originating from pulmonary veins. Circulation,1999.100(22):p.2237-43.
[3]. McCabe, J.M., et al., Protracted CRP elevation after atrial fibrillation ablation. Pacing Clin Electrophysiol,2008.31(9):p.1146-51.
[4]. Richter, B., et al., Markers of oxidative stress after ablation of atrial fibrillation are associated with inflammation, delivered radiofrequency energy and early recurrence of atrial fibrillation. Clin Res Cardiol, 2012.101(3):p.217-25.
[5]. Stein, A., et al., Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization. Europace,2008.10(4):p.444-9.
[1]. Calkins, H., et al.,2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation:recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design. Europace,2012.14(4):p. 528-606.
[2]. Lang, R.M., et al., Recommendations for chamber quantification:a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr,2005.18(12):p.1440-63.
[3]. Andrade, J.G., et al., Early recurrence of atrial tachyarrhythmias following radiofrequency catheter ablation of atrial fibrillation. Pacing Clin Electrophysiol,2012.35(1):p.106-16.
[4].McCabe, J.M., et al., Protracted CRP elevation after atrial fibrillation ablation. Pacing Clin Electrophysiol,2008.31(9):p.1146-51.
[5]. Stein, A., et al., Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization. Europace,2008.10(4):p.444-9.
[6]. Richter, B., et al., Markers of oxidative stress after ablation of atrial fibrillation are associated with inflammation, delivered radiofrequency energy and early recurrence of atrial fibrillation. Clin Res Cardiol, 2012.101(3):p.217-25.
[7]. Hsieh, M.H., et al., Alterations of heart rate variability after radiofrequency catheter ablation of focal atrial fibrillation originating from pulmonary veins. Circulation,1999.100(22):p.2237-43.
[8].Koyama, T., et al., Comparison of characteristics and significance of immediate versus early versus no recurrence of atrial fibrillation after catheter ablation. Am J Cardiol,2009.103(9):p.1249-54.
[9]. Koyama, T., et al., Prevention of atrial fibrillation recurrence with corticosteroids after radiofrequency catheter ablation:a randomized controlled trial. J Am Coll Cardiol,2010.56(18):p.1463-72.
[10].Themistoclakis, S., et al., Clinical predictors and relationship between early and late atrial tachyarrhythmias after pulmonary vein antrum isolation. Heart Rhythm,2008.5(5):p.679-85.
[11]. Liu, J., et al., High-sensitivity C-reactive protein as a predictor of atrial fibrillation recurrence after primary circumferential pulmonary vein isolation. Pacing Clin Electrophysiol,2011.34(4):p.398-406.
[12].Letsas, K.P., et al., Pre-ablative predictors of atrial fibrillation recurrence following pulmonary vein isolation:the potential role of inflammation. Europace,2009.11(2):p.158-63.
[13].Okumura, Y., et al., Impact of biomarkers of inflammation and extracellular matrix turnover on the outcome of atrial fibrillation ablation:importance of matrix metalloproteinase-2 as a predictor of atrial fibrillation recurrence. J Cardiovasc Electrophysiol,2011.22(9):p.987-93.
[14].Eugen-Olsen, J., et al., Circulating soluble urokinase plasminogen activator receptor predicts cancer, cardiovascular disease, diabetes and mortality in the general population. J Intern Med,2010.268(3):p. 296-308.
[15]. Sehestedt, T., et al., Soluble urokinase plasminogen activator receptor is associated with subclinical organ damage and cardiovascular events. Atherosclerosis,2011.216(1):p.237-43.
[16].Lyngbaek, S., et al., CRP and suPAR are differently related to anthropometry and subclinical organ damage. Int J Cardiol,2012.
[17].Pawlak, K., D. Pawlak and M. Mysliwiec, Urokinase-type plasminogen activator and metalloproteinase-2 are independently related to the carotid atherosclerosis in haemodialysis patients. Thromb Res,2008.121(4):p.543-8.
[18]. Donadello, K., et al., suPAR as a prognostic biomarker in sepsis. BMC Med,2012.10:p.2.
[19]. Koch, A., et al., Circulating soluble urokinase plasminogen activator receptor is stably elevated during the first week of treatment in the intensive care unit and predicts mortality in critically ill patients. Crit Care,2011.15(1):p. R63.
[20]. Vergara, G.R. and N.F. Marrouche, Tailored management of atrial fibrillation using a LGE-MRI based model:from the clinic to the electrophysiology laboratory. J Cardiovasc Electrophysiol,2011. 22(4):p.481-7.
[21]. Badger, T.J., et al., Temporal left atrial lesion formation after ablation of atrial fibrillation. Heart Rhythm,2009.6(2):p.161-8.
[22]. Wylie, J.J., et al., Left atrial function and scar after catheter ablation of atrial fibrillation. Heart Rhythm,2008.5(5):p.656-62.
[23]. Marsan, N.A., et al., Comparison of left atrial volumes and function by real-time three-dimensional echocardiography in patients having catheter ablation for atrial fibrillation with persistence of sinus rhythm versus recurrent atrial fibrillation three months later. Am J Cardiol,2008.102(7):p.847-53.
[24]. Tops, L.F., et al., Left atrial strain predicts reverse remodeling after catheter ablation for atrial fibrillation. J Am Coll Cardiol,2011.57(3):p.324-31.
1 Shu Zhang, Atrial fibrillation in mainland China:epidemiology and current management. Heart 2009 95:1052-1055
2 Haissaguerre, M., et al., Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med,1998.339(10):p.659-66.
3 Mina K. Chung, David O. Martin, et al. C-Reactive Protein Elevation in Patients With Atrial Arrhythmias Inflammatory Mechanisms and Persistence of Atrial Fibrillation. Circulation. 2001;104:2886-2891.
4 Bruins P, te Velthuis H, Yazdanbakhsh AP, et al. Activation of the complement system during and after cardiopulmonary bypass surgery:postsurgery activation involves C-reactive protein and is associated with postoperative arrhythmia. Circulation.1997;96:3542-3548.
5 Abdelhadi RH, Gurm HS, Van Wagoner DR, Chung MK. Relation of an exaggerated rise in white blood cells after coronary bypass or cardiac valve surgery to development of atrial fibrillation postoperatively. Am J Cardiol 2004;93:1176-8.
6 Gaudino M, Andreotti F, et al., The-174G/C interleukin-6 polymorphism influences postoperative interleukin-6 levels and postoperative atrial fibrillation. Is atrial fibrillation an inflammatory complication? Circulation 2003 Sep 9;108 Suppl 1:11195-9.
7 Prasongsukarn, K. et al. (2005) The effects of steroids on the occurrence of postoperative atrial fibrillation after coronary artery bypass grafting surgery:a prospective randomized trial. J. Thorac. Cardiovasc. Surg.130,93-98
8 Ronnier J. Aviles, David O. Martin, et al., Inflammation as a Risk Factor for Atrial Fibrillation, Circulation.2003;108:3006-3010
9 Stavroula N. Psychari, Thomas S. Apostolou, et al., Relation of Elevated C-Reactive Protein and Interleukin-6 Levels to Left Atrial Size and Duration of Episodes in Patients With Atrial Fibrillation. Am J Cardiol 2005;95:764-767
10 Ying Luan, Yuanyuan Guo, et al., Interleukin-18 among atrial fibrillation patients in the absence of structural heart disease. Europace (2010) 12,1713-1718.
11 Leftheriotis, D.I. et al. The predictive value of inflammatory and oxidative markers following the successful cardioversion of persistent lone atrial fibrillation. Int. J. Cardiol.2009,361-369
12 Frustaci, A. et al. Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation 1997,1180-1184
13 Mihm, M.J. et al. Impaired myofibrillar energetics and oxidative injury during human atrial fibrillation. Circulation 2001,174-180
14 Carnes CA et al. Ascorbate attenuates atrial pacing-induced peroxynitrite formation and electrical remodeling and decreases the incidence of postoperative atrial fibrillation. Circ Res 2011, (89): E32-E38
15 Ide, T. et al. (2000) Direct evidence for increased hydroxyl radicals originating from superoxide in the failing myocardium. Circ. Res.2000, (86):152-157
16 Chen, C.L. et al. Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metalloproteinases in rapid atrial pacinginduced atrial fibrillation. J. Mol. Cell. Cardiol.2008, (45), 742-753
17 Saba, S. et al. Atrial contractile dysfunction, fibrosis, and arrhythmias in a mouse model of cardiomyopathy secondary to cardiac-specific overexpression of tumor necrosis factor-a. Am. J. Physiol. Heart Circ. Physiol.2005, H1456-H1467
18 Corradi D et al., Myocyte changes and their left atrial distribution in patients with chronic atrial fibrillation related to mitral valve disease. Hum Pathol 2005 (36):1080-1089
19 Eleftherios M. Kallergis, Emmanuel G Manios, Extracellular Matrix Alterations in Patients With Paroxysmal and Persistent Atrial Fibrillation, Journal of the American College of Cardiology,2008(52): 211-215
20 Kalogeropoulos et al., Novel association patterns of cardiac remodeling markers in patients with essential hypertension and atrial fibrillation, BMC Cardiovascular Disorders 2011,11:77-86
21 Burstein B, Nattel S Atrial fibrosis:mechanisms and clinical relevance in atrial fibrillation. J Am Coll Cardiol,2008, (51):802-809
22 Goette A, Stack T, Rocken C, et al. Increased expression of extracellular signal-regulated kinase and angiotensin-converting enzyme in human atria during atrial fibrillation. J Am Coll Cardiol, 2000;35:1669-77.
23 Sugden PH, Clerk A. Stress-responsivemitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen-activated protein kinases) in the myocardium. Circ Res.1998; 83:345-352
24 Khan R, Sheppard R. Fibrosis in heart disease:understanding the role of transforming growth factor-1 in cardiomyopathy, valvular disease and arrhythmia. Immunology 2006;118:10-24.
25 Stockand JD, Meszaros JG. Aldosterone stimulates proliferation of cardiac fibroblasts by activating Ki-RasA and MAPK1/2 signaling. Am J Physiol Heart Circ Physiol 2003;284:H176-84.
26 Rude MK, Duhaney T-AS, Kuster GM, et al. Aldosterone stimulates matrix metalloproteinases and reactive oxygen species in adult rat ventricular cardiomyocytes. Hypertension 2005;46:555-61.
27 Rudolph V, Andrie'RP, Rudolph TK, et al. Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation. Nat Med.2010; 16:470-474.
28 Chen CL, Huang SK, Lin JL, et al. Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metal loproteinases in rapid atrial pacing-induced atrial fibrillation. J Mol Cell Cardiol. 2008;45:742-753.
29 Galis ZS, Asanuma K, Godin D, Meng X. N-acetyl-cysteine decreases the matrix-degrading capacity of macrophage-derived foam cells:new target for antioxidant therapy? Circulation 1998; 97:2445-53.
30 Fu X, Kassim SY, Parks WC, Heinecke JW. Hypochlorous acid oxygenates the cysteine switch domain of pro-matrilysin (MMP-7). A mechanism for matrix metalloproteinase activation and atherosclerotic plaque rupture by myeloperoxidase. J Biol Chem 2001;276:41279-87.
31 Rajagopalan S, Meng XP, Ramasamy S, Harrison DG, Galis ZS. Reactive oxygen species produced by macrophage-derived foam cells regulate the activity of vascular matrix metalloproteinases in vitro. Implications for atherosclerotic plaque stability. J Clin Invest 1996; 98:2572-9.
32 Eiichi Watanabea, Tomoharu Arakawa, High-sensitivity C-reactive protein is predictive of successful cardioversion for atrial fibrillation and maintenance of sinus rhythm after conversion. International Journal of Cardiology 108 (2006) 346-353.
33 Tong Liu, Guangping Li, et al., Association Between C-Reactive Protein and Recurrence of Atrial Fibrillation After Successful Electrical Cardioversion. J Am Coll Cardiol 2007;49:1642-8.
34 Fujiki A, Sakamoto T, et al., Relation of interleukin-6 and C-reactive protein levels to sinus maintenance after pharmacological cardioversion in persistent atrial fibrillation. J Cardiovasc Pharmacol.2007 Sep;50(3):264-6.
35 Rizos I, Tsiodras S, et al., Interleukin-2 serum levels variations in recent onset atrial fibrillation are related with cardioversion outcome. Cytokine.2007 Dec;40(3):157-64. Epub 2007 Oct 17.
36 JUN LIU, PI-HUA FAN, et al., High-Sensitivity C-Reactive Protein as a Predictor of Atrial Fibrillation Recurrence after Primary Circumferential Pulmonary Vein Isolation. PACE 2011; 34:398-406.
37 Takashi Koyama, Yukio Sekiguchi, et al., Comparison of Characteristics and Significance of Immediate Versus Early Versus No Recurrence of Atrial Fibrillation After Catheter Ablation. Am J Cardiol 2009;103:1249-1254
38 Bernhard Richter, Marianne Gwechenberger, et al., Markers of oxidative stress after ablation of atrial fibrillation are associated with inflammation, delivered radiofrequency energy and early recurrence of atrial fibrillation. Clin Res Cardiol.2012 Mar;101(3):217-25.
39 Yasuo Okumura, Ichiro Watanabe, et al., Impact of Biomarkers of Inflammation and Extracellular Matrix Turnover on the Outcome of Atrial Fibrillation Ablation:Importance of Matrix Metalloproteinase-2 as a Predictor of Atrial Fibrillation Recurrence. J Cardiovasc Electrophysiol, Vol. 22, pp.987-993, September 2011.
40 Laurens F. Tops, Victoria Delgado, et al., Left Atrial Strain Predicts Reverse Remodeling After Catheter Ablation for Atrial Fibrillation. J Am Coll Cardiol 2011;57:324-31.
41 Christoph Hammerstingl, et al., Left Atrial Deformation Imaging with Ultrasound Based Two-Dimensional Speckle-Tracking Predicts the Rate of Recurrence of Paroxysmal and Persistent Atrial Fibrillation After Successful Ablation Procedures. J Cardiovasc Electrophysiol, Vol., pp.1-9.
42 Andreas Stein, Gabi Wessling, Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization. Europace (2008) 10,444-449.
43 Badger TJ, Oakes RS, et al., Temporal left atrial lesion formation after ablation of atrial fibrillation. Heart Rhythm 2009;6:161-168.
44 Tops LF, Bax JJ, Zeppenfeld K, Jongbloed MR, van der Wall EE, chalij MJ. Effect of radiofrequency catheter ablation for atrial ibrillation on left atrial cavity size. Am J Cardiol 2006;97:1220-2.
45 Marsan NA, Tops LF, Holman ER, et al. Comparison of left atrial vlumes and function by real-time three-dimensional echocardiography in patients having catheter ablation for atrial fibrillation with persistence of sinus rhythm versus recurrent atrial fibrillation three months later. Am J Cardiol 2008;102:847-53.
46 Laurens F. Tops, Victoria Delgado, et al., Left Atrial Strain Predicts Reverse Remodeling After Catheter Ablation for Atrial Fibrillation. (J Am Coll Cardiol 2011;57:324-31).
[2].Camm, A.J., et al., Guidelines for the management of atrial fibrillation:the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Europace,2010.12(10):p. 1360-420.
[3].Haissaguerre, M., et al., Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med,1998.339(10):p.659-66.
[4]. Cox, J.L., et al., The surgical treatment of atrial fibrillation. II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg,1991.101(3):p.406-26.
[5]. Wijffels, M.C., et al., Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation,1995.92(7):p.1954-68.
[6]. Chung, M.K., et al., C-reactive protein elevation in patients with atrial arrhythmias:inflammatory mechanisms and persistence of atrial fibrillation. Circulation,2001.104(24):p.2886-91.
[7]. Rizos, I., et al., Interleukin-2 serum levels variations in recent onset atrial fibrillation are related with cardioversion outcome. Cytokine,2007.40(3):p.157-64.
[8].Luan, Y., et al., Interleukin-18 among atrial fibrillation patients in the absence of structural heart disease. Europace,2010.12(12):p.1713-8.
[9]. Conway, D.S., et al., Relationship of interleukin-6 and C-reactive protein to the prothrombotic state in chronic atrial fibrillation. J Am Coll Cardiol,2004.43(11):p.2075-82.
[10]. Kallergis, E.M., et al., Extracellular matrix alterations in patients with paroxysmal and persistent atrial fibrillation:biochemical assessment of collagen type-I turnover. J Am Coll Cardiol,2008.52(3):p.211-5.
[11].Kalogeropoulos, A.S., et al., Novel association patterns of cardiac remodeling markers in patients with essential hypertension and atrial fibrillation. BMC Cardiovasc Disord,2011.11:p.77.
[12]. Spinale, F.G., Myocardial matrix remodeling and the matrix metalloproteinases:influence on cardiac form and function. Physiol Rev,2007.87(4):p.1285-342.
[13]. Chen, C.L., et al., Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metalloproteinases in rapid atrial pacing-induced atrial fibrillation. J Mol Cell Cardiol,2008.45(6):p. 742-53.
[14].Stockand, J.D. and J.G. Meszaros, Aldosterone stimulates proliferation of cardiac fibroblasts by activating Ki-RasA and MAPK1/2 signaling. Am J Physiol Heart Circ Physiol,2003.284(1):p. H176-84.
[15]. Alfonso-Jaume, M.A., et al., Cardiac ischemia-reperfusion injury induces matrix metalloproteinase-2 expression through the AP-1 components FosB and JunB. Am J Physiol Heart Circ Physiol,2006.291(4): p. H1838-46.
[16]. Mountain, D.J., et al., Interleukin-1beta increases expression and activity of matrix metalloproteinase-2 in cardiac microvascular endothelial cells:role of PKCalpha/betal and MAPKs. Am J Physiol Cell Physiol,2007.292(2):p. C867-75.
[17]. Bergman, M.R., et al., A functional activating protein 1 (AP-1) site regulates matrix metalloproteinase-2 (MMP-2) transcription by cardiac cells through interactions with JunB-Fral and JunB-FosB heterodimers. Biochem J,2003.369(Pt 3):p.485-96.
[18]. Wary, K.K., et al., A requirement for caveolin-1 and associated kinase Fyn in integrin signaling and anchorage-dependent cell growth. Cell,1998.94(5):p.625-34.
[19].Ossowski, L. and J.A. Aguirre-Ghiso, Urokinase receptor and integrin partnership:coordination of signaling for cell adhesion, migration and growth. Curr Opin Cell Biol,2000.12(5):p.613-20.
[20]. He, Y., et al., Interaction between cancer cells and stromal fibroblasts is required for activation of the uPAR-uPA-MMP-2 cascade in pancreatic cancer metastasis. Clin Cancer Res,2007.13(11):p.3115-24.
[21], Pliyev, B.K., Activated human neutrophils rapidly release the chemotactically active D2D3 form of the urokinase-type plasminogen activator receptor (uPAR/CD87). Mol Cell Biochem,2009.321(1-2):p. 111-22.
[22]. Donadello, K., et al., suPAR as a prognostic biomarker in sepsis. BMC Med,2012.10:p.2.
[23]. Persson, M., et al., Soluble urokinase plasminogen activator receptor in plasma is associated with incidence of CVD. Results from the Malmo Diet and Cancer Study. Atherosclerosis,2012.220(2):p. 502-5.
[24]. Liu, J., et al., High-sensitivity C-reactive protein as a predictor of atrial fibrillation recurrence after primary circumferential pulmonary vein isolation. Pacing Clin Electrophysiol,2011.34(4):p.398-406.
[25].Okumura, Y., et al., Impact of biomarkers of inflammation and extracellular matrix turnover on the outcome of atrial fibrillation ablation:importance of matrix metalloproteinase-2 as a predictor of atrial fibrillation recurrence. J Cardiovasc Electrophysiol,2011.22(9):p.987-93.
[1]. Nabauer, M., et al., The Registry of the German Competence NETwork on Atrial Fibrillation:patient characteristics and initial management. Europace,2009.11(4):p.423-34.
[2]. Guglin, M., et al., Relation of Obesity to Recurrence Rate and Burden of Atrial Fibrillation. The American Journal of Cardiology,2011.107(4):p.579-582.
[3]. Wijffels, M.C., et al., Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation,1995.92(7):p.1954-68.
[1]. Kalogeropoulos, A.S., et al., Novel association patterns of cardiac remodeling markers in patients with essential hypertension and atrial fibrillation. BMC Cardiovasc Disord,2011.11:p.77.
[2]. Xu, J., et al., Atrial extracellular matrix remodeling and the maintenance of atrial fibrillation. Circulation,2004.109(3):p.363-8.
[3]. Spinale, F.G., Myocardial matrix remodeling and the matrix metalloproteinases:influence on cardiac form and function. Physiol Rev,2007.87(4):p.1285-342.
[4]. Frustaci, A., et al., Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation,1997.96(4):p.1180-4.
[5]. Corradi, D., et al., Myocyte changes and their left atrial distribution in patients with chronic atrial fibrillation related to mitral valve disease. Hum Pathol,2005.36(10):p.1080-9.
[6]. Ossowski, L. and J.A. Aguirre-Ghiso, Urokinase receptor and integrin partnership:coordination of signaling for cell adhesion, migration and growth. Curr Opin Cell Biol,2000.12(5):p.613-20.
[7]. Pliyev, B.K. and M.Y. Menshikov, Release of the soluble urokinase-type plasminogen activator receptor (suPAR) by activated neutrophils in rheumatoid arthritis. Inflammation,2010.33(1):p.1-9.
[8]. Andersen, O., et al., Soluble urokinase plasminogen activator receptor is a marker of dysmetabolism in HIV-infected patients receiving highly active antiretroviral therapy. J Med Virol,2008.80(2):p. 209-16.
[9]. Slot, O., et al., Soluble urokinase plasminogen activator receptor in plasma of patients with inflammatory rheumatic disorders:increased concentrations in rheumatoid arthritis. Ann Rheum Dis,1999. 58(8):p.488-92.
[10].Fazioli, F., et al., A urokinase-sensitive region of the human urokinase receptor is responsible for its chemotactic activity. EMBO J,1997.16(24):p.7279-86.
[11]. Huttunen, R., et al., Plasma level of soluble urokinase-type plasminogen activator receptor as a predictor of disease severity and case fatality in patients with bacteraemia:a prospective cohort study. J Intern Med,2011.270(1):p.32-40.
[12].Persson, M., et al., Soluble urokinase plasminogen activator receptor in plasma is associated with incidence of CVD. Results from the Malmo Diet and Cancer Study. Atherosclerosis,2012.220(2):p. 502-5.
[13]. Pliyev, B.K., Activated human neutrophils rapidly release the chemotactically active D2D3 form of the urokinase-type plasminogen activator receptor (uPAR/CD87). Mol Cell Biochem,2009.321(1-2):p. 111-22.
[14]. Ostrowski, S.R., et al., Interleukin-6 infusion during human endotoxaemia inhibits in vitro release of the urokinase receptor from peripheral blood mononuclear cells. Scand J Immunol,2005.61(2):p. 197-206.
[15].Lyngbaek, S., et al., CRP and suPAR are differently related to anthropometry and subclinical organ damage. Int J Cardiol,2012.
[16].Sehestedt, T., et al., Soluble urokinase plasminogen activator receptor is associated with subclinical organ damage and cardiovascular events. Atherosclerosis,2011.216(1):p.237-43.
[17].Eugen-Olsen, J., et al., Circulating soluble urokinase plasminogen activator receptor predicts cancer, cardiovascular disease, diabetes and mortality in the general population. J Intern Med,2010.268(3):p. 296-308.
[18].Pawlak, K., D. Pawlak and M. Mysliwiec, Urokinase-type plasminogen activator and metalloproteinase-2 are independently related to the carotid atherosclerosis in haemodialysis patients. Thromb Res,2008.121(4):p.543-8.
[1]. Stein, A., et al., Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization. Europace,2008.10(4):p.444-9.
[2]. Hsieh, M.H., et al., Alterations of heart rate variability after radiofrequency catheter ablation of focal atrial fibrillation originating from pulmonary veins. Circulation,1999.100(22):p.2237-43.
[3]. McCabe, J.M., et al., Protracted CRP elevation after atrial fibrillation ablation. Pacing Clin Electrophysiol,2008.31(9):p.1146-51.
[4]. Richter, B., et al., Markers of oxidative stress after ablation of atrial fibrillation are associated with inflammation, delivered radiofrequency energy and early recurrence of atrial fibrillation. Clin Res Cardiol, 2012.101(3):p.217-25.
[5]. Stein, A., et al., Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization. Europace,2008.10(4):p.444-9.
[1]. Calkins, H., et al.,2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation:recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design. Europace,2012.14(4):p. 528-606.
[2]. Lang, R.M., et al., Recommendations for chamber quantification:a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr,2005.18(12):p.1440-63.
[3]. Andrade, J.G., et al., Early recurrence of atrial tachyarrhythmias following radiofrequency catheter ablation of atrial fibrillation. Pacing Clin Electrophysiol,2012.35(1):p.106-16.
[4].McCabe, J.M., et al., Protracted CRP elevation after atrial fibrillation ablation. Pacing Clin Electrophysiol,2008.31(9):p.1146-51.
[5]. Stein, A., et al., Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization. Europace,2008.10(4):p.444-9.
[6]. Richter, B., et al., Markers of oxidative stress after ablation of atrial fibrillation are associated with inflammation, delivered radiofrequency energy and early recurrence of atrial fibrillation. Clin Res Cardiol, 2012.101(3):p.217-25.
[7]. Hsieh, M.H., et al., Alterations of heart rate variability after radiofrequency catheter ablation of focal atrial fibrillation originating from pulmonary veins. Circulation,1999.100(22):p.2237-43.
[8].Koyama, T., et al., Comparison of characteristics and significance of immediate versus early versus no recurrence of atrial fibrillation after catheter ablation. Am J Cardiol,2009.103(9):p.1249-54.
[9]. Koyama, T., et al., Prevention of atrial fibrillation recurrence with corticosteroids after radiofrequency catheter ablation:a randomized controlled trial. J Am Coll Cardiol,2010.56(18):p.1463-72.
[10].Themistoclakis, S., et al., Clinical predictors and relationship between early and late atrial tachyarrhythmias after pulmonary vein antrum isolation. Heart Rhythm,2008.5(5):p.679-85.
[11]. Liu, J., et al., High-sensitivity C-reactive protein as a predictor of atrial fibrillation recurrence after primary circumferential pulmonary vein isolation. Pacing Clin Electrophysiol,2011.34(4):p.398-406.
[12].Letsas, K.P., et al., Pre-ablative predictors of atrial fibrillation recurrence following pulmonary vein isolation:the potential role of inflammation. Europace,2009.11(2):p.158-63.
[13].Okumura, Y., et al., Impact of biomarkers of inflammation and extracellular matrix turnover on the outcome of atrial fibrillation ablation:importance of matrix metalloproteinase-2 as a predictor of atrial fibrillation recurrence. J Cardiovasc Electrophysiol,2011.22(9):p.987-93.
[14].Eugen-Olsen, J., et al., Circulating soluble urokinase plasminogen activator receptor predicts cancer, cardiovascular disease, diabetes and mortality in the general population. J Intern Med,2010.268(3):p. 296-308.
[15]. Sehestedt, T., et al., Soluble urokinase plasminogen activator receptor is associated with subclinical organ damage and cardiovascular events. Atherosclerosis,2011.216(1):p.237-43.
[16].Lyngbaek, S., et al., CRP and suPAR are differently related to anthropometry and subclinical organ damage. Int J Cardiol,2012.
[17].Pawlak, K., D. Pawlak and M. Mysliwiec, Urokinase-type plasminogen activator and metalloproteinase-2 are independently related to the carotid atherosclerosis in haemodialysis patients. Thromb Res,2008.121(4):p.543-8.
[18]. Donadello, K., et al., suPAR as a prognostic biomarker in sepsis. BMC Med,2012.10:p.2.
[19]. Koch, A., et al., Circulating soluble urokinase plasminogen activator receptor is stably elevated during the first week of treatment in the intensive care unit and predicts mortality in critically ill patients. Crit Care,2011.15(1):p. R63.
[20]. Vergara, G.R. and N.F. Marrouche, Tailored management of atrial fibrillation using a LGE-MRI based model:from the clinic to the electrophysiology laboratory. J Cardiovasc Electrophysiol,2011. 22(4):p.481-7.
[21]. Badger, T.J., et al., Temporal left atrial lesion formation after ablation of atrial fibrillation. Heart Rhythm,2009.6(2):p.161-8.
[22]. Wylie, J.J., et al., Left atrial function and scar after catheter ablation of atrial fibrillation. Heart Rhythm,2008.5(5):p.656-62.
[23]. Marsan, N.A., et al., Comparison of left atrial volumes and function by real-time three-dimensional echocardiography in patients having catheter ablation for atrial fibrillation with persistence of sinus rhythm versus recurrent atrial fibrillation three months later. Am J Cardiol,2008.102(7):p.847-53.
[24]. Tops, L.F., et al., Left atrial strain predicts reverse remodeling after catheter ablation for atrial fibrillation. J Am Coll Cardiol,2011.57(3):p.324-31.
1 Shu Zhang, Atrial fibrillation in mainland China:epidemiology and current management. Heart 2009 95:1052-1055
2 Haissaguerre, M., et al., Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med,1998.339(10):p.659-66.
3 Mina K. Chung, David O. Martin, et al. C-Reactive Protein Elevation in Patients With Atrial Arrhythmias Inflammatory Mechanisms and Persistence of Atrial Fibrillation. Circulation. 2001;104:2886-2891.
4 Bruins P, te Velthuis H, Yazdanbakhsh AP, et al. Activation of the complement system during and after cardiopulmonary bypass surgery:postsurgery activation involves C-reactive protein and is associated with postoperative arrhythmia. Circulation.1997;96:3542-3548.
5 Abdelhadi RH, Gurm HS, Van Wagoner DR, Chung MK. Relation of an exaggerated rise in white blood cells after coronary bypass or cardiac valve surgery to development of atrial fibrillation postoperatively. Am J Cardiol 2004;93:1176-8.
6 Gaudino M, Andreotti F, et al., The-174G/C interleukin-6 polymorphism influences postoperative interleukin-6 levels and postoperative atrial fibrillation. Is atrial fibrillation an inflammatory complication? Circulation 2003 Sep 9;108 Suppl 1:11195-9.
7 Prasongsukarn, K. et al. (2005) The effects of steroids on the occurrence of postoperative atrial fibrillation after coronary artery bypass grafting surgery:a prospective randomized trial. J. Thorac. Cardiovasc. Surg.130,93-98
8 Ronnier J. Aviles, David O. Martin, et al., Inflammation as a Risk Factor for Atrial Fibrillation, Circulation.2003;108:3006-3010
9 Stavroula N. Psychari, Thomas S. Apostolou, et al., Relation of Elevated C-Reactive Protein and Interleukin-6 Levels to Left Atrial Size and Duration of Episodes in Patients With Atrial Fibrillation. Am J Cardiol 2005;95:764-767
10 Ying Luan, Yuanyuan Guo, et al., Interleukin-18 among atrial fibrillation patients in the absence of structural heart disease. Europace (2010) 12,1713-1718.
11 Leftheriotis, D.I. et al. The predictive value of inflammatory and oxidative markers following the successful cardioversion of persistent lone atrial fibrillation. Int. J. Cardiol.2009,361-369
12 Frustaci, A. et al. Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation 1997,1180-1184
13 Mihm, M.J. et al. Impaired myofibrillar energetics and oxidative injury during human atrial fibrillation. Circulation 2001,174-180
14 Carnes CA et al. Ascorbate attenuates atrial pacing-induced peroxynitrite formation and electrical remodeling and decreases the incidence of postoperative atrial fibrillation. Circ Res 2011, (89): E32-E38
15 Ide, T. et al. (2000) Direct evidence for increased hydroxyl radicals originating from superoxide in the failing myocardium. Circ. Res.2000, (86):152-157
16 Chen, C.L. et al. Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metalloproteinases in rapid atrial pacinginduced atrial fibrillation. J. Mol. Cell. Cardiol.2008, (45), 742-753
17 Saba, S. et al. Atrial contractile dysfunction, fibrosis, and arrhythmias in a mouse model of cardiomyopathy secondary to cardiac-specific overexpression of tumor necrosis factor-a. Am. J. Physiol. Heart Circ. Physiol.2005, H1456-H1467
18 Corradi D et al., Myocyte changes and their left atrial distribution in patients with chronic atrial fibrillation related to mitral valve disease. Hum Pathol 2005 (36):1080-1089
19 Eleftherios M. Kallergis, Emmanuel G Manios, Extracellular Matrix Alterations in Patients With Paroxysmal and Persistent Atrial Fibrillation, Journal of the American College of Cardiology,2008(52): 211-215
20 Kalogeropoulos et al., Novel association patterns of cardiac remodeling markers in patients with essential hypertension and atrial fibrillation, BMC Cardiovascular Disorders 2011,11:77-86
21 Burstein B, Nattel S Atrial fibrosis:mechanisms and clinical relevance in atrial fibrillation. J Am Coll Cardiol,2008, (51):802-809
22 Goette A, Stack T, Rocken C, et al. Increased expression of extracellular signal-regulated kinase and angiotensin-converting enzyme in human atria during atrial fibrillation. J Am Coll Cardiol, 2000;35:1669-77.
23 Sugden PH, Clerk A. Stress-responsivemitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen-activated protein kinases) in the myocardium. Circ Res.1998; 83:345-352
24 Khan R, Sheppard R. Fibrosis in heart disease:understanding the role of transforming growth factor-1 in cardiomyopathy, valvular disease and arrhythmia. Immunology 2006;118:10-24.
25 Stockand JD, Meszaros JG. Aldosterone stimulates proliferation of cardiac fibroblasts by activating Ki-RasA and MAPK1/2 signaling. Am J Physiol Heart Circ Physiol 2003;284:H176-84.
26 Rude MK, Duhaney T-AS, Kuster GM, et al. Aldosterone stimulates matrix metalloproteinases and reactive oxygen species in adult rat ventricular cardiomyocytes. Hypertension 2005;46:555-61.
27 Rudolph V, Andrie'RP, Rudolph TK, et al. Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation. Nat Med.2010; 16:470-474.
28 Chen CL, Huang SK, Lin JL, et al. Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metal loproteinases in rapid atrial pacing-induced atrial fibrillation. J Mol Cell Cardiol. 2008;45:742-753.
29 Galis ZS, Asanuma K, Godin D, Meng X. N-acetyl-cysteine decreases the matrix-degrading capacity of macrophage-derived foam cells:new target for antioxidant therapy? Circulation 1998; 97:2445-53.
30 Fu X, Kassim SY, Parks WC, Heinecke JW. Hypochlorous acid oxygenates the cysteine switch domain of pro-matrilysin (MMP-7). A mechanism for matrix metalloproteinase activation and atherosclerotic plaque rupture by myeloperoxidase. J Biol Chem 2001;276:41279-87.
31 Rajagopalan S, Meng XP, Ramasamy S, Harrison DG, Galis ZS. Reactive oxygen species produced by macrophage-derived foam cells regulate the activity of vascular matrix metalloproteinases in vitro. Implications for atherosclerotic plaque stability. J Clin Invest 1996; 98:2572-9.
32 Eiichi Watanabea, Tomoharu Arakawa, High-sensitivity C-reactive protein is predictive of successful cardioversion for atrial fibrillation and maintenance of sinus rhythm after conversion. International Journal of Cardiology 108 (2006) 346-353.
33 Tong Liu, Guangping Li, et al., Association Between C-Reactive Protein and Recurrence of Atrial Fibrillation After Successful Electrical Cardioversion. J Am Coll Cardiol 2007;49:1642-8.
34 Fujiki A, Sakamoto T, et al., Relation of interleukin-6 and C-reactive protein levels to sinus maintenance after pharmacological cardioversion in persistent atrial fibrillation. J Cardiovasc Pharmacol.2007 Sep;50(3):264-6.
35 Rizos I, Tsiodras S, et al., Interleukin-2 serum levels variations in recent onset atrial fibrillation are related with cardioversion outcome. Cytokine.2007 Dec;40(3):157-64. Epub 2007 Oct 17.
36 JUN LIU, PI-HUA FAN, et al., High-Sensitivity C-Reactive Protein as a Predictor of Atrial Fibrillation Recurrence after Primary Circumferential Pulmonary Vein Isolation. PACE 2011; 34:398-406.
37 Takashi Koyama, Yukio Sekiguchi, et al., Comparison of Characteristics and Significance of Immediate Versus Early Versus No Recurrence of Atrial Fibrillation After Catheter Ablation. Am J Cardiol 2009;103:1249-1254
38 Bernhard Richter, Marianne Gwechenberger, et al., Markers of oxidative stress after ablation of atrial fibrillation are associated with inflammation, delivered radiofrequency energy and early recurrence of atrial fibrillation. Clin Res Cardiol.2012 Mar;101(3):217-25.
39 Yasuo Okumura, Ichiro Watanabe, et al., Impact of Biomarkers of Inflammation and Extracellular Matrix Turnover on the Outcome of Atrial Fibrillation Ablation:Importance of Matrix Metalloproteinase-2 as a Predictor of Atrial Fibrillation Recurrence. J Cardiovasc Electrophysiol, Vol. 22, pp.987-993, September 2011.
40 Laurens F. Tops, Victoria Delgado, et al., Left Atrial Strain Predicts Reverse Remodeling After Catheter Ablation for Atrial Fibrillation. J Am Coll Cardiol 2011;57:324-31.
41 Christoph Hammerstingl, et al., Left Atrial Deformation Imaging with Ultrasound Based Two-Dimensional Speckle-Tracking Predicts the Rate of Recurrence of Paroxysmal and Persistent Atrial Fibrillation After Successful Ablation Procedures. J Cardiovasc Electrophysiol, Vol., pp.1-9.
42 Andreas Stein, Gabi Wessling, Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization. Europace (2008) 10,444-449.
43 Badger TJ, Oakes RS, et al., Temporal left atrial lesion formation after ablation of atrial fibrillation. Heart Rhythm 2009;6:161-168.
44 Tops LF, Bax JJ, Zeppenfeld K, Jongbloed MR, van der Wall EE, chalij MJ. Effect of radiofrequency catheter ablation for atrial ibrillation on left atrial cavity size. Am J Cardiol 2006;97:1220-2.
45 Marsan NA, Tops LF, Holman ER, et al. Comparison of left atrial vlumes and function by real-time three-dimensional echocardiography in patients having catheter ablation for atrial fibrillation with persistence of sinus rhythm versus recurrent atrial fibrillation three months later. Am J Cardiol 2008;102:847-53.
46 Laurens F. Tops, Victoria Delgado, et al., Left Atrial Strain Predicts Reverse Remodeling After Catheter Ablation for Atrial Fibrillation. (J Am Coll Cardiol 2011;57:324-31).
© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号 地址：北京市海淀区学院路29号 邮编：100083 电话：办公室：(+86 10)66554848；文献借阅、咨询服务、科技查新：66554700 |