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卡维地洛对不稳定型心绞痛患者血浆炎症因子的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第3期
页码:
315-317
栏目:
临床研究
出版日期:
2007-06-01

文章信息/Info

Title:
Effects of Carvedilol on function of endothelium in patients with unstable angina pectoris
作者:
程如峰1赵慧强2肖四海1邵利1
1.解放军255医院心内科,河北 唐山 063000;2.沈阳军区总医院心内科,辽宁 沈阳 110016
Author(s):
CHENG Rufeng1 ZHAO Huiqiang2 XIAO Sihai1 SHAO Li1
1.Department of Cardiovasology, PLA 255 Hospital, Tangshan 063000 Hebei,China; 2.Department of Cardiovasology, General Hospital, Shenyang Military Area Command, Shenyang 110016,Liaoning, China
关键词:
卡维地洛心绞痛不稳定型C反应蛋白高敏白介素6可溶性细胞间黏附分子1
Keywords:
carvedilol unstable angina pectoris high sensitivity Creactive proteininterleukin6 soluble intercellular adhesion molecule1
分类号:
R541.4
DOI:
-
文献标识码:
A
摘要:
目的 观察卡维地洛对不稳定型心绞痛(UAP)患者高敏C反应蛋白(hsCRP)、白介素6(IL6)及细胞间可溶性黏附分子1(sICAM1)水平的影响。方法 UAP患者62例采用完全随机化方法分成对照组(n=30)和治疗组(n=32),在常规抗血小板、扩血管治疗基础上,对照组予美托洛尔(12.5 mg,2次/d ×3 d)口服,治疗组服卡维地洛(6.25 mg,2次/d×3 d),在治疗前后分别测定hsCRP、IL6、sICAM1值。结果 对照组和治疗组在治疗前hsCRP、IL6、sICAM1均无显著性差异;用药后两组3指标均较用药前显著降低(P<0.05);治疗组在用药后IL6、sICAM1显著低于对照组(P<0.05)。同时,用药后两组患者的心率、血压、心肌耗氧量均较用药前显著降低(P<0.05),治疗组的心肌耗氧量显著低于对照组(P<0.05)。结论 卡维地洛可显著降低UAP患者的炎症因子IL6、sICMA1水平。
Abstract:
AIM To observe the effect of Carvedilol on the circulating levels of high sensitivity Creactive protein(hsCRP), interleukin6(IL6)and soluble intercellular adhesion molecule1(sICAM1) in patients with unstable angina pectoris (UAP). METHODS Sixtytwo patients with UAP were randomly divided into two groups. On the basis of ant iplatelet and vasodilator remedy, the patients in control group (n= 30) were given Metoprolol, while the patients in therapeutic group (n= 32) were given carvedilol. Before and 3 d after the treatment, venous blood samples were taken and the levels of serum hsCRP, IL6 and sICAM1 were measured. RESULTS The levels of circulating hsCRP, IL6 and sICAM1 between control group and carvedilol group were not significantly different before the treatment. After the treatment, the levels of hsCRP, IL6 and sICAM1 in control group and carvedilol group were significantly lower than the base line (P<0.05), whereas the levels of IL6 and sICAM1 in carvedilol group were significantly lower than those in control group (P<0.05). The levels rate, blood pressure,myocardial consumption of oxygen in control group and carvediol group were significantly lower than base line(P<0.05). CONCLUSION Carvedilol can decrease the circulating levels of IL6, sICAM1 inflammatory factors in patients with UAP.

参考文献/References

[1]中华医学会心血管病分会,中华心血管病杂志编辑委员会.不稳定型心绞痛诊断和治疗建议[J].中华心血管病杂志,2000,28(6):409-412.

[2]Maseri A. Inflammation, atherosclerosis, and ischemic events exploringthe hidden side of the moon[J]. N Engl J Med,1997,336(14):1014-1016.[3]Ross R. Atherosclerosis—an inflammatory disease[J]. N Engl J Med,1999,340(2):115-126.

[4]Mazzone A, De Servi S, Ricevuti G, et al. Increased expression of neutrophil and monocyte adhesion molecules in unstable coronary artery disease[J]. Circulation,1993,88(2):358-363.

[5]Van der Wal AC, Becker AE, Van der Loos CM, et al. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology[J]. Circulation, 1994, 89 (1):36-44.

[6]Yoshikawa T,Port JD,Asano K,et al.Cardiac adrenergic receptor effect of carvedilol[J]. Eur Heart J,1996,17(suppl B):8-16.

[7]Brunner M,Faber TS,Greve B,et al.sefulness of carvedilol in unstable angina pectoris[J]. Am J Cardiol,2000,85(10):1173-1178.

[8]Dandona P,Karne R,Ghanim H,et al.Carvedilol inhibits reactive oxygen species generation by leukocytes and oxidative damage to amino acids[J]. Circulation,2000,101(2):122-124

[9]Prabhu SD, chandrasekar B,Murray DR,et al.βadrenergic blockade in developing heart failure effects on myocardial inflamatory cytokines,nitric oxide, and remodeling[J]. Circulation, 2000,101(17):2103-2109.

[10]Richardson M, Kurowska EM, Carroll KK. Early lesion development in the aortas of rabbits fed lowfat, cholesterolfree, semipurified casein diet[J]. Atherosclerosis,1994,107(2):165-178.

[11]Crea F,Biasucci LM,Buffon A,et al.Role of inflammation in the pathogenesis of unstable coronary artery disease[J]. Am J Cardiol,1997,80(5A):10E-16E.

[12]Schieffer B, Schieffer E, HilfikerKleiner D,et al. Expression of angiotensin II and interleukin 6 in human coronary atherosclerotic plaques: potential implications for inflammation and plaque instability[J]. Circulation,2000,101(12):1372-1378.

[13]Anderson JL, Carlquist JF, Muhlestein JB,et al. Evaluation of Creactive protein, an inflammatory marker, and infectious serology as risk factors for coronary artery disease and myocardial infarction[J]. J Am Coll Cardiol,1998,32 (1):35-41.

备注/Memo

备注/Memo:
收稿日期:2006-02-22.作者简介:程如峰,硕士,主治医师Email:tangshanch@sohu.com
更新日期/Last Update: