体外心脏震波(CSWT)治疗冠心病的疗效、安全性和方法学研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
冠心病是指冠状动脉粥样硬化使血管管腔狭窄或阻塞,或(和)冠脉功能性改变(痉挛)导致心肌缺血缺氧或坏死而引起的心脏病。以药物治疗为基础,辅以冠脉介入、外科开胸搭桥、激光心肌打孔和心肌干细胞移植等多种冠心病治疗方法相继问世。众多方法在使千千万万患者受益的同时,由于疗效有限或疗效短暂或费用昂贵或技术复杂或并发症凶险或存在治疗禁忌证或处于研发期……等等,迄今尚无任何1种方法可以根治或基本解决冠心病。如何突破冠心病治疗局限、促进人体自身”冠脉搭桥”形成是国际上冠心病治疗的热点也是难点。体外心脏震波(CSWT)是一种新型的血管再生疗法,它通过低能脉冲波产生的机械剪切力和空穴效应促进心肌内微血管修复再生,缓解心绞痛,提高运动耐力。昆明医学院第一附属医院率先在国内引进了该治疗系统,并成立科技攻关项目小组,现综合1年的应用情况作一报告。
     目的评价CSWT的安全性和有效性,探讨CSWT治疗中国冠心病患者的适应证和禁忌证,总结CSWT的方法学要点和技术细节。
     方法2008年12月-2009年12月入住我院心内科的陈旧性心肌梗死、稳定型心绞痛和不稳定型心绞痛患者55例。病史1-16年。55例患者分为治疗A组、治疗B组和对照C组。A组20例,男18例,女2例,年龄35-79岁;B组21例,男17例,女4例,年龄41-79岁;C组14例,男12例,女2例,年龄55-81岁。所有患者经冠状动脉造影或多层螺旋CT冠状动脉造影提示冠脉中、重度狭窄、经正规药物(伴或不伴支架或旁路移植)治疗后,仍有胸闷、气促发作,运动耐力差,1年内因上述相同问题住院2次以上。排除标准为急性心肌梗死1月内;左室射血分数低于30%的血流动力学不稳定者;严重的慢性阻塞性肺病。使用多巴酚丁胺负荷超声心动图(DSE)和基础及负荷状态下99m锝甲氧基异丁基异腈(99mTc-MIBI)心肌灌注显像(MPI)识别并定位缺血/存活心肌:使用活动平板运动试验(Treadmill)和动态心电监测分析系统(Holter)评价运动耐力、缺血程度和范围;使用瑞士STORZ MEDICAL公司生产的CSWT仪行心脏CSWT,依治疗周期不同分为2个亚组:A组3月内完成9次治疗,B组1月内完成9次治疗,之后根据病情需要重复1-4个疗程。治疗时经机载实时超声探头锁定缺血靶区,每个靶区实施-1-0-+1两两组合的9点治疗,每点发放200次脉冲,每次脉冲能量为0.09mJ/mm2。整个过程实时心电、血压、血氧饱合度监测。随访采用NYHA心功能分级、加拿大心血管学会(CCS)心绞痛分级、西雅图心绞痛量表(SAQ)、6分钟步行试验(6MWT)、硝酸甘油用量、Treadmill和Holter行临床评估;采用静息及负荷状态下收缩期峰值应变率(PSSR)和MPI评价局部心肌收缩功能和血流灌注,测量静息及负荷状态下局部心肌运动幅度,测量左室舒张末内径(LVDd)、左室舒张末容积(EDV),左室收缩末容积(ESV)和左室射血分数(LVEF)。A, B 2组在震波前、第3次及第9次震波后分别行心肌酶学和肝肾功能检测。结果治疗组41例患者除第6个月随防时有1例死亡、2例行PCI术外,其余38例均按期及顺利完成相关疗程的CSWT,无心力衰竭、心悸晕厥、呼吸困难、出血、栓塞或休克等并发症发生。55例患者完成了0月、3个月、6个月的随访,A组18人、B组10人、C组14人完成了第12个月随防。A组7人,B组17人,C组5人完成了期满12个月的Treadmill和Holter随防。CSWT治疗前后的心肌酶学和肝肾功能指标差异无统计学意义(P>0.05)。DSE和负荷MPI共同检出存活/缺血心肌节段94个,A组和B组各35个,C组24个。A组1例诊断为“缺血性心肌病“的患者,在随防至6月、接受了2个疗程CSWT后猝死于家中,死因考虑为恶性心律失常致呼吸心跳骤停。A组和B组各有1例CABG患者在CSWT后6月因胸闷加重再次行CA加PCI术。A组2例患者治疗前心电图表现为胸导V1-V5 T波倒置,接受3次CSWT后T波由倒置转为直立维持至12月随防时。与C组相比,A组在随访3月、6月及12月、B组在随访12月时,6MWT. CCS及SAQ明显改善(P<0.05),A、B 2组在12月随访时硝酸脂类用量明显减少(P<0.01)。与C组相比,基础和负荷状态下的MPI. A组在6月随访时明显增加(P<0.05);PSSR,A组在3月随访时负荷态增强(P<0.05),之后6月和12月随访,A组在基础和负荷状态下均明显增强(P<0.01)。与治疗前相比,治疗组多项临床指标和形态学指标明显改善(P<0.05),A组包含指标更多,维持时间更长。70个节段中,65.71%的MPI属于轻度改善。Treadmill与治疗前相比,A、B 2组伴随随访时间延长,运动时间明显增加,ST段下移幅度明显减少(A:P<0.01;B:P<0.05)。Holter与治疗前相比,ST段下移幅度及ST-T异常导联数A组在3个随防时期显著降低(下移幅度P<0.01;ST-T异常P<0.05);B组在3月和6月明显降低(P<0.05)。房性早搏发作次数B组在3月随防时较治疗前明显减少(P=0.021)。室性早搏发作次数A组在12月随防时较治疗前明显减少(P=0.03)。而C组以上指标改变甚微,EDV、ESV在3个月、6个月和12个月随访时较治疗前显著增加(P<0.05)。
     结论1、在国内首次开展采用CSWT治疗CAD的系统研究,为CSWT在中国推广提供了科学依据。
     2、该血管再生疗法是无创、安全、有效的,在治疗初期就可以使患者心绞痛症状缓解、冠脉储备增加、多项心肌灌注指标改善、生活质量提高。
     3、总结出适合中国患者的相关适应证和禁忌证:适应证中不仅包括了接受PCI/CABG和规范药物治疗后、仍有心绞痛频繁发作者;还包括了影像学提示冠脉中重度狭窄、正规药物治疗期间仍有胸闷、气促发作,运动耐力差,不能或不愿行冠脉血运重建的心绞痛人群。
     4、DSE联合负荷MPI可以发现更多微血管性缺血心肌,确保了CSWT对靶心肌治疗的精确性和有效性。
     5、国外普遍采用的3月治疗周期优于课题组首创的1月治疗周期;震波范围不应局限于每个缺血节段的9点治疗,而应扩大到20-40点治疗;在患者无新的心肌缺血证据时,不应盲目增加震波次数。
Coronary artery disease (CAD) is recognized as a leading cause of adult mortality worldwide. Current therapies in the treatment of CAD include drug interventions, percutaneous coronary intervention (PCI), coronary artery bypass graft (CABG) and transmyocardial laser revascularization (TMR). However, these approaches are invasive and often inadequate in the treatment of advanced CAD and are associated with serious cardiovascular risks and complications. Elevated patient risk factors including increased age and co-morbidities such as hypertension and diabetes may further limit treatment options. Prognosis for patients diagnosed with end stage CAD without indication of PCI or CABG surgery is poor. Thus, it is critical to note that a large number of CAD patients continue to experience angina, decreased exercise tolerance and the risk of sudden death. Understandably, there is need for a safe and effective, noninvasive approach toward the treatment of CAD. Cardiac shock wave therapy (CSWT) is a novel, noninvasive intervention that can ameliorate myocardial ischemia and improve cardiac function. To further investigate the potential benefits of CSWT we performed a preliminary study of CSWT administered regularly over a 12 month period in 41 patients with advanced CAD. Patients were clinically assessed before initiation and at 3 month,6 month and 12 month following completion of the CSWT treatment program.
     Purpose. To evaluate the feasibility and efficiency of CSWT for treatment of CAD and to establish the inclusion and exclusion criteria and summarize the methodological outlines of CSWT in China.
     Methods. Fifty-five patients with 1-16 years history of chronic angina pectoris admitted to the Cardiology Department from August 2008 to December 2009 were enrolled in this study. All patients received standard medical treatment and the CSWT procedure was explained to each patient. Patients were divided group A and group B. twenty patients in group A,18 males, ranged from 55-70 years were applied 9 sessions on 35 segments within 3 month. Twenty-one patients in group B,17 males, ranged from 41-79 years were applied 9 sessions on 35 segments within 1 month. Fourteen patients in group C,12 males, ranged from 55-81 years were enrolled as medical-controlled group. The reasons for hospitalization included repeated episodes of chest tightness, shortness of breath, and fatigue after PCI/CABG. Exclusion criteria were absence of the inclusion criteria, acute myocardial infarction (AMI) with 1 month, uncontrolled heart failure, severe chronic obstructive pulmonary disease. Prior to initiation of CSWT, all patients received Dobutamine stress echocardiography (DSE) and 99mTc-MIBI myocardial perfusion imaging(MPI) at rest and stress state to identify areas of ischemic myocardium. Treadmill and Holter were performed to assess the exercise tolerance and ischemic threshold. Under the guidance of echocardiography, we applied shock wave in R-wave-triggered manner with low energy(0.09mJ/mm2) at 200 shoots/spot for 9 spots (-l--0-+1 combination). During the procedure, ECG, blood pressure, breathing, and blood oxygen saturation were concurrently monitored and vital signs and symptoms including palpitations, chest pain, breathing difficulty, and dizziness were closely inquired. We followed-up all patients at 3 month,6 month and 12 month after 1st time therapy and enzyme markers of myocardial, liver and renal injury were measured prior to CSWT and at 3 times,9 times following completion of CSWT. The efficacy of CSWT was assessed using the Canada Cardiovascular Society (CCS) angina scale, NYHA class, SAQ scale (angina),6-min walk test (6MWT) and nitroglycerin dose. Myocardial perfusion, regional myocardium function and wall motion were evaluated by MPI, peak systolic strain rate (PSSR) and M-mode measure at rest and Dob stress state. The left ventricular ejection fraction (LVEF), end-diastolic volume (EDV)and end-systolic volume(ESV) were measured by Simpson method.
     Results. A total of 94 viable ischemic myocardial segments were identified by stress MPI and SE。Forty-one patients with 70 ischemic segments underwent the CSWT without procedural complications or adverse effects. Patients did not experience any serious cardiovascular health complications (heart failure, bleeding, thrombosis, shock or death) either during or after CSWT. At 6 month follow-up, one died because of serious heart failure not related to CSWT and two CABG patients received the stent implantation because of refractory angina pectoris. There was ECG changing from T wave inversion to positive T wave after 3 times CSWT and stay the course of 12 month. Plasma levels of enzyme markers had no significant difference before and after CSWT. CSWT significantly improved symptoms, as evaluated by NYHA, CCS class score, SAQ score,6MWT and the use of nitroglycerin. Also, CSWT improved myocardial perfusion and regional myocardium function as evaluated by MPI and PSSR both at rest and stress. 65.71% segments have a mild improvement in MPI of 70 ischemic segments. The exercise tolerance and ischemic threshold were increased significantly measured by treadmill and Holter. There was a evident decrease in the number of ventricular premature in group A and the number of atrial premature in group B. Whereas, group C had little difference, even had a malignant tendency in EDV and ESV following 3,6 and 12 month. And many indicators improved preferably and lasted longer in group A compared with group B.
     Conclusions.
     1. We provide scientific basis of CSWT for the first time in China.
     2. CSWT is a safe and effective non-invasive intervention in the management of patients with CAD.
     3. Indications and contraindications of CSWT in China are concluded, not only for refractory CAD, but also for those chronic pectoris which are reluctant or have no condition to undergo the invasive therapy.
     4. DSE combined with MPI is a preferable method to locate the viable ischemic myocardial segments and guarantees the accuracy and effect of CSWT.
     5.9 sessions CSWT within 3 month have an advantage over the same times within 1 month. Maybe the expanded treatment areas like 20-40 spots each time can make better results. Unless there is an ischemic evidence, it is no need to repeat CSWT frequently.
引文
[1]胡大一,马长生.心脏病学实践2007[M].北京:人民卫生出版社,2007:8-18.
    [2]国家“九五”科技攻关课题协作组.我国人群心血管主要危险因素流行现状及从20世纪80年代初至90年代末的变化趋势.中华心血管病杂志,2001,29:74-80.
    [3]赵冬,吴兆苏,王薇,等.北京地区1984-1997年急性冠心病事件死亡率变化趋势(中国MONICA方案的研究).中华心血管病杂志,2000,28:14-17.
    [4]Yusuf S, Reddy S, Ounpuu S, et al. Global burden of cardiovascular disease: Part Ⅱ:variation in cardiovascular disease by specific ethnic groups and geographic regions and prevention strategies. Circulation,2001,104:2855-2864.
    [5]Weintraub WS, Jones EL, Craver JM, et al. Frequency of repeat coronary bypass or coronary angioplasty after coronary artery bypass surgery using saphenous venous grafts. Am J cardiol,1994,73:103-112.
    [6]Doyle BJ, Rihal CS, Gastineau DA, Holmes DR Jr:Bleeding, blood transfusion, and increased mortality after percutaneous coronary intervention:implications for contemporary practice. J Am Coll Cardiol 2009;53:2019-2027.
    [7]Wann S and Balkhy H:Evaluation of patients after coronary artery bypass grafting. Cardiol Rev 2009; 17:176-80.
    [8]Allen KB, Kelly J, Borkon AM, et al. Transmyocardial revascularization:from randomized trials to clinical practice. A review of techniques, evidence-based outcomes, and future directions. Anesthesiology Clin,2008,26:501-519.
    [9]Singh M, Rihal CS, Roger VL, et al. Comorbid conditions and outcomes after percutaneous coronary intervention. Heart,2008,4:1424-1428.
    [10]Beltrami P, Barlucchi L, Torella D, et al. Adult cardiac stem cells are multipotent and support myocardial regeneration.Cell,2003,114,114:763-776.
    [11]TA Khan,et al.Gene therapy progressand prospects:therapeutic angiogenesis for limb and myocardial ischemia. Gene Therapy,2003,10:285-291.
    [12]罗兴华,李凤英,王晓东.冠心病的运动疗法.解放军体育学院学报,2002,4:32-36.
    [13]Erbel R, Gutersohn A. Cardiac shock wave therapy, a successful workshop at ESC 2003 [DB/OL]. http://www.storzmedica.lch/English/News,2003-09-01.
    [14]Folberth W, KEhler G, Rohwedder A, et al. Pressure distribution and energy flow in the focal region of two different electromagnetic shock wave sources Journal of Stone Disease,1992,4 (1):108-115.
    [15]Ichioka S, Shibata M, Kosaki K, et al. Effects of shear stress on wound healing angiogenesis in the rabbit ear chamber. J Surg Res,1997,72:29-35.
    [16]Chaussy C, Brendel,W, Schmiedt E. Extracorporeal induced destruction of kidney stone by shock waves. Lancet,1980,226:1265-1268.
    [17]Mariotto S, Cavalieri E, Amelio E, et al. Extracorporeal shock waves:from lithotripsy to anti-inflammatory action by NO production. Nitric Oxide, 2005,12:89-96.
    [18]Anna R, Alessandra C, Ernesto A, et al. Nitric oxide mediates anti-inflammatory action of extracorporeal shock waves. FEBS Letters,2005,579:6839-6845.
    [19]Gutersohn A, Gaspari G.. Shock waves upregulate vascular endothelial growth factor m-RNA in human umbilical vascular endothelial cells. Circulation,2000, 102(supll):1-18.
    [20]Smith RS Jr, Agata J, Xia CF, et al. Human endothelial nitric oxide synthase gene delivery protects against cardiac remodeling and reduces oxidative stress after myocardial infarction. Life Sci,2005,76:2457-2471.
    [21]Gutersohn A, Gaspari G. Shock waves upregulate vascular endothelial growth factor m-RNA in human umbilical vascular endothelial cells. Circulation,2000, 102(supll):1-18.
    [22]Smith RS Jr, Agata J, Xia CF, Chao J. Human endothelial nitric oxide synthase gene delivery protects against cardiac remodeling and reduces oxidative stress after myocardial infarction. Life Sci,2005,76:2457-2471.
    [23]Nurzynska D, Meglio DF, Castaldo C, et al. Shock waves activate in vitro cultured progenitors and precursors of cardiac cell lineages from the human heart. Ultrasound in Med. & Biol.2007,33:1-9.
    [24]Nishida T, Shimokawa H, Oi K, et al. Extracorporeal cardiac shock wave therapy markedly ameliorates ischemia-induced myocardial dysfunction in pigs in vivo. Circulation,2004,110:3055-3061.
    [25]Uwatoku T, Ito K, Abe K, et al. Extracorporeal cardiac shock wave therapy proves left ventricular remodeling after acute myocardial infarction in pigs. Coron Artery Dis,2007,18:397-404.
    [26]Fukumoto Y, Ito A, Uwatoku T, et al. Extracorporeal cardiac shock wave therapy ameliorates myocardial ischemia in patients with severe coronary artery disease. Coron Artery Dis.,2006,17:63-70.
    [27]Khattab AA, Brodersen B, Schuermann-Kuchenbrandt D,et al. Extracorporeal cardiac shock wave therapy:first experience in the everyday practice for treatment of chronic refractory angina pectoris. Int J Cardiol,2007,121:84-85.
    [28]Kikuchi Y, Ito K, Ito Y, et al. Double-blind and placebo-controlled study of the effectiveness and safety of extracorporeal cardiac shock wave therapy for severe angina pectoris. Circulation J,2010,74:589-591.
    [29]Meluzin J, Cerny J, Frelich M, et al. Prognostic value of the amount of dysfunction but viable myocardium in revascularized patients with coronary artery disease and left ventricular disfunction. Am Coll Cardiol,1998, 32:912-920.
    [30]Jeroen B, Frans V, Don P. Time course of functional recovery of stunned and hibernating segments after surgical revascularization. Circulation,2001, 140:314-318.
    [31]Carlos C, Christopher F, Elizabeth B, et al. Dobutamine stress echocardiography identifies hibernating myocardium and predicts recovery of left ventricular function after coronary revascularization. circulation,1993,88:430-436.
    [32]Bax JJ, Wijins W, Cornel, JH, et al. Accuracy of current available techniques for prediction of functional recovery after revascularization in patients with left ventricular dysfunction due to chronic coronary artery disease:comparison of pooled data. J Am Coll Cardiol,1997,30:1451-1460.
    [33]Afidi 1, Kleiman NS, Raizner AE, et al. Dobutamine echocardiography in myocardial hibernation:optimal dose and accuracy in predicting recovery of ventricular function after angioplasty. Circulation,1995,91:663-670.
    [34]朱天刚.定量多巴酚丁胺负荷超声心动图.中华超声影像学杂志,2003,12:468.
    [35]杨跃进,杨伟宪,史荣芳,等.药物负荷超声心动图与双核素心肌显像对比检测存活心肌.2005,33(4):356-360.
    [36]Mandalapu BP, Amato M, Stratmann HG. Technetium Tc 99m sestamibi myocardial perfusion imaging:current role for evaluation of prognosis. Chest, 1999,115(6):1684-1694.
    [37]李少林,张永学主编.核医学.人民卫生出版社,2002年第五版:136-137.
    [38]何作祥.心肌灌注显像的临床应用.中华心血管病杂志,2004,32(:7)665-667.
    [39]Hachamovitch R, Berman DS, Shaw LJ, et al. Incremental prognostic value of myocardial perfusion single photon emission computed tomography for the prediction of cardiac death:differential Stratification for risk of cardiac death and myocardial infarction. Circulation,1998,97(6):535-543.
    [40]Elhendy A, Bax JJ, Poldermans D. Dobutamine stress mycardial perfusion imaging in coronary artery disease.J Nuel Med,2002,43(2):1634-646.
    [41]Sutherland GR, Di Salvo G, Claus P, et al. Strain and train rate imaging:a new clinical approach to quantifying regional myocardial function. J Am Soc Echocardiogr,2004,17:788-802.
    [42]Armstrong G, Pasquet A, Fukamachi K, et al. Use of peak systolic strain as index of regional left ventricular function:comparison with tissue Doppler velocity during Dobutamine stress and myocardial ischemia. J Am Soc Echocardiogr,2000,13:731-737.
    [1]中华医学会心血管病学分会,中华心血管病杂志编辑委员会.慢性稳定性心绞痛诊断与治疗指南.中华心血管病杂志,2007,35:195-206.
    [2]柯元南,陈纪林.不稳定性心绞痛和非ST段抬高心肌梗死诊断与治疗指南.中华心血管病杂志,2007,35:212-225.
    [3]Fukumoto Y, Ito A, Uwatoku T, et al. Extracorporeal cardiac shock wave therapy ameliorates myocardial ischemia in patients with severe coronary artery disease. Coron Artery Dis.,2006,17:63-70.
    [4]Khattab AA, Brodersen B, Schuermann-Kuchenbrandt D,et al. Extracorporeal cardiac shock wave therapy:first experience in the everyday practice for treatment of chronic refractory angina pectoris. Int J Cardiol,2007,121:84-85.
    [5]朱天刚.定量多巴酚丁胺负荷超声心动图.中华超声影像学杂志,2003,12:468.
    [6]Gottdiener SJ, Bednarz J, Devereux R, et al. American society of echocardiography recommendations for use of echocardiography in clinical trials: a report from the American society of echocardiography's guidelines and standards committee and the task force on echocardiography in clinical trials. J Am Soc Echocardiagr,2004,17:1086-1119.
    [7]Zweng A, Bachl C, Schragel D, et al. The role of dobutamine stress echocardiography in the clinical routine of a department of cardiology. Acta Med Austriaca.2001,28:123-128.
    [8]San Roman JA, Sanz Ruiz R, Ortega JR, et al. Safety and predictors of complications with a new accelerated Dobutamine stress echocardiography protocol. J Am Soc Echocardiogr.2008,21:53-57.
    [9]Mertes H, Sawada SG,Ryan T,et al.Symptoms.adverse effects and complications associated with Dobutamine stress echocardiography. experience in 1118 patients.Circulation,1993,88:15-19.
    [10]Sutherland GR, Di Salvo G, Claus P, et al. Strain and strain rate imaging:a new clinical approach to quantifying regional myocardial function. J Am Soc Echocardiogr,2004,17:788-802.
    [11]Armstrong G, Pasquet A, Fukamachi K, et al. Use of peak systolic strain as index of regional left ventricular function:comparison with tissue Doppler velocity during Dobutamine stress and myocardial ischemia. J Am Soc Echocardiogr,2000,13:731-737.
    [12]Deng YB, Liu R, Wu YH et al. Evaluation of short-axis and long-axis myocardial function with two-dimensional strain echocardiography in patients with different degrees of coronary artery stenosis. Ultrasound Med Biol.2010, 36:227-233.
    [13]Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart:a statement for healthcare professionals from the cardiac imaging committee of the council on clinical cardiology of the American Heart Association. J Nucl Cardiol,2002,9:240-245.
    [14]Mandalapu BP, Amato M, Stratmann HG. Technetium Tc 99m sestamibi myocardial perfusion imaging:current role for evaluation of Prognosis. Chest, 1999,115(6):1684-1694.
    [15]李少林,张永学主编.核医学.人民卫生出版社,2002年第五版:136-137.
    [16]何作祥.心肌灌注显像的临床应用.中华心血管病杂志,2004,32(:7)665-667.
    [17]Long Y, Mi Y, Li Y. The diagnostic value of 99mTc-MIBI myocardial perfusion imaging for coronary artery disease:a systematic review. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi.2008,25:686-693.
    [18]Kim C, Kwok YS, Heagerty P, et al. Pharmacologic stress testing for coronary disease diagnosis:a meta- analysis.Am Heart J,2001,142:934-944.
    [19]Bruce R. Exercise testing in patients with coronary artery disease. Ann Clin Res, 1971,3:323-325.
    [20]张忆湘.活动平板运动试验阳性对冠心病诊断的临床价值分析.基层医学论坛,2005,9:304.
    [21]郭继鸿,张萍.动态心电图(M).北京:人民卫生出版社,2003:630-632.
    [22]Peeters P, Mets T, The 6-minute walk as an appropriate exercise test in elderly patients with chronic heart failure. J Gerontol A Biol Sci Med Sci,1996, 54:M147-151.
    [23]张萍.六分钟步行试验及在心功能评价中的作用.中华临床医师杂志(电子版),2007,1:10-11.
    [24]Nishida T, Shimokawa H, Oi K, et al. Extracorporeal cardiac shock wave therapy markedly ameliorates ischemia-induced myocardial dysfunction in pigs in vivo. Circulation,2004,110:3055-3061.
    [25]Gibbons RJ, Chatterrjee K, Daley J. et al. ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic stable angina:a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines(Committee on Management of Patients With Chronic Stable Angina. J Am Coll Cardiol,1999,33:2092-2197.
    [26]SPertUs JA, Winders JA, Dewhurst TA, et al. Development and evaluation of the Seattle Angina Questionnaire:a new functional status measure for coronary artery disease. JAM Coll cardiol,1995 Feb; 25(2):333-341.
    [27]Wang Y, Guo T, Cai HY, et al. Cardiac shock wave therapy reduces angina and improves myocardial function in patients with refractory coronary artery disease. Clin. Cardiol.2010,33 [Epub ahead of print]
    [28]王钰,郭涛,蔡红雁,等.体外心脏震波治疗冠心病的应用研究.中华心血管病杂志,2010,38(8):711-715.
    [29]Nurzynska D, Meglio FD, Castaldo C, et al. Shock waves activate in vitro cultured progenitors and precursors of cardiac cell lineages from the human heart. Ultrasound in Med & Biol,2008,34:334-342.
    [30]Kikuchi Y, Ito K, Ito Y, et al. Double-blind and placebo-controlled study of the effectiveness and safety of extracorporeal cardiac shock wave therapy for severe angina pectoris. Circulation J,2010,74:589-591.
    [31]Mariotto,S.,Cavalieri,E.,Amelio,E., et al. Extracorporeal shock waves:from lithotripsy to anti-inflammatory action by NO production. Nitric Oxide. 2005,12:89-96.
    [32]Fisher, A.B., Chien, S., Barakat, A.I.,et al. Endothelial cellular response to altered shear stress. Am. J. Physiol.2001;28:, L529-L533.
    [33]Ichioka S, Shibata M, Kosaki K, et al. Effects of shear stress on wound healing angiogenesis in the rabbit ear chamber. J Surg Res 1997; 72:29-35.
    [34]Andre Pasternac, Martial G Bourassa. Pathogenesis of chest pain in patients with cardiomyopathies and normal coronary arteries. Inter.J.Cardiol. 1983(3):273-280.
    [35]Uwatoku T, Ito K, Abe K, et al. Extracorporeal cardiac shock wave therapy proves left ventricular remodeling after acute myocardial infarction in pigs. Coron Artery Dis.2007,18:397-404.
    [36]Ito Y, Ito K, Shiroto T, et al. Extracorporeal cardiac shock wave therapy ameliorates left ventricular remodeling after myocardial ischemia-reperfusion injury in pigs in vivo. European Heart Journal.2008.29(Abstract Supplement): 199.
    [37]Gutersohn A, Gaspari G. Shock waves upregulate vascular endothelial growth factor m-RNA in human umbilical vascular endothelial cells. Circulation.2000, 102(supll):1-18.
    [38]Dougherty CM, Dewhurst T, Nichol WP, et al. Comparison of three quality of life instruments in stable angina pectoris:Seattle Angina Questionnaire, Short Form Health Survey(SF236)and Quality of Life Index-Cardiac VersionⅢ. J Clin Epidemiol,1998,51:569-575.
    [39]Rentrop KP, Cohen M, Blanke H, et al. Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. J Am Coll Ca rdiol,1985;5:587-592.
    [40]Koerselman J, de Jaegere PP, Verhaar MC, et al.Cardiac ischemic score determines the presence of coronary collateral circulation. Cardiovasc Drugs Ther,2005,19(4):283-289.
    [41]Rihal CS, Raco DL, Gersh BJ, Yusuf S:Indications for coronary artery bypass surgery and percutaneous coronary intervention in chronic stable angina:review of the evidence and methodological considerations. Circulation 2003; 108:2439-2445.
    [42]Shimokawa H, Ito K, Fukumoto Y, Yasuda S:Extracorporeal cardiac shock wave therapy for ischemic heart disease. Shock Waves 2008;17:449-455.
    [43]Prinz C, Lindner O, Bitter T, et al:Extracorporeal cardiac shock wave therapy ameliorates clinical symptoms and improves regional myocardial blood flow in a patient with severe coronary artery disease and refractory angina. Case Report Med 2009; 2009:639594. Epub Aug 20.
    1. Erbel R, Gutersohn A. Cardiac shock wave therapy, a successful workshop at ESC 2003 [DB/OL]. http://www.storzmedica.lch/English/News,2003-09-01.
    2. Ichioka S, Shibata M, Kosaki K, et al. Effects of shear stress on wound healing angiogenesis in the rabbit ear chamber. J Surg Res 1997;72:29-35
    3. Chaussy C, Brendel,W, Schmiedt E. Extracorpo-really induced destruction of kidney stone by shock waves. Lancet.1980,1265-1268.
    4. Mariotto S, Cavalieri E, Amelio E, et al. Extracorporeal shock waves:from 1 ithotripsy to anti-inflammatory action by NO production. Nitric Oxide. 2005,12:89-96.
    5. Anna R, Alessandra C, Ernesto A, et al. Nitric oxide mediates anti-inflammatory action of extracorporeal shock waves. FEBS Letters,2005,579:6839-6845.
    6. Gutersohn A, Gaspari G. Shock waves upregulate vascular endothelial growth factor m-RNA in human umbilical vascular endothelial cells. Circulation.2000, 102(supll):1-18.
    7. Smith RS Jr, Agata J, Xia CF, et al. Human endothelial nitric oxide synthase gene delivery protects against cardiac remodeling and reduces oxidative stress after myocardial infarction. Life Sci.2005,76:2457-2471.
    8. Nishida T, Shimokawa H, Oi K, et al. Extracorporeal cardiac shock wave therapy markedly ameliorates ischemia-induced myocardial dysfunction in pigs in vivo. Circulation.2004,110:3055-61.
    9. Uwatoku T, Ito K, Abe K, et al. Extracorporeal cardiac shock wave therapy proves left ventricular remodeling after acute myocardial infarction in pigs. Coron Artery Dis.2007,18:397-404.
    10. Ito Y, Ito K, Shiroto T, et al. Extracorporeal cardiac shock wave therapy ameliorates left ventricular remodeling after myocardial ischemia-reperfusion injury in pigs in vivo. European Heart Journal.2008,29 (Abstract Supplement): 199.
    11. Ito Y, Ito K, Shiroto T, et al. Cardiac shock wave therapy ameliorates left ventricular remodeling after myocardial ischemia-reperfusion injury in pigs in vivo. Coron Artery Dis.2010,21:304-311.
    12. Fukumoto Y, Ito A, Uwatoku T, et al. Extracorporeal cardiac shock wave therapy ameliorates myocardial ischemia in patients with severe coronary artery disease. Coron Artery Dis.2006,17:63-70.
    13. Khattab AA, Brodersen B, Schuermann-Kuchenbrandt D,et al. Extracorporeal cardiac shock wave therapy:first experience in the everyday practice for treatment of chronic refractory angina pectoris. Int J Cardiol.2007,121:84-5.
    14. Kikuchi Y, Ito K, Ito Y, et al. Double-blind and placebo-controlled study of the effectiveness and safety of extracorporeal cardiac shock wave therapy for severe angina pectoris. Circ J 2010;74:589-591

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700