Rho激酶对急性冠状动脉综合征患者复合心血管不良事件的影响

李文华; 何国平; 李勇; 徐波; 肖建强; 顾君; 季建国; 施有为

doi:10.13201/j.issn.1001-1439.2016.03.008

Rho激酶对急性冠状动脉综合征患者复合心血管不良事件的影响

- 常州市武进人民医院心内科(江苏常州, 213000)

详细信息

通讯作者: 何国平,E-mail:guopinghe6@sina.com

中图分类号: R541.4

收稿日期: 2015-08-30

The influence of Rho-kinase on prognosis of medium-to-long term adverse cardiovascular outcomes in patients with acute coronary syndrome

- Department of Cardiology, Changzhou Wujin People's Hospital, Changzhou, Jiangsu, 213000, China

More Information

Corresponding author: HE Guoping, E-mail: guopinghe6@sina.com

Received Date: 30 August 2015

摘要

摘要: 目的:探讨Rho激酶活性对急性冠状动脉综合征(ACS)患者长期预后的影响。方法:入选ACS患者280例为观察组,同期冠状动脉(冠脉)造影证实冠脉无异常的患者120例为对照组,观察组根据Rho激酶活性的高低分为高活性组和低活性组,记录观察组和对照组在Rho激酶、高敏C反应蛋白(hs-CRP)水平上的差异,记录观察组亚组间Rho激酶、hs-CRP水平和6个月复合心血管不良事件(非致命的心肌梗死、心力衰竭、心绞痛、再次血运重建和心源性死亡)发生率的差异,评价Rho激酶对ACS患者中长期预后的影响。结果:观察组Rho激酶和hs-CRP水平明显高于对照组(P＜0.05);观察组亚组间高活性组的hs-CRP水平明显高于低活性组(P＜0.05);随访1个月高活性组Rho激酶和hs-CRP水平仍显著高于低活性组(P＜0.05);随访6个月观察组亚组间Rho激酶和hs-CRP水平无显著差异,Rho激酶高活性组复合心血管事件的发生率高于低活性组,有显著差异(P＜0.05)。相关性分析显示,Rho激酶与hs-CRP呈正相关,Logistic回归分析显示Rho激酶活性是影响ACS患者6个月复合心血管事件发生率的独立预测因素(P=0.028)。结论:Rho激酶是一个与ACS患者相关的炎性因子,与hs-CRP呈正相关,可作为ACS患者中长期预后的独立预测因子。
- Rho激酶 /
- 急性冠脉综合征 /
- 高敏C反应蛋白 /
- 复合心血管不良事件
Abstract: Objective:To explore the prognostic value of Rho-kinase activity in patients with acute coronary syndrome.Method:A total of 400 patients with chest pain, according to the results of coronary angiography, were divided into observation group (ACS, n=280) and control group (n=120). The patients in the observation group were further divided into 2 subgroups according the activity of Rho kinase:high active group and lowactive group. The Rho-kinase activity and high sensitivity C reactive protein (hs-CRP)were detected in each group. The adverse cardiovascular outcomes with 6 months were analyzed in the observation group.Result:The Rho-kinase activity and hs-CRP level were significantly higher in observation group compared with control group (P<0.05). In hospital and 30-day follow-up, the Rho-kinase activity and hs-CRP level were significantly higher in high activity group compared with low activity group(P<0.05). At 6-month follow-up, patients in highactivity group had a significantly higher incidence of combined adverse cardiovascular outcomes than those in lowactivity group (P<0.05). There was positive correlation between Rho-kinase activity and hs-CRP level. The logistic regression analysis displayed that Rho-kinase activity was an independent risk factor which may predict the combined adverse cardiovascular outcomes of ACS patients within 6 months after admission. Conclusion:Rho-kinase is an inflammatory factor associated with ACS, may be an independent predictive biomarker in the ACS patients within medium-to-long term.
- Rho-kinase /
- acute coronary syndrome /
- high sensitivity C reactive protein /
- combined adeverse cardiovascular outcomes

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参考文献(22)

[1]	黄兆章,周希敏.急性冠脉综合征早期的识别和救治[J].实用临床医药杂志,2007,11(6):82-84.
[2]	WANG H W,LIU P Y,OYAMA N,et al.Deficiency of ROCK1 in bone marrow-derived cells protects against atherosclerosis in LDLR-/-mice[J].FASEB J,2008,22:3561-3570.
[3]	CANNON C P,BRINDIS R G,CHAITMAN B R,et al.2013 ACCF/AHA key data elements and definitions for measuring the clinical management and outcomes of patients with acute coronary syndromes and coronary artery disease[J].J Am Coll Cardiol,2013,61:992-1025.
[4]	LIESTING C,BRUGTS J J,KOFFLARD M J,et al.Acute coronary syndrome in a patient with a single coronary artery arising from the right sinus of valsalva[J].World J Cardiol,2012,4:264-266.
[5]	KOLTOWSKI L,FILIPIAK K J,RDZANEK A,et al.IgG,IgM and inflammatory markers serum concentration in patients with acute coronary syndrome:a pilot study[J].Kardiol Pol,2012,70:1023-1028.
[6]	AKABAME S,HAMAGUCHI M,TOMIYASU K,et al.Evaluation of vulnerable coronary plaques and Non-alcoholic fatty liver disease(NAFLD)by 64-detector multislice computed tomography(MAST)[J].Cire J,2009,72:618-625.
[7]	YAMAGUCHI K,WAKATSUKI T,SOEKI T,et al.Effects of telmisartan on inflammatory cytokines and coronary plaque component as assessed on integrated backscatter intravascular ultrasound in hypertensive patients[J].Circ J,2013,78:240-247.
[8]	RIENTO K,RIDLEY A J.Rocks:multifunctional kinases in cell behaviour[J].Nat Rev Mol Cell Biol,2003,4:446-456.
[9]	FUKATA Y,AMANO M,KAIBUCHI K.RhoRho-kinase pathway in smooth muscle contraction and cytoskeletal reorganization of non-muscle cells[J].Trends Pharmacol Sci,2001,22:32-39.
[10]	TAKEMOTO M,SUN J,HIROKI J,et al.Rho-kinase mediates hypoxia-induced downregulation of endothelial nitric oxidesynthase[J].Circulation,2002,106:57-62.
[11]	MIYATA K,SHIMOKAWA H,KANDABASHI T,et al.Rho-kinase is involved in macrophage-mediated formation of coronary vascular lesions in pigs in vivo[J].Arterioscler Thromb Vasc Biol,2000,20:2351-2358.
[12]	YAMAKAWA T,TANAKA S,NUMAGUCHI K,et al.Involvement of Rho-kinase in angiotensin II-induced hypertrophy of rat vascular smooth muscle cells[J].Hypertension,2000,35:313-318.
[13]	SHIBATA R,KAI H,SEKI Y,et al.Rho-kinase inhibition reduces neointima formation after vascular injury by enhancing Bax expression and apoptosis[J].J Cardiovasc Pharmacol,2003,42:S43-S47.
[14]	MING X F,VISWAMBHARAN H,BARANDIER C,et al.Rho GTPase/Rho kinase negtively regulates endothelial nitric oxide synthase phosphorylation through the inhibition of protein kinase B/Akt in human endothelial cells[J].Mol Cell Biol,2002,22:8467-8477.
[15]	SEASHOLTZ T M,MAJUMDAR M,KAPLAN D D,et al.Rho and Rho kinase mediate thrombin-stimulated vascular smooth muscle cell DNA synthesis and migration[J].Circ Res,1999,84:1186-1193.
[16]	YONEDA A,MULTHAUPT H A,COUCHMAN J R.The Rho kinasesⅠandⅡregulate different aspects of myosinⅡactivity[J].J Cell Biol,2005,170:443-453.
[17]	MATSUMOTO Y,UWATOKU T,ABE K,et al.Long-term inhibition of Rho-kinase suppresses neointimal formation after stent implantation in porcine coronary arteries.Involvement of multiple mechanisms[J].Arterioscler Thromb Vasc Biol,2004,24:181-186.
[18]	HATTORI T,SHIMOKAWA H,HIGASHI M,et al.Long-term treatment with a specific Rho-kinase inhibitor suppresses cardiac allograft vasculopathy in mice[J].Circ Res,2004,94:46-52.
[19]	SHIMOKAWA H,MORISHIGE K,MIYATA K,et al.Long-term inhibition of Rho-kinase induces a marked regression of arteriosclerotic coronary lesions in a porcine model in vivo[J].Cardiovasc Res,2001,51:169-177.
[20]	HISAOKA T,YANO M,OHKUSA T,et al.Enhancement of Rho/Rhokinase system in regulation of vascular smooth muscle contraction in tachycardia-induced heat failure[J].Cardiovasc Res,2001,49:319-329.
[21]	MASUMOTO A,MOHRI M,SHIMOKAWA H,et al.Suppression of coronary artery spasm by a Rho-kinase inhibitor fasudil in patients with vasospastic angina[J].Circulation,2002,105:1545-1547.
[22]	MOHRI M,SHIMOKAWA H,HIRAKAWA Y,et al.Rho-kinase inhibition with intracoronary fasudil prevents myocardial ischemia in patients with angina and normal coronary angiograms[J].J Am Coll Cardiol,2003,41:15-19.