凝血因子Ⅺ和Ⅻ活性与冠状动脉慢血流的关系
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摘要
目的探讨血浆凝血因子Ⅺ和Ⅻ活性与冠状动脉慢血流(CSF)的关系。方法选择经冠脉造影证实的冠状动脉慢血流(CSF)患者49例,另选同期经冠脉造影证实冠状动脉血流正常(NCF)者49例。测定比较两组患者血浆凝血因子活性水平。结果与NCF组比较,CSF组凝血因子Ⅺ[(109.3±18.9)]vs(96.8±15.7)]及凝血因子Ⅻ活性[(130.1±18.7)vs(116.7±16.6)]均增高(P均<0.05)。Pearson相关性分析显示,FⅪ活性水平与CSF的冠脉血流速度呈正相关(r=0.90,P<0.01),FⅫ活性水平与CSF的冠脉血流速度呈正相关(r=0.79,P<0.01)。结论 CSF现象与凝血因子Ⅺ和Ⅻ活性增高导致的促凝状态有关,凝血因子Ⅺ和Ⅻ活性增高可能参与了CSF的发病。
Objective To investigate the relationship between plasma coagulation factors activity and coronary slow flow(CSF). Methods The study included 49 patients with angiographically proven CSF(group CSF)and 49 individuals with normal coronary flow(group NCF). Blood samples were collected from both groups to determine the plasma coagulation factor activity. Results Compared with NCF group, the activity of coagulation factorⅪ[(109.3±18.9)vs(96.8±15.7)]and coagulation factorⅫ[(130.1±18.7) vs(116.7±16.6)]in CSF group increased(P<0.05). Pearson correlation analysis showed that FⅪ activity level was positively correlated with coronary flow velocity of CSF(r=0.90,P<0.001),and FⅫ activity level was positively correlated with coronary flow velocity of CSF(r=0.79,P<0.001). Conclusion The phenomenon of CSF is related to the coagulation state caused by the increase of coagulation factor activity. The increase of coagulation factor activity may be involved in the pathogenesis of coronary slow blood flow.
Objective To investigate the relationship between plasma coagulation factors activity and coronary slow flow(CSF). Methods The study included 49 patients with angiographically proven CSF(group CSF)and 49 individuals with normal coronary flow(group NCF). Blood samples were collected from both groups to determine the plasma coagulation factor activity. Results Compared with NCF group, the activity of coagulation factorⅪ[(109.3±18.9)vs(96.8±15.7)]and coagulation factorⅫ[(130.1±18.7) vs(116.7±16.6)]in CSF group increased(P<0.05). Pearson correlation analysis showed that FⅪ activity level was positively correlated with coronary flow velocity of CSF(r=0.90,P<0.001),and FⅫ activity level was positively correlated with coronary flow velocity of CSF(r=0.79,P<0.001). Conclusion The phenomenon of CSF is related to the coagulation state caused by the increase of coagulation factor activity. The increase of coagulation factor activity may be involved in the pathogenesis of coronary slow blood flow.
引文
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[10] Siegerink B,Rosendaal FR,Algra A. Antigen levels of coagulation factor XII,coagulation factor XI and prekallikrein,and the risk of myocardial infarction and ischemic stroke in young women[J]. Journal of Thrombosis and Haemostasis,2014,12(5):606-613.
[11] Cheng Q,Tucker EI,Pine MS,et al. A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo[J]. Blood,2010,116(19):3981-3989.
[12] Pham M,Stoll G,Nieswandt B,et al. Blood coagulation factor XII—a neglected player in stroke pathophysiology[J]. Journal of Molecular Medicine-jmm,2012,90(2):119-126.
[13] Konings J,Govers-Riemslag JWP,Philippou H,et al.Factor XIIa regulates the structure of the fibrin clot independently of thrombin generation through direct interaction with fibrin[J]. Blood,2011,118(14):3942-3951.
[2]何永福,孙林,林志.冠状动脉慢血流现象病理生理机制及治疗进展[J].心血管病学进展,2018,39(3):448-452.
[3] Gibson CM,Cannon CP,Murphy SA,et al. Relationship of the TIMI myocardial perfusion grades,flow grades,frame count,and percutaneous coronary intervention to long-term outcomes after thrombolytic administration in acute myocardial infarction[J]. Circulation,2002,105(16):1909-1913.
[4] Zaman AG,Helft G,Worthley SG,et al. The role of plaque rapture and thrombosis in coronary artery disease[J]. Atherosclerosis,2000,149(2):251-266.
[5] Emsley J,Mcewan PA,Gailani D.Structure and function of factor XI[J]. Blood,2010,115(13):2569-2577.
[6] Meijers JC,Tekelenburg WL,Bouma BN,et al. High levels of coagulation factor XI as a risk factor for venous thrombosis[J]. N Engl J Med,2000,342(10):696-701.
[7] Yang DT,Flanders MM,Kim H,et al. Elevated factor XI activity levels are associated with an increased odds ratio for cerebrovascular events[J]. American Journal of Clinical Pathology,2006,126(3):411-415.
[8] Doggen CJ,Rosendaal FR,Meijers JC. Levels of intrinsic coagulation factors and the risk of myocardial infarction among men:Opposite and synergistic effects of factors XI and XII[J]. Blood,2006,108(13):4045-4051.
[9] RennéT,PozgajováM,Grüner S,et al. Defective thrombus formation in mice lacking coagulation factorⅫ[J]. J Exp Med,2005,202(2):271-281.
[10] Siegerink B,Rosendaal FR,Algra A. Antigen levels of coagulation factor XII,coagulation factor XI and prekallikrein,and the risk of myocardial infarction and ischemic stroke in young women[J]. Journal of Thrombosis and Haemostasis,2014,12(5):606-613.
[11] Cheng Q,Tucker EI,Pine MS,et al. A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo[J]. Blood,2010,116(19):3981-3989.
[12] Pham M,Stoll G,Nieswandt B,et al. Blood coagulation factor XII—a neglected player in stroke pathophysiology[J]. Journal of Molecular Medicine-jmm,2012,90(2):119-126.
[13] Konings J,Govers-Riemslag JWP,Philippou H,et al.Factor XIIa regulates the structure of the fibrin clot independently of thrombin generation through direct interaction with fibrin[J]. Blood,2011,118(14):3942-3951.