期刊文献+

波生坦对房间隔缺损合并重度肺动脉高压女性患者血管内皮舒张功能的影响 被引量:1

Bosentan on vascular endothelial diastolic function in female patients with secundum atrial septal defect and severe pulmonary artery hypertension
下载PDF
导出
摘要 目的:观察波生坦对继发孔型房间隔缺损(ASD)合并重度肺动脉高压(PAH)女性患者血管内皮舒张功能的短期影响。方法:给予11例经右心导管检查确诊为先天性心脏病,ASD合并PAH的女性患者,给予波生坦62.5mg,每日2次,口服4周治疗。记录并比较患者治疗前、后6分钟步行距离(6MWD)、WHO心功能分级、内皮依赖性(FMD)和非内皮依赖性血管舒张功能(EID)及超声心动图检测指标。结果:波生坦治疗4周后,患者6MWD由(238±173.0)m增至(307±141.4)m(P=0.005);WHO心功能分级3例患者(27%)降低1级,8例患者维持原有分级不变;治疗前、后患者的肺动脉收缩压和平均压呈下降趋势,但差异无统计学意义;FMD由治疗前的2.7(2.0,3.3)%升至4.4(3.3,5.6)%(P=0.033),EID无显著变化。患者随访期间未观察到严重不良反应。结论:半剂量波生坦短期治疗,可以显著改善ASD合并PAH女性患者肱动脉内皮依赖性血管舒张功能。 Objectives: To observe the short-time effect of bosentan in female patients with congenital secundum atrial septal defect( ASD) and severe pulmonary artery hypertension( PAH). Methods: 11 female patients definitely diagnosed of ASD and PAH by right heart catheterization were enrolled and prescribed of bosentan 62. 5mg,bid for 4 weeks. 6 minutes walking distance( 6MWD),WHO heart function,echocardiographic results and branchial flow-mediated dilation( FMD) were recorded for statistical analysis before and 4weeks after the treatment. Results: 6MWD increased from( 238 ± 173. 0) m to( 307 ± 141. 4) m( P = 0. 005) after 4 weeks( P 0. 01). 3( 27%) patients decreased with 1 grade of WHO heart function classification and 8patients maintained the initial grade. No significant changes were seen in pulmonary artery systolic pressure and pulmonary artery mean pressure. Branchial FMD elevated from 2. 7( 2. 0,3. 3) % to 4. 4( 3. 3,5. 6) %( P =0. 033). No severe side effects were seen during follow-up. Conclusion: 4-weeks 'treatment of half-dose Bosentan improved FMD significantly in female patients with congenital secundum ASD and severe PAH.
出处 《心肺血管病杂志》 2015年第11期812-815,共4页 Journal of Cardiovascular and Pulmonary Diseases
关键词 内皮素受体拮抗剂 房间隔缺损 肺动脉高压 血管内皮舒张功能 Endothelin receptor antagonist Secundum atrial septal defect Pulmonary artery hypertension Vascular endothelial diastolic function
  • 相关文献

参考文献11

  • 1阮英茆.从先天性心脏病肺血管病理学资料看心外科临床发展中的困惑[J].心肺血管病杂志,2014,33(2):150-151. 被引量:2
  • 2GalieN,Rubin LJ,Hoeper M,et al.Treatment of patients with mildly symptomatic pulmonary arterial hypertension with bosentan(EARLY study):a double-blind,randomized controlled trial.Lancet,2008,371:2093-2100.
  • 3Galie N,Beghetti M,Gatzoulis MA,et al.Bosentan therapy in patients with Eisenmenger syndrome:a multicenter,doubleblind,randomized,placebo-controlled study.Circulation,2006,114:48-54.
  • 4GalièN1,Hoeper MM,Humbert M,et al.Guidelines for the diagnosis and treatment of pulmonary hypertension:the task force for the diagnosis and treatment of pulmonary hypertension of the european society of cardiology(ESC)and the european respiratory society(ERS),endorsed by the International society of heart and lung transplantation(ISHLT).Eur Heart J,2009,30:2493-537.
  • 5Corretti MC,Anderson TJ,Benjamin EJ,et al.Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery:a report of the International Brachial Artery Reactivity Task Force.J Am Coll Cardiol,2002,16,39:257-65.
  • 6Therrien J,Rambihar S,Newman B,et al.Eisenmenger syndrome and atrial septal defect:nature or nurture?Can J Cardiol,2006,22:1133-6.
  • 7陈普文,黄石安.肺动脉高压分子机制的研究进展[J].心肺血管病杂志,2014,33(1):130-132. 被引量:3
  • 8田丹,管丽华,李明飞,潘文志,蔡卫民,周达新,吕迁洲.波生坦治疗中重度特发性及先天性心脏病相关肺动脉高压40例[J].中国新药与临床杂志,2014,33(6):450-455. 被引量:12
  • 9Strange G,Keogh A,Williams T,et al.Bosentan therapy in patients with pulmonary arterial hypertension:the relationship between improvements in 6 minute walk distance and quality of life.Respirology,2008,13:674-682.
  • 10Chen SJ,Chen YF,Meng QC,et al.Endothelin-receptor antagonist bosentan prevents and reverses hypoxic pulmonary hypertension in rats.J Appl Physiol,1995,79:2122-2131.

二级参考文献55

  • 1陈新军,刘亚萍,温绍君,罗毅.肾上腺髓质素与肺动脉高压[J].中华胸心血管外科杂志,2005,21(6):381-382. 被引量:4
  • 2Rabinovitch M. Molecular pathogenesis of pulmonary arterial hy- pertension. J Clin Invest. 2012, 122 : 4306.
  • 3Deng Z, Morse JH, Slager SL, et al. Familial primary pulmonary hypertension ( Gene(i) PPH1 </i) ) Is Caused by mutations in the bone morphogenetic protein receptor-II gene. Am J Hum Gen- et, 2000, 67: 737-744.
  • 4Maehado RD, Aldred MA, James V, et al. Mutations of the TGF - 13 type II receptor BMPR2 in pulmonary arterial hypertension. Hum Murat, 2006, 27: 121-132.
  • 5Roberts KE, MeElroy JJ, Wong WP, et al. BMPP,2 mutations in pulmonary arterial hypertension with congenital heart disease. Eur Respir J, 2004, 24: 371-374.
  • 6Jiang BH, Zheng JZ, Leung SW, et al. Transactivation and in- hibitory domains of hypoxia-induciblefactor let. Modulation oftranscriptional activity by oxygentension. J Biol Chem, 1997, 272 : 19253-19260.
  • 7Suzuki H, Tomida A, Tsuruo T. Dephosphorylated hypoxia-in- ducible factor lalpha as a mediator of p53-dependent apoptosis during hypoxia. Oncogene, 2001,20:5779-5788.
  • 8Semenza GL. Regulation of physiological responses to continuous and intermittent hypoxia by hypoxia-inducible factor 1. Exp Phys- iol, 2006, 91: 803-806.
  • 9MacLean MR. Pulmonary hypertension, anorexigens and 5-HT: pharmacological synergism in action7. Trends Pharmacol Sci, 1999,20:490-495.
  • 10Kaumann AJ, Levy FO. 5-hydroxytryptamine receptors in the hu- man cardiovascular system. Pharmacol Ther,2006,111:674-706.

共引文献14

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部