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|本期目录/Table of Contents|

法舒地尔治疗先天性心脏病相关性重度肺动脉高压短期疗效观察

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2016年第1期
页码:
60-063
栏目:
临床研究
出版日期:
2015-09-15

文章信息/Info

Title:
Short-term effects of fasudil on patients with severe pulmonary arterial hypertension secondary to congenital heart disease
作者:
肖家旺; 朱鲜阳; 王琦光; 张端珍; 崔春生; 陈火元; 孟立立
（沈阳军区总医院全军心血管病研究所先心病内科，辽宁 沈阳 110016）
Author(s):
XIAO Jia-wang;  ZHU Xian-yang;  WANG Qi-guang;  ZHANG Duan-zhen;  CUI Chun-sheng;  CHEN Huo-yuan;  MENG Li-li
(Department of Congenital Heart Disease, General Hospital, Shenyang Military Area Command, Shenyang 110840, Liaoning, China)
关键词:
Rho 激酶; 法舒地尔; 心脏病; 先天性; 高血压; 肺性
Keywords:
Rho kinase;  fasudil;  congenital heart disease;  pulmonary arterial hypertension
分类号:
R541.1
DOI:
-
文献标识码:
A
摘要:
目的 探讨法舒地尔治疗先天性心脏病相关性重度肺动脉高压短期应用的有效性及安全性。方法 入选2011年1月~2012年8月我科住院的先天性心脏病相关性重度肺动脉高压患者，法舒地尔60 mg静脉滴注，每天2次，连续用药14 d后观察6分钟步行距离、血流动力学参数、超声心动图指标以及血浆N末端脑钠尿肽前体(NT-proBNP)变化情况。结果 共纳入21(男4,女17)例患者，年龄16~54(32±14)岁；用药14 d后6分钟步行距离由（445±49）m显著增加至（471±40）m，差异有统计学意义；且WHO肺动脉高压心功能分级显著改善（P<0.05）。血浆NT-pro BNP亦明显下降，从（788±623）pg/ml降低至（464±393）pg/ml（P<0.05）。右房平均压从（6.1±2.3）mmHg降低至(5.2±1.8)mmHg（P<0.05）；右向左分流量从（23±16）% 明显减少至（18±16）%（P<0.05）；而肺动脉平均压、肺血管阻力、体肺循环血流量比值、体肺循环阻力比值、股动脉氧饱和度、心脏指数等指标虽无显著统计学差异，但较用药前均有所改善，仅体循环压力及阻力均无统计学差异。结论 法舒地尔短期内应用可显著提高先天性心脏病相关重度肺动脉高压患者的运动耐量、WHO肺动脉高压心功能分级，有效改善肺动脉高压的血流动力学指标，而且安全性与耐受性良好。
Abstract:
AIM To investigate the short-term efficacy and safety of fasudil (a Rho kinase inhibitor) monotherapy in patients with severe pulmonary arterial hypertension (PAH) secondary to congenital heart disease (CHD). METHODSEnrolled in the study were 21 patients with severe PAH secondary to CHD from January 2011 to August 2012 in our Department. All patients were given basic drug treatment for PAH and then continuously given fasudil 60 mg i.v. twice a day for 14 days. After fasudil treatment, changes were observed in the 6-min walking distance according to all relevant hemodynamic parameters (including pulmonary arterial pressure, left to right and right to left shunt volume, pulmonary vascular resistance, systemic and pulmonary blood flow, systemic pressure, systemic vascular resistance, and cardiac output and femoral arterial blood oxygen saturation), anatomy parameters (including each chamber size and left ventricular ejection fraction) and plasma brain natriuretic peptide and liver and kidney functions after medication. RESULTSAfter continuous administration of fasudil for 14 days, the 6-min walking distance increased dramatically from (445±490) m to (471±40) m, with significant statistical difference. WHO cardiac functions improved significantly (P<0.05). Compared with baseline, plasma NT-proBNP significantly decreased from (788±622.61) pg/ml to (464±392.80) pg/ml (P=0.043), with significant statistical difference. Compared with baseline, mean right atrial pressure decreased from (6.12±2.26) mmHg to (5.2±1.84) mmHg (P<0.05) and right to left shunt volume significantly reduced from (22.9±16.21)% to (18.3±15.98)% (P<0.05). No significant difference was observed in mean pulmonary artery pressure, pulmonary vascular resistance, systemic and pulmonary blood flow ratio, systemic and pulmonary vascular resistance ratio, femoral arterial oxygen saturation and cardiac indexes, but all improved to some extent. No statistical differences were found in systemic arterial pressure and systemic vascular resistance and no obvious changes were seen in liver and kidney functions. CONCLUSIONShort-term treatment of fasudil is safe and well tolerated and can effectively improve exercise capacity and hemodynamic parameters in patients with severe pulmonary arterial hypertension secondary to CHD.

参考文献/References

[1]McMurtry IF,Abe K,Ota H,et al.Rho kinase-mediated vasoconstriction in pulmonary hypertension[J].Adv Exp Med Biol,2010,661:299-308.
[2]Abe K,Tawara S,Oi K,et al.Long-term inhibition of Rho-kinase ameliorates hypoxia-induced pulmonary hypertension in mice[J].J Cardiovasc Pharmacol,2006,48(6):280-285.
[3]Abe K,Shimokawa H,Morikawa K,et al.Long-term treatment with a Rho kinase inhibitor improves monocrotaline-induced fatal pulmonary hypertension[J].Circ Res,2004,94(3):385-393.
[4]Ishikura K,Yamada N,Ito M,et al.Beneficial acute effects of Rho kinase inhibitor in patients with pulmonary arterial hypertension[J].Circ J,2006,70(2):174-178.
[5]Li F,Xia W,Yuan S,et al.Acute inhibition of Rho-kinase attenuates pulmonary hypertension in patients with congenital heart disease[J].Pediatr Cardiol,2009,30(3):363-366.
[6]Satoh K,Fukumoto Y,Shimokawa H.Rho-kinase:Important new therapeutic target in cardiovascular diseases[J].Am J Physiol Heart Circ Physiol,2011,301(2):H287-H296.
[7]Doggrell SA.Rho-kinase inhibitors show promise in pulmonary hypertension[J].Expert Opin Investig Drugs,2005,14(9):1157-1159.
[8]Fujita H,Fukumoto Y,Saji K,et al.Acute vasodilator effects of inhaled fasudil,a specific Rho-kinase inhibitor,in patients with pulmonary arterial hypertension[J].Heart Vessels,2010,25(2):144-149.
[9]Jiang X,Han ZY,Wang Y,et al.Hemodynamic variables and clinical features were correlated to serum uric acid in patients with pulmonary arterial hypertension[J].Chin Med J(Engl),2008,121(24):2497-2503.
[10]Benza RL,Miller DP,Gomberg-Maitland M,et al.Predicting survival in pulmonary arterial hypertension:insights from the Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management(REVEAL)[J].Circulation,2010,122(2):164-172.
[11]Oka M,Fagan KA,Jones PL,et al.Therapeutic potential of Rho A/Rho kinase inhibitors in pulmonary hypertension[J].Br J Pharmacol,2008,155(4):44-54.
[12]Viswanathan S,Kumar RK.Assessment of operability of congenital cardiac shunts with increased pulmonary vascular resistance[J].Catheter Cardiovase Interv,2008,71(5):665-670.

备注/Memo

备注/Memo:
收稿日期：2014-11-02.
通讯作者：朱鲜阳，主任医师，主要从事结构性心脏病影像诊断和介入治疗 Email：xyangz@yahoo.com.cn
作者简介：肖家旺，住院医师,硕士 Email：xjw492918837@126.com
更新日期/Last Update: 2015-09-16