疏血通改善低氧肺动脉高压作用与NO通路相关性

目的观察疏血通降低低氧肺动脉高压患者肺动脉压力作用与NO通路间的相关性。方法将34例确诊低氧肺动脉高压患者随机分为对照组及疏血通组,分别给予常规治疗和常规加疏血通治疗,分别测量治疗前及用药2周后两组患者mPAP、RVAW及RVAW/LVPW变化情况,采用Western Blot法测定治疗前、后两组患者组织中NOs、NO含量的变化,采用SPSS13.0软件分析数据。结果疏血通组及对照组治疗后mPAP、RVAW均明显降低(P<0.05),RVAW/LVPW比值下降(P<0.05),疏血通组及对照组治疗后组织中NOs、NO含量均明显增高(P<0.05),疏血通组mPAP、RVAW、RVAW/LVPW比值下降较对照组下降更为明显(P<0.05),疏血通组较对照组治疗后组织中NOs、NO含量增高更明显(P<0.05)。结论疏血通可降低低氧肺动脉高压患者肺动脉压力,其降低肺动脉压力作用可能与激活NOs提高组织中NO含量相关。     

肾上腺髓质素与缺氧性肺动脉高压的关系

目的本研究探讨缺氧对肾上腺髓质素(AM)合成分泌的影响及AM在缺氧性肺动脉高压中的作用和意义。方法制备大鼠缺氧性肺动脉高压模型,分为对照组和缺氧组(10,20,30d)。每组6只。慢性肺心病患者23例,对照组16名。测量肺动脉压力和右心室收缩最大上升速率。应用放射免疫法检测血浆和支气管肺泡灌洗液中AM含量的动态变化。测定慢性肺心病患者急性期和缓解期血浆AM含量变化。结果缺氧组实验大鼠肺动脉压和右心室最大上升速率高于对照组(P<0.01);血浆和支气管肺泡灌洗液中AM含量高于对照组(P<0.01),且与肺动脉高压变化趋势一致。慢性肺心病患者不同病期血浆AM亦明显高于对照组(P<0.01)。结论AM参与缺氧性肺动脉高压的病理生理过程,在肺血管张力调节中起重要作用。局部和全身性AM增高可能是机体自身内源性抗损伤的代偿反应。     

定量组织速度显像与应变率显像技术评价COPD患者右心室功能的价值

目的应用定量组织速度显像(quantita tissue velocity imaging,QTVI)和应变率显像(strain rate imaging,SRI)检测COPD患者右心室功能。方法对89例COPD患者及32例健康对照组行常规超声心动图及组织多普勒成像检查,并计算右室Tei指数。结果 COPD患者肺动脉高压组(pul monary hypertension,PH)右心系统增大,右心室前壁增厚,主肺动脉内径增宽(P<0.01);PH组三尖瓣环右室游离壁处Vs、Ve、Vs/Ve均减低,Tei指数增高,随肺动脉压力增高更为显著;右室游离壁各节段峰值运动速度沿心室壁长轴方向递减,COPD患者右心室游离壁Vs、Ve、SRs、SRe均显著降低。结论 COPD患者右心室局部与整体功能已经受损,肺动脉高压患者右心室功能受损更重,组织速度显像和应变率显像能有效评价COPD患者右心室功能。     

COPD患者静息和运动时右心室功能(两种放射性核素技术的比较)

重症COPD 患者常发生肺动脉高压.慢性肺泡缺氧引起肺血管结构上的改变及肺血管阻力和肺动脉压力的增加,导致右心室肥大及肺心病.右心室射血分数(RVEF,可作为右心室功能指标,与肺动脉压及肺血管阻力指数呈负相关.用放射性核素~(99m)锝(~(99m)Tc)血池和~(81m)氪(~(81m)Kr)平衡心室显影术测定24例COPD 患者静息及次极量运动时~(99m)To RVEF 及~(81m)Kr RVEF,     

长期无创机械通气对终末期肺心病患者右心室结构和功能变化的临床观察

目的观察长期无创机械通气对肺心病右心室结构及功能的改善作用。方法采用病例-对照研究,对纳入本研究患者随机分为观察组（27例）与对照组（25例）,观察组在常规治疗基础上,采用长期无创机械通气治疗1年,观察治疗前后肺动脉收缩压、右心室结构参数如右心室流出道内径（RVOT）、右心室舒服张末期内径（RVD）、右心室壁厚度（RVWT）、右肺动脉内径（RPA）、左、右心室内径的比值（LV/RV）和脑钠肽前体（pro-BNP）等指标。结果两组患者治疗后pro-BNP明显降低,与治疗前比较差异有统计学意义（P〈0.01）,且观察组治疗后较对照组下降更明显,差异有统计学意义（P〈0.05）;两组患者治疗后肺动脉收缩压显著降低,同治疗前比较差异有统计学意义（P〈0.05）,但治疗后两组差异无统计学意义（P〉0.05）。两组患者治疗后右心室各结构参数显著改善,同治疗前比较差异具有统计学意义（P〈0.05,〈0.01）,但治疗后两组组间比较差异无统计学意义（P〉0.05）。pearson相关分析显示肺动脉收缩压同右心室各结构参数呈显著正相关（r=0.47-0.65）,P〈0.01）。结论长期无创机械通气可以明显降低肺心病患者肺动脉高压,改善右心室结构和功能。     

131例慢性肺原性心脏病患者心电图分析

慢性肺原性心脏病（简称肺心病）由于肺组织、肺血管或胸廓的慢性病变引起肺组织结构和（或）功能异常，产生血管阻力增加，肺动脉压力增高，使右心室扩张或肥厚。心肌重构主要表现为右心室肥大的心电图改变。现对131例慢性肺心病患者的心电图表现分析如下。     

维拉帕米治疗慢性阻塞性支气管炎患者的肺动脉高压

慢性阻塞性支气管炎患者的死亡原因主要是肺心病,而肺心病的发展是由于肺阻力和肺动脉压升高。为研究维拉帕米对肺动脉高压的治疗作用,观察慢性阻塞性支气管炎加重期患者30例,男20例,女10例,年龄21～65岁,平均46岁。病程5～15年,均有中度阻塞型呼吸功能障碍。临床X线和心电图检查没有查出肺心病的表现。进行多普勒超声心动图和心振动图(Kinetocardiogram)检查,查出肺阻力和肺动脉压升高(P<0.01),右心室前壁厚度增加(P<0.05),右室收缩力降低,证明有隐匿性肺心病。     

内源性硫化氢与高原地区慢性肺心病肺动脉高压的相关性研究

目的探讨内源性硫化氢(H2S)与高原地区慢性肺心病肺动脉高压的相关性。方法高原地区慢性肺心病稳定期患者72例和健康对照组40例,分别测定血浆H2S、内皮素-1(ET-1)、平均肺动脉压(mPAP)、动脉血氧分压(PaO2)和二氧化碳分压(PaCO2)。结果肺心病稳定期患者血浆H2S、PaO2水平显著低于健康对照组(均P<0.01),而血浆ET-1、mPAP和PaCO2水平显著高于健康对照组(均P<0.01)。肺心病组患者血浆H2S水平与ET-1、mPAP、PaCO2呈显著负相关(分别为r=-0.718、-0.692、-0.556,均P<0.01),与PaO2呈显著正相关(r=0.583,P<0.01)。结论内源性H2S可能参与了高原肺心病患者肺动脉高压的发生发展,血浆H2S作为一种无创指标监测PAH的严重程度和预后具有一定意义。     

超声心动图二维斑点追踪技术评价慢性阻塞性肺疾病患者右心室收缩功能

目的:应用超声心动图二维斑点追踪技术评价慢性阻塞性肺疾病患者(COPD)右心室收缩功能,研究二维斑点追踪技术参数用于评价不同肺动脉高压程度COPD患者右心室收缩功能的可行性。方法:研究纳入COPD患者37例,根据肺动脉收缩压程度分为:肺动脉压正常组,肺动脉高压组。同时选取19例健康成人作为对照组。所有受试者均进行肺功能测定和超声心动图检查,比较三组之间右心室收缩功能的差异。结果:COPD患者无肺动脉高压组和肺动脉高压组的右心室面积变化率,纵向右心室室间隔应变,径向右心室室间隔应变,纵向右心室整体心内膜应变均小于对照组(P0.05);PH组纵向右心室游离壁应变,纵向右心室室间隔应变,纵向右心室整体心内膜应变小于NPH组(P0.05);PH组纵向右心室游离壁应变,径向右心室游离壁应变,纵向右室整体心肌应变,径向右室整体心肌应变小于对照组(P0.05)。结论:超声心动图二维斑点追踪技术可以用于评价COPD患者右心室收缩功能,相比常规的用于评价右心室收缩功能的超声心动图参数更加敏感。     

超声心动图评价急、慢性肺栓塞患者右心室重构的研究

目的:探讨超声心动图技术评价急、慢性肺栓塞患者右心室功能及重构的临床价值。方法:选取急性肺栓塞患者30例(急性肺栓塞组)和慢性肺栓塞患者30例(慢性肺栓塞组),另选30例健康者为正常对照组。二维超声测量右心室前壁厚度(RVAWTd);多普勒超声测量三尖瓣反流压力阶差(TRPG)及肺动脉压力(SPAP);实时三维超声心动图(RT-3DE)技术测量各组患者的右心室舒张末期容积(RVEDV)、右心室收缩末期容积(RVESV)及右心室射血分数(RVEF);组织多普勒成像技术(TDI)测量三尖瓣环心肌运动舒张早期峰值速度(Em)、舒张晚期峰值速度(Am)及Em/Am。结果:与正常对照组比较,急性肺栓塞组及慢性肺栓塞组RVAWTd、TRPG、SPAP、RVEDV、RVESV、Am值增大(P<0.01～0.05),Em、Em/Am、RVEF值减小(P<0.01);与急性肺栓塞组比较,慢性肺栓塞组TRPG、SPAP、RVAWTd、RVEDV值均增大(P<0.01～0.05)。结论:急、慢性肺栓塞患者可发生右心室功能变化及形成右心室重构,慢性肺栓塞患者较急性肺栓塞患者更为严重,超声心动图评价肺栓塞患者右心室重构简便、客观、有效。     

Hemodynamic correlates of right ventricular ejection fraction measured with gated radionuclide angiography

Right ventricular function was studied in 60 patients with equilibrium gated radionuclide angiography. The mean (± standard deviation) right ventricular ejection fraction in 20 normal subjects was 53 ± 6 percent, a value in agreement with previous data from both radionuclide and contrast angiographie studies. This value was similar (55 ± 7 percent) in 11 patients with coronary artery disease but normal left ventricular function.Radionuclide measurements of right ventricular ejection fraction were correlated with right heart hemodynamics. There was a significant negative linear correlation between right ventricular ejection fraction and mean pulmonary arterial pressure (r = ?0.82) and between right ventricular ejection fraction and right ventricular end-diastolic pressure (r = ?0.67). Furthermore, patients with elevated right ventricular enddiastolic pressure and mean pulmonary arterial pressure had a more severely depressed ejection fraction than did those with an elevated mean pulmonary arterial pressure alone.Thus, an abnormal value for right ventricular ejection fraction by gated radionuclide angiography in the absence of primary right ventricular volume overload suggests abnormal right heart pressures, whereas a normal value excludes severe pulmonary arterial hypertension or an elevated right ventricular end-diastolic pressure.     

Right ventricular diastolic pressure in coronary artery disease

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P < 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P < 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P < 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.     

Pulmonary hypertension and respiratory failure in the development of right ventricular hypertrophy in patients with chronic obstructive airway disease

The high incidence of right ventricular hypertrophy in patients with chronic obstructive pulmonary disease is a well-known fact. In clinical medicine according to our present status of thinking, severe impairment of ventilatory function and pulmonary hypertension are the two essential prerequisites for right ventricular involvement. To investigate this accepted assumption we studied 51 patients with chronic obstructive pulmonary disease, while they were in a remission period. The patients were subjected to clinical examination, chest roentgenography, spirometry, blood gas examination, electrocardiography, vectorcardiography, echocardiography, and right heart catheterization. The majority of the patients with significantly compromised ventilatory function and abnormal blood gases had right ventricular hypertrophy with elevation of the pulmonary artery pressure. Two subgroups of patients could be distinguished: One included 15 patients (29.4% of all patients) with normal pulmonary artery pressure and evidence of right ventricular hypertrophy. In this subgroup are included 10 patients (19.6% of all patients) showing mild ventilatory impairment and mild hypoxaemia. The second subgroup consisted of 5 patients (9.8% of all patients) with elevated mean pulmonary artery pressure at rest and right ventricular hypertrophy showing relatively mild ventilatory impairment and moderate hypoxaemia. Two conclusions could be drawn: (1) the pulmonary artery pressure at rest could be normal despite the evidence of right ventricular hypertrophy, and (2) a mild ventilatory impairment does not exclude an elevated pulmonary artery pressure or the development of right ventricular hypertrophy in patients with chronic obstructive pulmonary disease.     

Effect of single lung transplantation on pulmonary hypertension in patients with end stage fibrosing lung disease.

OBJECTIVE--To investigate the effect of successful single lung transplantation on pulmonary haemodynamic variables and right ventricular function. DESIGN--Pulmonary haemodynamic variables and right ventricular function were measured at right heart catheterisation after single lung transplantation. The results were compared with the preoperative pulmonary haemodynamic variables measured at the time of assessment for transplantation. SETTING--A tertiary referral centre. PATIENTS--Five survivors of single lung transplantation performed for end stage lung disease. INTERVENTIONS--Cardiac catheterisation in all five patients at a mean of 18 months postoperatively. Preoperative catheter data were available for comparison in four. Right heart pressures and cardiac output were measured and right ventricular angiography was performed. Perfusion scans performed for clinical reasons were used to assess the percentage of cardiac output passing through each lung. MAIN OUTCOME MEASURES--Right heart pressures, cardiac output, right ventricular function, percentage perfusion to lungs. RESULTS--After operation mean peak right ventricular pressure fell from 53 mm Hg to 33 mm Hg, mean pulmonary artery pressure from 33 mm Hg to 18 mm Hg, total pulmonary resistance from 11.2 U x m2 to 5.8 U x m2, and pulmonary arteriolar resistance from 8.9 U x m2 to 3.6 U x m2. Pulmonary artery wedge pressure and cardiac index were unchanged. Right ventricular function improved in all patients. The transplanted lung received most of the cardiac output. CONCLUSION--In patients with moderate pulmonary hypertension and right ventricular dysfunction secondary to end stage fibrosing lung disease single lung transplantation was followed by an improvement in pulmonary haemodynamic variables and right ventricular function.     

Effect of single lung transplantation on pulmonary hypertension in patients with end stage fibrosing lung disease.

OBJECTIVE--To investigate the effect of successful single lung transplantation on pulmonary haemodynamic variables and right ventricular function. DESIGN--Pulmonary haemodynamic variables and right ventricular function were measured at right heart catheterisation after single lung transplantation. The results were compared with the preoperative pulmonary haemodynamic variables measured at the time of assessment for transplantation. SETTING--A tertiary referral centre. PATIENTS--Five survivors of single lung transplantation performed for end stage lung disease. INTERVENTIONS--Cardiac catheterisation in all five patients at a mean of 18 months postoperatively. Preoperative catheter data were available for comparison in four. Right heart pressures and cardiac output were measured and right ventricular angiography was performed. Perfusion scans performed for clinical reasons were used to assess the percentage of cardiac output passing through each lung. MAIN OUTCOME MEASURES--Right heart pressures, cardiac output, right ventricular function, percentage perfusion to lungs. RESULTS--After operation mean peak right ventricular pressure fell from 53 mm Hg to 33 mm Hg, mean pulmonary artery pressure from 33 mm Hg to 18 mm Hg, total pulmonary resistance from 11.2 U x m2 to 5.8 U x m2, and pulmonary arteriolar resistance from 8.9 U x m2 to 3.6 U x m2. Pulmonary artery wedge pressure and cardiac index were unchanged. Right ventricular function improved in all patients. The transplanted lung received most of the cardiac output. CONCLUSION--In patients with moderate pulmonary hypertension and right ventricular dysfunction secondary to end stage fibrosing lung disease single lung transplantation was followed by an improvement in pulmonary haemodynamic variables and right ventricular function.     

丹参川芎嗪治疗慢性肺源性心脏病急性发作的疗效

目的：观察丹参川芎嗪注射液对慢性肺源性心脏病急性发作患者肺动脉压（PAP）、动脉氧分压（PaO。）、C反应蛋白（CRP）和内皮素-1（ET-1）的影响。方法：40例慢性肺源性心脏病肺动脉高压患者被随机分为两组,常规治疗组：20例,接受常规治疗;观察组：20例,在常规治疗基础上加用丹参川芎嗪。另选20例健康查体者作为健康对照组。观察治疗后各组PAP、PaO：、CRP、ET-1水平和左室射血分数（LVEF）变化,并进行分析。结果：治疗后与常规治疗组比较,观察组总有效率明显提高（75％比90％）,PaOz[（83．87±14．53）mmHg比（92．95±13．54）mmHg]显著升高,平均肺动脉压（mPAP）[（55．43±9．65）mmHg比（45．52±8．89）mm-Hg]显著下降,CRP[（6．37±2．12）mg／L比（3．29±0．84）mg／L]和ET-1[（52．37±20．79）ng／L比（40．29±16．04）ng／L]水平明显下降（P〈0．05～〈0．01）。两组治疗后LVEF升高幅度无显著差异（P〉0．05）。结论：对于慢性肺心病急性发作患者丹参JIJ芎嗪注射液能显著提高临床疗效,改善右心功能,降低平均肺动脉压,改善内皮功能,抑制炎症反应。     

长期低氧暴露对健康青年男性心脏结构和功能的影响

目的 通过对长期低氧暴露下健康青年男性心脏彩超基础数据的分析比较,揭示低氧暴露下心脏结构和功能的变化特征,探索防治高原肺动脉高压及慢性高原性心脏病的临床意义。 方法 纳入37名健康青年男性,采用低氧暴露前后自身对照的方法,利用心脏彩超测量左心房内径（LAD）、右心房内径（RAD）、左心室内径（LVD）、主动脉内径（AOD）、室间隔厚度（VST）、左室后壁厚度（LVPWT）、肺动脉内径（PAD）、右室流出道内径（RVOT）、左室短轴缩短率（LVFS）、左心室射血分数（LVEF）、左室舒张早期充盈流速（LVEDFV）、左室舒张晚期充盈流速（LVLDFV）、左室舒张早期/晚期充盈流速比（E/A）和肺动脉收缩压(PASP),进行对比分析。 结果 低氧暴露后,HR显著升高（P<0.01）,LVEF、LVFS及E/A均显著降低(均P<0.01);低氧暴露对心脏结构和功能有显著影响,低氧暴露后LAD、LVD、AOD、VST、LVPWT均显著降低（均P<0.01）,RAD（P<0.05）、PAD、RVOT（P<0.01）均显著升高。低氧暴露后,56.8%的受试对象肺动脉收缩压明显增高。PAH-组在低氧暴露后LVEDFV及E/A显著降低(均P<0.01),LVLDFV显著升高(均P<0.01);而PAH+组在低氧暴露后LVEF、LVFS、LVEDFV及E/A显著降低(均P<0.01),在低氧暴露前,PAH+组受试对象LVFS和LVEF均显著高于PAH-组(均P<0.05);PAH+组△LVFS和△LVEF的变化幅度均高于PAH-组（均P<0.01）。 结论 长期高原低氧暴露可引起肺动脉压升高以及心脏结构和功能发生显著变化;低氧暴露前LVFS和LVEF基础水平较高者或更易成为PAH易感人群。     

Right ventricular function at rest and during exercise in aortic and mitral valve disease

Right ventricular function at rest and during exercise was examined in a group of patients with symptomatic aortic or mitral valve disease, or both. The right ventricular ejection fraction was less than 45% in 22 of 36 patients at rest and in 12 of 17 subjects at symptom-limited, supine bicycle exercise. The right ventricular ejection fraction failed to increase more than 5% with exercise in 17 of 17 patients. The central venous pressure was greater than 5 mm Hg in 18 of 36 patients at rest and in 13 of 17 patients at maximal exercise. There was a significant inverse relation between rest right ventricular ejection fraction and mean pulmonary artery pressure (r = -0.47, p less than 0.05) and between rest right ventricular ejection fraction and mean central venous pressure (r = -0.39, p less than 0.05). There was no significant relation between the exercise values of these variables. In individual patients, the changes in right ventricular ejection fraction and pulmonary artery pressure with graded exercise were nonlinear. It is concluded that right ventricular function is not a simple function of pulmonary artery pressure at rest or during exercise in aortic and mitral valve disease. Less than one-quarter of the variation in right ventricular ejection fraction at rest can be explained by the variation in pulmonary artery pressure, and the finding of a normal (greater than 45%) right ventricular ejection fraction does not reliably exclude the possibility of pulmonary hypertension in a patient with valvular heart disease.     

房间隔缺损患者手术前后Tei指数与右心功能相关

目的:探讨应用Tei指数评价房间隔缺损(ASD)患者手术前后右心室功能的变化,评估介入及手术的近期疗效。方法:应用多普勒超声技术测定47例ASD(其中26例伴肺动脉高压)术前及术后3月的右室横径(RVDd)、右室射血分数(RVEF)、肺动脉收缩压(PASP)及Tei指数,25例健康成人作为对照组。结果:ASD患者的RVDd及右室Tei指数较正常对照组明显增大;肺动脉高压组的RVDd,ASD大小及右室Tei指数较无肺动脉高压组明显增大。经介入或手术治疗后,肺动脉高压阴性组患者右室Tei指数较术前降低,较对照组无统计学意义;肺动脉高压组右室Tei指数较术前降低,但仍较对照组大。结论:ASD患者右心功能有减退,介入及手术治疗对肺动脉高压阴性组患者右心功能改善近期疗效明显;对肺动脉高压组患者右心功能改善近期疗效不显著。