房间隔缺损封堵术患者血浆F1+2水平及血小板CD62P、CD41a表达的研究
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摘要
目的:观察先天性心脏病房间隔缺损(ASD)患者植入封堵器后血浆凝血酶原片段1+2(F1+2)及血小板P选择素(CD62P)、血小板膜糖蛋白Ⅱb/Ⅲa受体(CD41a)的变化及其意义。
方法:选择40例成功以Amplatzer进行房缺封堵术的病人,用EHSA法及流式细胞术(FCM)分别测定他们术前、术后1-2d、术后1m、术后3m F1+2水平及血小板CD62P、CD41a的表达。
结果:(1)ASD患者术后1-2d较术前组的F1+2水平明显增高,由0.96±1.19nmol/L增高到术后1-2d的1.43±1.49nmol/L,术后1月降低明显,术后3m时恢复到接近术前的0.98±1.10nmol/L。(2)ASD患者术后1-2d、术后1m、术后3m的CD62P及CD41a表达均较术前明显下降,由(8.22±2.11)%及(79.36±14.15)%降至术后3月时的(4.41±1.11)%及(54.88±11.62)%。(3)ASD病人在术后1-2d及术后1m、术后3m右室内径(RVD)均较术前缩小,而左室舒末径(LVDd)较术前增大。(4)ASD患者术前RVD与术前血小板CD62P、CD41a呈正相关;ASD大小与术前血小板CD62P呈正相关,与术前CD41a无相关关系。
结论:ASD封堵术后凝血功能一过性增强,1月后开始明显下降,3月后大致恢复术前水平;而血小板活性在术后却降低;房缺封堵术后患者的RVD、LVDd呈现出逐渐恢复正常大小的趋势;术前血小板活化程度与RVD及房缺大小呈正相关。
Objective To investigate the changes of the levels of prothrombin fragment 1 + 2(F1 + 2),P-selectin(CD62P)and platelet glycoproteinⅡb/Ⅲa receptor(CD41a)among patients following transcatheter ASD closure.
Methods Forty consecutive patients who underwent successful transcatheter closure of an ASD defect with the Amplatzer septal occluder were prospectively studied.Measurements of the F1 + 2 levels and the percentage of activated platelets(evaluated by CD62P and CD41a) expression detected by flow cytometry)were taken at baseline just before the procedure as baseline,and at 1,30 and 90 days following device implantation.We therefore evaluated the presence,degree and timing of the activation of the coagulation and platelet systems following transcatheter closure of ASDs.
Result(1)F1 + 2 levels increased from 0.96±1.19 nmol/1 at baseline to a maximal value of 1.43±1.49 nmol/1 at 1 days,gradually returning to the baseline levels at 90 days(0.98±1.10 nmol/1)(p＜0.05).(2)CD62P and CD41a decreased from(8.22±2.11)%and(79.36±14.15)%to(4.41±1.11)% and(54.88±11.62)%at 90 days.(3)RVD of patient with ASD dicreased after operation 1-2 day,1 month and 3 month,while LVDd increased at the same time.(4)Before the operation,CD62P and CD41a were both positive correlated with RVD;The size of ASD was positive correlated with CD62P, but not with CD41a.
Conclusions Transcatheter closure of ASDs with the Amplatzer septal occluder was associated with significant increase coagulation activation and a significant decrease in the platelet system activation.The patient's RVD,and LVDd tended to be normal following transcatheter closure of ASDs.Before the procedure,the degree of platelet activation, RVD and the size of Atrial septal defects were positive correlated.
方法:选择40例成功以Amplatzer进行房缺封堵术的病人,用EHSA法及流式细胞术(FCM)分别测定他们术前、术后1-2d、术后1m、术后3m F1+2水平及血小板CD62P、CD41a的表达。
结果:(1)ASD患者术后1-2d较术前组的F1+2水平明显增高,由0.96±1.19nmol/L增高到术后1-2d的1.43±1.49nmol/L,术后1月降低明显,术后3m时恢复到接近术前的0.98±1.10nmol/L。(2)ASD患者术后1-2d、术后1m、术后3m的CD62P及CD41a表达均较术前明显下降,由(8.22±2.11)%及(79.36±14.15)%降至术后3月时的(4.41±1.11)%及(54.88±11.62)%。(3)ASD病人在术后1-2d及术后1m、术后3m右室内径(RVD)均较术前缩小,而左室舒末径(LVDd)较术前增大。(4)ASD患者术前RVD与术前血小板CD62P、CD41a呈正相关;ASD大小与术前血小板CD62P呈正相关,与术前CD41a无相关关系。
结论:ASD封堵术后凝血功能一过性增强,1月后开始明显下降,3月后大致恢复术前水平;而血小板活性在术后却降低;房缺封堵术后患者的RVD、LVDd呈现出逐渐恢复正常大小的趋势;术前血小板活化程度与RVD及房缺大小呈正相关。
Objective To investigate the changes of the levels of prothrombin fragment 1 + 2(F1 + 2),P-selectin(CD62P)and platelet glycoproteinⅡb/Ⅲa receptor(CD41a)among patients following transcatheter ASD closure.
Methods Forty consecutive patients who underwent successful transcatheter closure of an ASD defect with the Amplatzer septal occluder were prospectively studied.Measurements of the F1 + 2 levels and the percentage of activated platelets(evaluated by CD62P and CD41a) expression detected by flow cytometry)were taken at baseline just before the procedure as baseline,and at 1,30 and 90 days following device implantation.We therefore evaluated the presence,degree and timing of the activation of the coagulation and platelet systems following transcatheter closure of ASDs.
Result(1)F1 + 2 levels increased from 0.96±1.19 nmol/1 at baseline to a maximal value of 1.43±1.49 nmol/1 at 1 days,gradually returning to the baseline levels at 90 days(0.98±1.10 nmol/1)(p＜0.05).(2)CD62P and CD41a decreased from(8.22±2.11)%and(79.36±14.15)%to(4.41±1.11)% and(54.88±11.62)%at 90 days.(3)RVD of patient with ASD dicreased after operation 1-2 day,1 month and 3 month,while LVDd increased at the same time.(4)Before the operation,CD62P and CD41a were both positive correlated with RVD;The size of ASD was positive correlated with CD62P, but not with CD41a.
Conclusions Transcatheter closure of ASDs with the Amplatzer septal occluder was associated with significant increase coagulation activation and a significant decrease in the platelet system activation.The patient's RVD,and LVDd tended to be normal following transcatheter closure of ASDs.Before the procedure,the degree of platelet activation, RVD and the size of Atrial septal defects were positive correlated.
引文
[1]Jeffrey W,Delaney,MD,Jennifer S.Li,MD,et al.Major Complications Associated with Transcatheter Atrial Septal Occluder Implantation:A Review of the Medical Literature and the Manufacturer and User Facility Device Experience(MAUDE)Database.Congenit Heart Dis,2007,2:256-264.
[2]Josep Rode's-Cabaua,Andre's Palaciosb,Carles Palaciob,et al.Assessment of the markers of platelet and coagulation activation following transcatheter closure of atrial septal defects.International Journal of Cardiology,2005,98:107-112.
[3]E Mackie,M Dawson,A McKenzie,et al.Platelet activation is increased in patients with atrial septal defects suitable for transcatheter closure with the amplatzer device[J].Heart.London:May 2003.Vol.89,pg.A12,ProQuest Medical Library.
[4]Rubin LJ.Diagnosis and management of pulmonary arterial hypertension:ACCP evidence-based clinical practice guidelines[J].Chest,2004,126(1 suppl):7S-10S.
[5]孔祥清主编.先天性心脏病介入治疗[M].第1版.江苏:江苏科学技术出版社,2003:2-6.
[6]中华儿科杂志编辑委员会,中华医学杂志英文版编辑委员会。先天性心脏病经导管介入治疗指南。中华儿科杂志,2004,423:234-239.
[7]Undar L,Akkoc N,Alakavuklar MN,et al.Flow cytometric analysis of circadian changes in platelet activation using anti-GMP-140 monoclonl antibody[J].Chronobiol Int,1999,16(3):335.
[8]彭作辉.弥散性血管内凝血前期诊断[J].中国实用内科杂志,2000,6(6): 338-342.
[9] Teitel JM, Bauer KA, Lau HK, et al.. Studies of the prothrombin activation pathway utilizing radioimmunoassays for the F2/prothrombin fragment1+2 fragment and trombin/antithrombin complex. Blood 1982;59:1086-97.
[10]SundaramM,Qi Y, Shriver Z, et al. Rational design of low molecular weight heparms with improved in vivo activity[J]. PNAS,2003, 100 (2) : 651-656.
[11] Lock JE, Rome JJ, Davis R, et al. Transcatheter closure of atrial septal defects— experimental studies. Circulation,1989,79:1091-1099.
[12] Sharafuddin MJA, Gu X, Titus JL, et al.Trans venous closure of secundum atrial septal defects.Preliminary results with a new self-expanding nitinol prosthesis in a swine model. Circulation, 1997, 95: 2162-2168.
[13] Cenni E, Ciapetti G, Cervellati M, et al. Activation of the plasma coagulation system induced by some biomaterials. J Biomed Mater Res,1996,31:145-148.
[14] Cenni E, Arciola CR, Ciapetti G, et al. Platelet and coagulation factor variations induced in vitro by polyethylene terephthalate (Dacron) coated with pyrolytic carbonl. Biomaterials, 1995,16:973 -976.
[15] Makkar R, Litvack F, Eigler N, et al. Effects of GP IIb/IIIa receptor monoclonal antibody (7E3), heparin, and aspirin in an ex vivo canine arteriovenous shunt model of stent thrombosis. Circulation,1997,95: 1015-21.
[16]Merten M , Thiagarajan P. P-selectin in arterial thrombosis[J]. Z Kardiol,2004,93(11):855-863.
[17]郭楠,鲁静朝,崔炜等.血小板活化标志物的研究进展.[J].临床荟萃,2006,21(23):1748-1749.
[18]AD Michelson.Flow cytometry:A clinical test of platelet function[J].Blood,1996,87(12):4925.
[19]王建中,王淑娟.当前流式细胞分析的发展趋势[J].中华医学检验杂志2002,25:5-6.
[20]徐杰,阮长耿,王爱青等.应用流式细胞仪检测血小板膜糖蛋白[J].中国小儿血液杂志,1997,20:216-219
[21]Olgun N,Uysal KM,Irken G,et al.Platelet activation in congenital heart disease[J].Acta Paediatr Jpn,1997,39(9):566
[22]杨杰,闫梅,杨兴季等.血小板活化状态在先天性心脏病中的作用.山东大学学报(医学版)2004,42(1):54-59
[23]俸勇强,伍伟锋.成人先天性心脏病介入封堵前后神经内分泌功能的变化。中国心血管病研究杂志,2006,3(4):175-177.
[24]Pernerstorfer T,Eichler HG,Stohlawetz P,et al.Effects of heparin and aspirin on circulating P-selectin,E-selectin and von Willebrand factor levels in healthy men.Atherosclerosis 2001;155:389-93.
[25]Chronos NA,Wilson DJ,Janes SL et al.Aspirin does not affect the flow cytometryc detection of fibrinogen binding to,or release of alpha-granules or lysosomes from,human platelets.Clin Sci(Lond)1994;87:575-80.
[26]Pernerstorfer T,Stohlawetz P,Stummvoll G,et al.Low-dose aspirin does not lower in vivo platelet activation in healthy smokers.Br J Haematol 1998;102:1229-31.
[27]Klinkhardt U,Bauersachs R,Adams J,et al.Clopidogrel but not aspirin reduces P-selectin expression and formation of platelet-leuko-cyte aggregates in patients with atherosclerotic vascular disease.Clin Pharmacol Ther 2003;73:232-41.
[28]Veldtman GR,Razack B,Siu S,et al.Right ventricular form and function after percutaneous atrial septal defect device closure[J].J Am Coll Cardiol,2001,37(8):2108-2113.
[29]吴栋梁,张玉顺,张军等。成人房间隔缺损封堵术后左心大小和功能的变化[J]。心脏杂志,2002,14(4):324
[1] Lock JE, Rome JJ, Davis R, et al. Transcatheter closure of atrial septal defects—experimental studies. Circulation,1989,79(5):1091-1099.
[2] Sharafuddin MJA, Gu X, Titus JL, Urness M, Cervera-Ceballos JJ,Amplatz K. Transvenous closure of secundum atrial septal defects.Preliminary results with a new self-expanding nitinol prosthesis in a swine model. Circulation, 1998, 95(8): 2162-2168.
[3] Josep Rode's-Cabaua,Andre's Palaciosb, Carles Palaciob, et al. Assessment of the markers of platelet and coagulation activation following transcatheter closure of atrial septal defects. Int J Cardiol, 2005, 98(1): 107- 112.
[4] Cenni E, Ciapetti G, Cervellati M, et al. Activation of the plasma coagulation system induced by some biomaterials. J Biomed Mater Res, 1996,31(1):145-148.
[5] Cenni E, Arciola CR, Ciapetti G, et al. Platelet and coagulation factor variations induced in vitro by polyethylene terephthalate (Dacron) coated with pyrolytic carbonl. Biomaterials,1995,16(13):973 -976.
[6] Makkar R, Litvack F, Eigler N, et al. Effects of GP IIb/IIIa receptor monoclonal antibody (7E3), heparin, and aspirin in an ex vivo canine arteriovenous shunt model of stent thrombosis. Circulation,1997,95(4): 1015-21.
[7] La Rosee K, Krause D, Becker M, et al. Transcatheter closure of atrialseptal defect in adults: practicability and safety of four different occluder systems used in 102 patients. German Medical Weekly,2001,126(38):1030-1036.
[8] Lambert V, Losay J, Piot JD, et al. Late complications of percutaneous closure of atrial septal defects with the Sideris occluder. Cardiovascular Diseases Periodicals, 1997, 90(2):245-251
[9] Krumsdorf U, Ostermayer S, Billinger K, Trepels T, Zadan E,Horvath K, et al.Incidence and clinical course of thrombus formationon atrial septal defect and patient foramen ovale closure devices in 1,000 consecutive patients. J Am Coll Cardiol,2004,43(2):302-309.
[10] Jeffrey W. Delaney, MD, Jennifer S. Li, MD, and John F. Rhodes, MD.Major Complications Associated with Transcatheter Atrial Septal Occluder Implantation: A Review of the Medical Literature and the Manufacturer and User Facility Device Experience (MAUDE) Database. Congenit Heart Dis,2007,2(4):256-264.
[11] Braun M, Fassbender D, Schoen S, et al. Transcatheter closure of patent foramen ovale in patients with cerebral ischemia. J Am Coll Cardiol,2002,39(12):2019- 2025.
[12] Krieg P, Lapp H, Pethig K, Gummert JF, Bossert T. Removal of a left atrial throm bus adherent to a patent foramen ovale occluder. Ann Thorac Surg,2007, 83(4): 1539-1541.
[13] La Rosee K, Deutsch HJ, Schnabel P, et al. Thrombus formation after transcatheter closure of atrial septal defect. Am J Cardiol, 1999,84(3): 356-359.
[14] Acar P, Aggoun Y, Abdel-Massih T, et al. Images in cardiology: Thrombus after transcatheter closure of ASD with an Amplatzer septal occluder assessed by three dimensional echocardio-graphic reconstruction. Heart, 2002 Jul,88(1):52.
[15] Moore JW, Levi DS. Transcatheter closure of atrial shunts Focus on a lingering issue. J Am Coll Cardiol, 2004, 43(2):310-312.
[16]Kawalsky D,Feldman M.Embolic stroke due to a left atrial thrombus two years after placement of an atrial septal defect closure device.Am J Cardiol,2006,98(9):1294-1296.
[17]Sievert H,Babic UU,Hausdorf G,et al.Transcatheter closure of atrial septal defect and patent foramen ovale with the ASDOS device(a multi-institutional European trial).Am J Cardiol 1998,82(11):1405-1413.
[18]Brandt RR,Neumann T,Neuzner J,et al.Transcatheter closure of atrial septal defect and patent foramen ovale in adult patients using the Amplatzer occlusion device:no evidence for thrombus deposition with antiplatelet agents.J Am Soc Echocardiogr,2002,15(10 pt1):1094-1098.
[19]Chessa M,Carminati M,Butera G,et al.Early and late complications associated with trans-catheter occlusion of secundum atrial septal defect.J Am Coll Cardiol,2002,39(6):1061-1065.
[20]中华儿科杂志编辑委员会,中华医学杂志英文版编辑委员会。先天性心脏病经导管介入治疗指南。中华儿科杂志,2004,42(3):234-239.
[21]Cetta F,Arruda MJ,Graham LC.Large left atrial thrombus formation despite warfarin therapy after device closure of a patent foramen ovale.Catheter Cardiovasc Interv,2003,59(3):396-398.
[2]Josep Rode's-Cabaua,Andre's Palaciosb,Carles Palaciob,et al.Assessment of the markers of platelet and coagulation activation following transcatheter closure of atrial septal defects.International Journal of Cardiology,2005,98:107-112.
[3]E Mackie,M Dawson,A McKenzie,et al.Platelet activation is increased in patients with atrial septal defects suitable for transcatheter closure with the amplatzer device[J].Heart.London:May 2003.Vol.89,pg.A12,ProQuest Medical Library.
[4]Rubin LJ.Diagnosis and management of pulmonary arterial hypertension:ACCP evidence-based clinical practice guidelines[J].Chest,2004,126(1 suppl):7S-10S.
[5]孔祥清主编.先天性心脏病介入治疗[M].第1版.江苏:江苏科学技术出版社,2003:2-6.
[6]中华儿科杂志编辑委员会,中华医学杂志英文版编辑委员会。先天性心脏病经导管介入治疗指南。中华儿科杂志,2004,423:234-239.
[7]Undar L,Akkoc N,Alakavuklar MN,et al.Flow cytometric analysis of circadian changes in platelet activation using anti-GMP-140 monoclonl antibody[J].Chronobiol Int,1999,16(3):335.
[8]彭作辉.弥散性血管内凝血前期诊断[J].中国实用内科杂志,2000,6(6): 338-342.
[9] Teitel JM, Bauer KA, Lau HK, et al.. Studies of the prothrombin activation pathway utilizing radioimmunoassays for the F2/prothrombin fragment1+2 fragment and trombin/antithrombin complex. Blood 1982;59:1086-97.
[10]SundaramM,Qi Y, Shriver Z, et al. Rational design of low molecular weight heparms with improved in vivo activity[J]. PNAS,2003, 100 (2) : 651-656.
[11] Lock JE, Rome JJ, Davis R, et al. Transcatheter closure of atrial septal defects— experimental studies. Circulation,1989,79:1091-1099.
[12] Sharafuddin MJA, Gu X, Titus JL, et al.Trans venous closure of secundum atrial septal defects.Preliminary results with a new self-expanding nitinol prosthesis in a swine model. Circulation, 1997, 95: 2162-2168.
[13] Cenni E, Ciapetti G, Cervellati M, et al. Activation of the plasma coagulation system induced by some biomaterials. J Biomed Mater Res,1996,31:145-148.
[14] Cenni E, Arciola CR, Ciapetti G, et al. Platelet and coagulation factor variations induced in vitro by polyethylene terephthalate (Dacron) coated with pyrolytic carbonl. Biomaterials, 1995,16:973 -976.
[15] Makkar R, Litvack F, Eigler N, et al. Effects of GP IIb/IIIa receptor monoclonal antibody (7E3), heparin, and aspirin in an ex vivo canine arteriovenous shunt model of stent thrombosis. Circulation,1997,95: 1015-21.
[16]Merten M , Thiagarajan P. P-selectin in arterial thrombosis[J]. Z Kardiol,2004,93(11):855-863.
[17]郭楠,鲁静朝,崔炜等.血小板活化标志物的研究进展.[J].临床荟萃,2006,21(23):1748-1749.
[18]AD Michelson.Flow cytometry:A clinical test of platelet function[J].Blood,1996,87(12):4925.
[19]王建中,王淑娟.当前流式细胞分析的发展趋势[J].中华医学检验杂志2002,25:5-6.
[20]徐杰,阮长耿,王爱青等.应用流式细胞仪检测血小板膜糖蛋白[J].中国小儿血液杂志,1997,20:216-219
[21]Olgun N,Uysal KM,Irken G,et al.Platelet activation in congenital heart disease[J].Acta Paediatr Jpn,1997,39(9):566
[22]杨杰,闫梅,杨兴季等.血小板活化状态在先天性心脏病中的作用.山东大学学报(医学版)2004,42(1):54-59
[23]俸勇强,伍伟锋.成人先天性心脏病介入封堵前后神经内分泌功能的变化。中国心血管病研究杂志,2006,3(4):175-177.
[24]Pernerstorfer T,Eichler HG,Stohlawetz P,et al.Effects of heparin and aspirin on circulating P-selectin,E-selectin and von Willebrand factor levels in healthy men.Atherosclerosis 2001;155:389-93.
[25]Chronos NA,Wilson DJ,Janes SL et al.Aspirin does not affect the flow cytometryc detection of fibrinogen binding to,or release of alpha-granules or lysosomes from,human platelets.Clin Sci(Lond)1994;87:575-80.
[26]Pernerstorfer T,Stohlawetz P,Stummvoll G,et al.Low-dose aspirin does not lower in vivo platelet activation in healthy smokers.Br J Haematol 1998;102:1229-31.
[27]Klinkhardt U,Bauersachs R,Adams J,et al.Clopidogrel but not aspirin reduces P-selectin expression and formation of platelet-leuko-cyte aggregates in patients with atherosclerotic vascular disease.Clin Pharmacol Ther 2003;73:232-41.
[28]Veldtman GR,Razack B,Siu S,et al.Right ventricular form and function after percutaneous atrial septal defect device closure[J].J Am Coll Cardiol,2001,37(8):2108-2113.
[29]吴栋梁,张玉顺,张军等。成人房间隔缺损封堵术后左心大小和功能的变化[J]。心脏杂志,2002,14(4):324
[1] Lock JE, Rome JJ, Davis R, et al. Transcatheter closure of atrial septal defects—experimental studies. Circulation,1989,79(5):1091-1099.
[2] Sharafuddin MJA, Gu X, Titus JL, Urness M, Cervera-Ceballos JJ,Amplatz K. Transvenous closure of secundum atrial septal defects.Preliminary results with a new self-expanding nitinol prosthesis in a swine model. Circulation, 1998, 95(8): 2162-2168.
[3] Josep Rode's-Cabaua,Andre's Palaciosb, Carles Palaciob, et al. Assessment of the markers of platelet and coagulation activation following transcatheter closure of atrial septal defects. Int J Cardiol, 2005, 98(1): 107- 112.
[4] Cenni E, Ciapetti G, Cervellati M, et al. Activation of the plasma coagulation system induced by some biomaterials. J Biomed Mater Res, 1996,31(1):145-148.
[5] Cenni E, Arciola CR, Ciapetti G, et al. Platelet and coagulation factor variations induced in vitro by polyethylene terephthalate (Dacron) coated with pyrolytic carbonl. Biomaterials,1995,16(13):973 -976.
[6] Makkar R, Litvack F, Eigler N, et al. Effects of GP IIb/IIIa receptor monoclonal antibody (7E3), heparin, and aspirin in an ex vivo canine arteriovenous shunt model of stent thrombosis. Circulation,1997,95(4): 1015-21.
[7] La Rosee K, Krause D, Becker M, et al. Transcatheter closure of atrialseptal defect in adults: practicability and safety of four different occluder systems used in 102 patients. German Medical Weekly,2001,126(38):1030-1036.
[8] Lambert V, Losay J, Piot JD, et al. Late complications of percutaneous closure of atrial septal defects with the Sideris occluder. Cardiovascular Diseases Periodicals, 1997, 90(2):245-251
[9] Krumsdorf U, Ostermayer S, Billinger K, Trepels T, Zadan E,Horvath K, et al.Incidence and clinical course of thrombus formationon atrial septal defect and patient foramen ovale closure devices in 1,000 consecutive patients. J Am Coll Cardiol,2004,43(2):302-309.
[10] Jeffrey W. Delaney, MD, Jennifer S. Li, MD, and John F. Rhodes, MD.Major Complications Associated with Transcatheter Atrial Septal Occluder Implantation: A Review of the Medical Literature and the Manufacturer and User Facility Device Experience (MAUDE) Database. Congenit Heart Dis,2007,2(4):256-264.
[11] Braun M, Fassbender D, Schoen S, et al. Transcatheter closure of patent foramen ovale in patients with cerebral ischemia. J Am Coll Cardiol,2002,39(12):2019- 2025.
[12] Krieg P, Lapp H, Pethig K, Gummert JF, Bossert T. Removal of a left atrial throm bus adherent to a patent foramen ovale occluder. Ann Thorac Surg,2007, 83(4): 1539-1541.
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