罗格列酮对ACS伴IGT患者PCI术后纤溶功能及再狭窄的影响
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摘要
目的:通过对急性冠脉综合征(acute coronary syndrome,ACS)伴糖耐量减低(impaired glucose tolerance,IGT)患者经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)后在常规治疗的基础上加用罗格列酮,检测其术前及用药1个月后组织型纤溶酶原激活剂(tissue-type plasminogen activator ,t-PA)、纤溶酶原激活剂抑制因子-1(plasminogen activator inhibitor–1,PAI-1)及高敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)水平,并于6个月后复查冠脉造影,以探讨罗格列酮对PCI术后纤溶功能及再狭窄的影响。
方法:选择76例ACS伴IGT患者,随机分为常规治疗组(n=38)和罗格列酮组(n=38),PCI术后分别给予常规治疗或常规加罗格列酮治疗共1个月。IGT组(n=20)为冠状动脉造影(coronary arteriography,CAG)正常的IGT患者,对照组(n=20)为CAG及口服葡萄糖耐量试验(oral glucose tolerance test,OGTT)正常者。检测所有研究对象术前及常规治疗组、罗格列酮组术后1个月t-PA、PAI-1和hs-CRP水平。对成功接受PCI的患者随访6个月,观察再狭窄相关症状的发生情况。随访结束时或出现再狭窄相关症状时复查CAG。
结果:
1.与IGT组比较,常规治疗组和罗格列酮组术前血浆PAI-1、血清hs-CRP水平较高,血浆t-PA水平较低,差异具有统计学意义(P<0.05);与对照组比较,IGT组、常规治疗组和罗格列酮组术前血浆PAI-1、血清hs-CRP水平较高,血浆t-PA水平较低,差异具有统计学意义(P<0.05;P<0.05);罗格列酮组和常规治疗组PCI术前血浆t-PA、PAI-1及血清hs-CRP水平差异无统计学意义(P>0.05)。
2.与术前比较,常规治疗组和罗格列酮组术后1个月血浆t-PA水平升高,血浆PAI-1及血清hs-CRP水平降低,差异具有统计学意义(P<0.05);与常规治疗组比较,罗格列酮组术后1个月血浆t-PA、PAI-1及血清hs-CRP水平变化程度较大,差异具有统计学意义(P<0.05)。
3.与常规治疗组比较,罗格列酮组术后6月再狭窄发生率较低,差异具有统计学意义(P<0.05);与未发生再狭窄者比较,再狭窄者血浆t-PA水平较低,血浆PAI-1及血清hs-CRP水平较高,差异具有统计学意义(P<0.05)。
4.血浆PAI-1水平与血清hs-CRP水平呈正相关(r=0.727,P<0.001),血浆t-PA水平与血清hs-CRP水平呈负相关(r=0.693,P<0.001)。
结论:
1. PAI-1、t-PA可能是IGT患者发生ACS的预测因子。
2. PAI-1与t-PA可能是ACS伴IGT患者PCI术后再狭窄的预测因子。
3.罗格列酮可能通过降低PAI-1,升高t-PA水平,促进纤溶的激活,从而减少再狭窄的发生。
Object: To investigate the effect of rosiglitazone on fibrinolytic system and in-stent restenosis in patients with acute coronary syndrome(ACS) combined with impaired glucose tolerance(IGT), by observing the variation of plasma levels of tissue-type plasminogen activator(t-PA), plasminogen activator inhibitor–1(PAI-1) and serum levels of high-sensitivity C-reactive protein(hs-CRP) of the patients who were treated with conventional therapy or conventional therapy with the addition of rosiglitazone before and 1 month after percutaneous coronary intervention(PCI) and the occurrence of in-stent restenosis.
Method: 76 patients with ACS combined with IGT were randomly divided into Conventional group and Rosiglitazone group who treated with conventional therapy or conventional therapy with the addition of rosiglitazone for 1 month after PCI. 20 patients with IGT who were normality in coronary arteriography(CAG) were enrolled in IGT group, and 20 who were normality in oral glucose tolerance test(OGTT) and CAG were assigned in Control group. Plasma levels of t-PA, PAI-1 and serum levels of hs-CRP were determined before and 1 month after PCI. Restenosis related symptoms were observed in 6-month follow-up. CAGs were reexamined when the follow-up was over or symptoms appeared.
Result:
1. Compared with IGT group, plasma levels of PAI-1 and serum levels of hs-CRP in Conventional group and Rosiglitazone group were higher while plasma levels of t-PA were lower with statistically significant(P<0.05); Compared with Control group, plasma levels of PAI-1, and serum leves of hs-CRP in IGT group,Conventional group and Rosiglitazone group were higher while plasma levels of t-PA were lower significantly(P<0.05 and P<0.05,respectively); No significant difference was found between Conventional group and Rosiglitazone group(P>0.05).
2. Plasma levels of t-PA were much higher 1 months later than before PCI in Conventional group and Rosiglitazone group while plasma levels of PAI-1 and serum levels of hs-CRP were much lower significantly(P<0.05); The increasing of t-PA levels and the decreasing of PAI-1 and hs-CRP levels were significantly higher in Rosiglitazone group than Conventional control group (P<0.05).
3. The occurrence of restenosis was lower in Rosiglitazone group than Conventional group significantly(P<0.05); Plasma levels of t-PA were lower while plasma levels of PAI-1 and serum levels of hs-CRP were higher significantly in those who with restenosis than those without (P<0.05).
4. Plasma levels of PAI-1were positively correlated with serum levels of hs-CRP (r=0.727,P<0.001)while plasma levels of t-PA were negatively correlated with it(r=0.693,P<0.001).
Conclusion:
1. Plasma levels of PAI-1 and t-PA may be valuable predictors of ACS in IGT patients.
2. Plasma levels of PAI-1 and t-PA like to be predictors of restenosis after PCI probably.
3. Rosiglitazone may reduce the occurrence of restenosis after PCI by raising the plasma level of t- PA and reducing the plasma level of PAI-1, indicating fibrinolytic system was activated.
方法:选择76例ACS伴IGT患者,随机分为常规治疗组(n=38)和罗格列酮组(n=38),PCI术后分别给予常规治疗或常规加罗格列酮治疗共1个月。IGT组(n=20)为冠状动脉造影(coronary arteriography,CAG)正常的IGT患者,对照组(n=20)为CAG及口服葡萄糖耐量试验(oral glucose tolerance test,OGTT)正常者。检测所有研究对象术前及常规治疗组、罗格列酮组术后1个月t-PA、PAI-1和hs-CRP水平。对成功接受PCI的患者随访6个月,观察再狭窄相关症状的发生情况。随访结束时或出现再狭窄相关症状时复查CAG。
结果:
1.与IGT组比较,常规治疗组和罗格列酮组术前血浆PAI-1、血清hs-CRP水平较高,血浆t-PA水平较低,差异具有统计学意义(P<0.05);与对照组比较,IGT组、常规治疗组和罗格列酮组术前血浆PAI-1、血清hs-CRP水平较高,血浆t-PA水平较低,差异具有统计学意义(P<0.05;P<0.05);罗格列酮组和常规治疗组PCI术前血浆t-PA、PAI-1及血清hs-CRP水平差异无统计学意义(P>0.05)。
2.与术前比较,常规治疗组和罗格列酮组术后1个月血浆t-PA水平升高,血浆PAI-1及血清hs-CRP水平降低,差异具有统计学意义(P<0.05);与常规治疗组比较,罗格列酮组术后1个月血浆t-PA、PAI-1及血清hs-CRP水平变化程度较大,差异具有统计学意义(P<0.05)。
3.与常规治疗组比较,罗格列酮组术后6月再狭窄发生率较低,差异具有统计学意义(P<0.05);与未发生再狭窄者比较,再狭窄者血浆t-PA水平较低,血浆PAI-1及血清hs-CRP水平较高,差异具有统计学意义(P<0.05)。
4.血浆PAI-1水平与血清hs-CRP水平呈正相关(r=0.727,P<0.001),血浆t-PA水平与血清hs-CRP水平呈负相关(r=0.693,P<0.001)。
结论:
1. PAI-1、t-PA可能是IGT患者发生ACS的预测因子。
2. PAI-1与t-PA可能是ACS伴IGT患者PCI术后再狭窄的预测因子。
3.罗格列酮可能通过降低PAI-1,升高t-PA水平,促进纤溶的激活,从而减少再狭窄的发生。
Object: To investigate the effect of rosiglitazone on fibrinolytic system and in-stent restenosis in patients with acute coronary syndrome(ACS) combined with impaired glucose tolerance(IGT), by observing the variation of plasma levels of tissue-type plasminogen activator(t-PA), plasminogen activator inhibitor–1(PAI-1) and serum levels of high-sensitivity C-reactive protein(hs-CRP) of the patients who were treated with conventional therapy or conventional therapy with the addition of rosiglitazone before and 1 month after percutaneous coronary intervention(PCI) and the occurrence of in-stent restenosis.
Method: 76 patients with ACS combined with IGT were randomly divided into Conventional group and Rosiglitazone group who treated with conventional therapy or conventional therapy with the addition of rosiglitazone for 1 month after PCI. 20 patients with IGT who were normality in coronary arteriography(CAG) were enrolled in IGT group, and 20 who were normality in oral glucose tolerance test(OGTT) and CAG were assigned in Control group. Plasma levels of t-PA, PAI-1 and serum levels of hs-CRP were determined before and 1 month after PCI. Restenosis related symptoms were observed in 6-month follow-up. CAGs were reexamined when the follow-up was over or symptoms appeared.
Result:
1. Compared with IGT group, plasma levels of PAI-1 and serum levels of hs-CRP in Conventional group and Rosiglitazone group were higher while plasma levels of t-PA were lower with statistically significant(P<0.05); Compared with Control group, plasma levels of PAI-1, and serum leves of hs-CRP in IGT group,Conventional group and Rosiglitazone group were higher while plasma levels of t-PA were lower significantly(P<0.05 and P<0.05,respectively); No significant difference was found between Conventional group and Rosiglitazone group(P>0.05).
2. Plasma levels of t-PA were much higher 1 months later than before PCI in Conventional group and Rosiglitazone group while plasma levels of PAI-1 and serum levels of hs-CRP were much lower significantly(P<0.05); The increasing of t-PA levels and the decreasing of PAI-1 and hs-CRP levels were significantly higher in Rosiglitazone group than Conventional control group (P<0.05).
3. The occurrence of restenosis was lower in Rosiglitazone group than Conventional group significantly(P<0.05); Plasma levels of t-PA were lower while plasma levels of PAI-1 and serum levels of hs-CRP were higher significantly in those who with restenosis than those without (P<0.05).
4. Plasma levels of PAI-1were positively correlated with serum levels of hs-CRP (r=0.727,P<0.001)while plasma levels of t-PA were negatively correlated with it(r=0.693,P<0.001).
Conclusion:
1. Plasma levels of PAI-1 and t-PA may be valuable predictors of ACS in IGT patients.
2. Plasma levels of PAI-1 and t-PA like to be predictors of restenosis after PCI probably.
3. Rosiglitazone may reduce the occurrence of restenosis after PCI by raising the plasma level of t- PA and reducing the plasma level of PAI-1, indicating fibrinolytic system was activated.
引文
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[1]陈晓文,戚文航.球囊血管成型术后局部PAI-1基因表达[J].上海第二医科大学学报,2001,21(3):220-222.
[2]陈晓文,戚文航.球囊血管成型术后局部PAI-1基因表达西拉普利的作用[J].中华心血管病杂志,2003,31(3):220-222.
[3] Sawa H,Lundgren C,Sobel BE,et al. Increased intramural expression of pla-sminogen activator inhibitor type 1 after balloon injury: a potential progenitor of restenosis[J]. J Am Coll Cardiol,1994,24 (7):1742-1748.
[4] DeYouny MB,Tom C,Dichek DA,et al. Plasminogen activator inhibitor type1 increases neointima formation in balloon-injured rat carotid arteries[J]. Circul-ation,2001,104(16):1972-1973.
[5] Sawa H,Sobel BE,Fujii S,et al. Potentiation by hypercholest-erolemia of th-e induction of aortic intramural synthesis of plasminogen activator inhibitor typ-e 1 by endothelial injury[J]. Circ Res,1993,73:671-680.
[6]王晔玲,赵利华,王延风.卡托普利对动脉损伤后内膜增生时纤溶系统的影响[J].中国介入心脏病学杂志,2002,4:214-216.
[7] Zidovetzki P,Wang JL,Kim JA,et al. Endothelin-1 enhances plasminogen activator inhibitor-1 production by human brain endothelial cells via protein kinas-e C dependent pathway[J]. Arterioscler Thromb Vasc Biol,1999,19(7):1768-1775.
[8] Sakata K,Miura F,Sugino H,et al. Impaired fibrinolysis early after percutan-eous transluminal coronary angioplasty is associated with restenosis[J]. Am He-art J,1996,131(1):1-6.
[9] Ishiwata S,Tukuda T,Nakanishi S,et al. Postangioplasty restenosis: platelet a-ctivation and the coagulation-fibrinolysis system as possible factors in the path-ogenesis of restenosis[J]. Am Heart J,1997,133(4): 387-392.
[10] Kato K,Satoh H,Endo Y,et al. Thiazolidinediones down-regulate plasminog-en activator inhibitor type 1 expression in human vascular endothelial cells: Apossible role for PPAR-γin endothelial function [J]. Biochem Biophys Res C-ommun,1999,258(2):431-435.
[11] Strauss BH,Lau HK,Bowman KA,et al. Plasma urokinase antigen and plas-minogen activator inhibitor-1 levels predict angiographic coronary restenosis[J].Circulation,1999,100(15):1616-1622.
[12] Inoue T,Yaguchi I,Mizoguchi K,et al. Accelerated plasminogen activetor i-nhibitor may prevent late restenosis after coronary stenting in acute myocardialinfarction[J]. Clin Cardiol,2003,26(3):153-157.
[13] BarbierO,Torra IP,Duguay Y,et al. Pleiotropic action of peroxisome prolif-erator-activated receptors in lipid metabolism and atherosclerosis[J]. ArteriosclerThromb Vasc Biol,2002,22 (5):717-726.
[14] Jozkowicz A,Dulak J,Nanobashvili J,et al. Role of peroxisome proliferator-activated receptor-γligands in vessel[J]. Eur Surg,2002,34(2):121-126.
[15] Sidhu JS,Kaski JC. Peroxisome proliferator activated receptorγ: a potentialtherapeutic target in the management of ischaemic heart disease [J]. Heart,2001,86(3):255-258.
[16] Marx N,Bourcier T,Sukhova GK,et al. PPARγactivation in human endot-helial cells increase plasminogen activator inhibitor type 1 expression[J]. Arteri-oscler Thromb Vasc Biol,1999,19(3):546-551.
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[18] Zidovetzki R,Wang JL,Kim JA,et al. Endothelin-1 enhances plasminogen activator inhibitor-1 production by human brain endothelial cells via protein kin-ase C dependent pathway[J]. Arterioscler Thromb Vasc Biol,1999,19(7):1768-1775.
[19] Birgel M,Gottschling-Zeller H, Rohrig K,et al. Role of cytokines in the r-egulation of plasmiogen activator inhibitor-1 expression and secretion in newlydifferentiated subcutaneous human adipocytes [J]. Arterioscler Thromb VascBiol,2000,20(6):1682-1687.
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[1]陈晓文,戚文航.球囊血管成型术后局部PAI-1基因表达[J].上海第二医科大学学报,2001,21(3):220-222.
[2]陈晓文,戚文航.球囊血管成型术后局部PAI-1基因表达西拉普利的作用[J].中华心血管病杂志,2003,31(3):220-222.
[3] Sawa H,Lundgren C,Sobel BE,et al. Increased intramural expression of pla-sminogen activator inhibitor type 1 after balloon injury: a potential progenitor of restenosis[J]. J Am Coll Cardiol,1994,24 (7):1742-1748.
[4] DeYouny MB,Tom C,Dichek DA,et al. Plasminogen activator inhibitor type1 increases neointima formation in balloon-injured rat carotid arteries[J]. Circul-ation,2001,104(16):1972-1973.
[5] Sawa H,Sobel BE,Fujii S,et al. Potentiation by hypercholest-erolemia of th-e induction of aortic intramural synthesis of plasminogen activator inhibitor typ-e 1 by endothelial injury[J]. Circ Res,1993,73:671-680.
[6]王晔玲,赵利华,王延风.卡托普利对动脉损伤后内膜增生时纤溶系统的影响[J].中国介入心脏病学杂志,2002,4:214-216.
[7] Zidovetzki P,Wang JL,Kim JA,et al. Endothelin-1 enhances plasminogen activator inhibitor-1 production by human brain endothelial cells via protein kinas-e C dependent pathway[J]. Arterioscler Thromb Vasc Biol,1999,19(7):1768-1775.
[8] Sakata K,Miura F,Sugino H,et al. Impaired fibrinolysis early after percutan-eous transluminal coronary angioplasty is associated with restenosis[J]. Am He-art J,1996,131(1):1-6.
[9] Ishiwata S,Tukuda T,Nakanishi S,et al. Postangioplasty restenosis: platelet a-ctivation and the coagulation-fibrinolysis system as possible factors in the path-ogenesis of restenosis[J]. Am Heart J,1997,133(4): 387-392.
[10] Kato K,Satoh H,Endo Y,et al. Thiazolidinediones down-regulate plasminog-en activator inhibitor type 1 expression in human vascular endothelial cells: Apossible role for PPAR-γin endothelial function [J]. Biochem Biophys Res C-ommun,1999,258(2):431-435.
[11] Strauss BH,Lau HK,Bowman KA,et al. Plasma urokinase antigen and plas-minogen activator inhibitor-1 levels predict angiographic coronary restenosis[J].Circulation,1999,100(15):1616-1622.
[12] Inoue T,Yaguchi I,Mizoguchi K,et al. Accelerated plasminogen activetor i-nhibitor may prevent late restenosis after coronary stenting in acute myocardialinfarction[J]. Clin Cardiol,2003,26(3):153-157.
[13] BarbierO,Torra IP,Duguay Y,et al. Pleiotropic action of peroxisome prolif-erator-activated receptors in lipid metabolism and atherosclerosis[J]. ArteriosclerThromb Vasc Biol,2002,22 (5):717-726.
[14] Jozkowicz A,Dulak J,Nanobashvili J,et al. Role of peroxisome proliferator-activated receptor-γligands in vessel[J]. Eur Surg,2002,34(2):121-126.
[15] Sidhu JS,Kaski JC. Peroxisome proliferator activated receptorγ: a potentialtherapeutic target in the management of ischaemic heart disease [J]. Heart,2001,86(3):255-258.
[16] Marx N,Bourcier T,Sukhova GK,et al. PPARγactivation in human endot-helial cells increase plasminogen activator inhibitor type 1 expression[J]. Arteri-oscler Thromb Vasc Biol,1999,19(3):546-551.
[17] Ihara H,Urano T,Takada A,et al.Induction of plasminogen activator inhibit-or 1 gene expression in adipocytes by thiazolidinediones[J].FASEB J,2001,15(7):1233-1235.
[18] Zidovetzki R,Wang JL,Kim JA,et al. Endothelin-1 enhances plasminogen activator inhibitor-1 production by human brain endothelial cells via protein kin-ase C dependent pathway[J]. Arterioscler Thromb Vasc Biol,1999,19(7):1768-1775.
[19] Birgel M,Gottschling-Zeller H, Rohrig K,et al. Role of cytokines in the r-egulation of plasmiogen activator inhibitor-1 expression and secretion in newlydifferentiated subcutaneous human adipocytes [J]. Arterioscler Thromb VascBiol,2000,20(6):1682-1687.
[20] Skurk T,Lee YM,Hauner H,et al. Angiotensin II and its metabolites stimu-late PAI-1 protein release from human adipocytes in primary culture[J]. Hypert-ension,2001,37(5):1336-1340.
[21] Sugawara A,Takeuchi K,Uruno A,et al. Differential effects among thiazoli-dine on the transcription of thromboxane receptor and angiotensinⅡtype 1 receptor genes[J]. Hypertens Res,2001,24(3): 229-233.