原发性肺动脉高压长期前列环素治疗效果评价

原发性肺动脉高压 (ＰＰＨ)是一种以肺血管阻力增加、肺动脉压升高、右心衰竭、呼吸困难为特点的病情进行性加重的罕见疾病 ,目前尚无有效疗法 ,本研究用右心导管和超声心动图检查评价前列环素连续注入的长期效果。一、资料与方法患者主要来自美国西部地区 ,符合ＰＰＨ诊断的患者 4 9例 (男 14例 ,女 3 5例 )。年龄 11～ 65岁 ,平均 4 6岁。球囊漂浮导管插入右心系统 ,采用多导生理仪记录右房压 (ＲＡＰ)、右室压 (ＲＶＰ)及肺动脉压 (ＰＡＰ)。用热稀释法测定心输出量(ＣＯ)并与心动图法测得者做相关性分析。用心动图法测定右房室压力阶差 …     

充血性心力衰竭对活体狗主动脉弹性的影响

用血管内超声等技术研究在不同被动扩张压力下,主动脉顺应性变化及硝普钠、多巴酚丁胺在心衰前后对主动脉顺应性的影响。 方法 符合条件的杂种犬七只,经右颈内静脉将一单极起搏电极送入右室心尖部,以250次/分超速起搏3～4周制成心衰模型。在心衰前、后未用药情况下分别做血流动力学(包括心率、血压、系统血管阻力)和超声心动图检查。以溴化六烃季胺阻滞神经结     

硝苯吡啶对充血性心衰的血液动力学效应

本研究的目的是探讨硝苯吡啶对心衰的血液动力学效果。 8例正常窦性心律的慢性心衰患者,年龄为31～64岁,男女各4人。血液动力学测量:采用常规心导管术或Swam-Gang导管连续测量肺动脉与压心输出量。体动脉和肺动脉压及心室内压力用Hewlett-Packard 1280c压力传感器进行测量。测量用药前(对照)和舌下含化20mg硝苯吡啶后10～30分钟的     

快速右心室起搏心力衰竭犬模型的建立

目的应用改进的快速右心室起搏的方法制备慢性心力衰竭犬模型,分析模型相应的临床和血流动力学及病理变化。方法选择比格犬12只,随机分为起搏组(7只)和对照组(5只),起搏组采用230 ppm的频率快速右心室起搏4周,之后改用180 ppm的频率维持右心室起搏4周。对照组正常喂养不处理,4周后测量相应指标。起搏组起搏前、起搏1、8周后,分别行心脏超声、血流动力学检测,之后处死取心脏做病理切片检查。结果与对照组和同组起搏前比较,起搏组犬起搏4、8周后,出现慢性心力衰竭的相应临床表现;超声心动图示各心腔内径均变大,左心室射血分数明显下降,左心导管示左心室舒张末压力增加,左心室收缩末压力及左心室内压最大上升及下降速率降低,差异有统计学意义(P<0.05,P<0.01)。结论经过改进的快速右心室起搏方法,可以产生相对稳定的慢性心力衰竭犬模型。     

应用彩色多普勒超声心动图评价终末期肾病患者肺动脉压力变化

目的 探讨应用彩色多普勒超声心动图评价终末期肾病( ESRD)及长期接受通过动-静脉通路进行血液透析的ESRD患者肺动脉高压的临床价值.方法 ESRD患者接受通过动-静脉通路进行血液透析组66例,ESRD患者无透析组42例,应用连续多普勒测量收缩期三尖瓣反流速度,并由峰速推算出收缩期三尖瓣口的跨瓣压差,进而推算出右室收缩压及肺动脉压力.透析组患者在完成透析后1h内进行超声心动图检查.结果 ESRD长期血液透析组肺动脉高压发病率、平均肺动脉压及心输出量明显增加,两组间肺动脉压及肺动脉高压发病率有显著性差异(P＜0.05).结论 彩色多普勒超声心动图能客观、无刨评价ESRD患者及经动-静脉内瘘血管通路进行血液透析的ESRD患者肺动脉压力,早期诊断ESRD相关肺动脉高压,有助于临床早期干预ESRD相关肺动脉高压,并改善预后.     

快速右房起搏致猪心动过速性心肌病

目的通过快速右房起搏建立心动过速性心肌病模型,观察该病不同时期血流动力学改变和心肌重构情况。方法将15头滇南小耳猪,按随机区组的方法分为起搏1周组、起搏4周组、假手术组,分别采用240次/分快速起搏右房1周、4周和只手术不起搏。运用超声心动图和左心导管检查测量窦性心律下的血流动力学参数并观察心脏大体结构变化。经Masson染色检测心肌纤维化,测定心肌胶原容积分数(CVF),比较房、室重塑差异。结果起搏1周组左室射血分数、左室收缩末压、左室压力上升最大速率、左室压力下降高峰速率均较假手术组降低(P<0.01);起搏4周组上述血流动力学指标继续恶化,且腔室扩大、室壁变薄,(P<0.01)。心房、心室CVF随起搏时间的延长逐渐增加(P<0.01)。结论采用快速右房起搏成功制作了心动过速性心肌病模型,证实该病是以严重的左、右室舒缩功能障碍,腔室扩大,室壁变薄,心肌重塑为特征。     

人重组生长激素对充血性心力衰竭猪强心作用的实验研究

目的　研究人重组生长激素 (hr- GH)对实验动物猪的强心作用。方法　利用起搏器快速 (2 2 0～ 2 4 0次 / min)起搏心脏 1 w造成猪充血性心力衰竭模型。将其分为心衰生长激素组、心衰生理盐水组 ,另设正常对照组 ,每组 5头猪。生长激素组给予 hr- GH 0 .5 mg· kg- 1· d- 1肌肉注射 ,连续 1 5 d;生理盐水组给予等量生理盐水肌肉注射 1 5 d。结果　左室舒张末压 (LVEDP)、心输出量 (CO)、外周血管阻力、、室内最大上升速度(+dp/ dtmax)均有明显改变 (P<0 .0 5或 <0 .0 1 )。结论　 hr- GH对充血性心力衰竭模型猪有强心作用 ,利用人工心脏起搏器快速起搏心脏制造猪充血性心力衰竭模型合理、适用、可靠。     

肺动脉高压患者超声心动图特点及其临床意义分析

目的探讨肺动脉高压(PH)患者超声心动图的特点及临床意义。方法选择2011年1月至2015年6月我院收治的经右心导管检查确诊的PH患者38例作为观察组,以同期在我院进行健康体检的志愿者35名作为对照组,对两组研究对象进行超声心动图检查比较。结果观察组患者的右室舒张末期容积(RVEDA)、右室和右房收缩末期容积(RVESA、RAESA)均明显高于对照组;而右室面积变化分数(RVFAC)、左室收缩末期容积(LVESV)、左室舒张末期容积(LVEDV)均明显低于对照组,差异有统计学意义(P0.05)。两组对象左室射血分数(LVEF)比较差异无统计学意义(P0.05)。采用超声心动图估测及右心导管检查观察组患者得到的平均肺动脉收缩压(PASP)分别为(83.51±6.02)mm Hg和(79.25±4.83)mm Hg,两种方法检测得出的结果比较差异无统计学意义(P0.05);Pearson相关性分析结果显示,通过超声心动图检查估测得到的PASP值与右心导管检测得到的结果呈正相关(r=0.824,P=0.003)。结论与正常健康人比较,肺动脉高压患者超声心动图各项指标均出现不同程度的异常,超声心动图估测患者的PASP与右心导管测得值相关性良好;超声心动图能够较好地检测PH患者肺动脉压的改变、反映患者心功能变化,检查操作简便、重复性好、费用低,具有较高的临床应用价值。     

血流频谱法估测慢性肺疾病患者肺动脉压的研究

目的研究慢性肺疾病患者肺动脉血流频谱与肺动脉压的关系，以期寻找能较好反映肺动脉压的指标，并推导多元回归方程，以便能更准确估测肺动脉压力。方法在行右心导管检查同时，用超声心动图观察５４例慢性肺疾病患者肺动脉血流频谱。将脱机分析的１４个多普勒参数分别与肺动脉压进行相关分析，并且进行多元逐步回归分析。结果多普勒参数右室射血前期（ＰＥＰ）／加速时间（ＡｃＴ）、平均加速度（ＡｃＶｍ）、速度积分（ＶＩ）／［心电图Ｑ～Ｔ点间期（ＱＴ）×最大速度（Ｖｍａｘ）］及右室射血时间（ＲＶＥＴ）／ＱＴ与肺动脉压相关较好；推算出多元回归方程。结论多元回归方程能用于慢性肺疾病患者的无创性肺动脉压估测     

Doppler超声心动图技术评价肺栓塞患者右心功能的价值

肺栓塞是一种常见的心血管疾病 ,无论是急性肺栓塞或栓塞性肺动脉高压均可能影响右心功能 ,因此评价肺栓塞患者的右心功能对该疾病的诊断、治疗及评价预后均有重要的临床意义。早在 1992年 Torbicki等[1] 就探讨了关于多普勒超声心动图在肺栓塞诊断中的意义及其优势。本文就 Doppler超声心动图技术对肺栓塞患者右心功能的评价作一简要的综述。1　二维超声心动图用传统的二维超声心动图方法评价右心室收缩功能。右室的收缩功能主要包括以下指标 :(1)右室的容量 ;(2 )右室舒张末期和收缩末期容积 ;(3)右室每搏量 ;(4 )右室心输出量 ;(5 )右室…     

Effects of chronic, rapid right atrial pacing on cardiac hemodynamics and myofibrillar ATPase activity in piglets

OBJECTIVES: To determine whether chronic, rapid right atrial pacing in newborn neonatal piglets has any effects on cardiac hemodynamics, and whether these changes are associated with intrinsic alterations in cardiac contractile potential as shown by cardiac myofibrillar calcium ATPase activity. BACKGROUND: Although many studies have examined aspects of heart function in models of supraventricular tachycardia, far less is known about its effects in neonatal animals. It is thought that rapid pacing induces a dilated cardiomyopathy in immature pigs. ANIMALS AND METHODS: Two-week-old piglets underwent rapid right atrial pacing (250 beats/min) for 10 days, and their cardiac hemodynamic response was monitored. To obtain subcellular mechanistic information regarding systolic dysfunction, cardiac myofibrils were isolated and calcium adenosine triphosphatase activity was measured. RESULTS: Control piglets had a heart rate of 185 beats/min at the end of the experimental period. Pulmonary artery flow, pulmonary artery flow index and left ventricular end-diastolic diameter were unchanged as a function of rapid, chronic right atrial pacing. Aortic pressure decreased in the paced piglets. Left atrial pressure increased approximately threefold in the paced animals. Left ventricular end-systolic diameter was also significantly higher after pacing, but left ventricular end-diastolic diameter was unchanged. Left ventricular shortening fraction was depressed approximately 50%. Myofibrillar calcium adenosine triphosphatase activity was significantly depressed as a function of pacing. CONCLUSIONS: Neonatal piglets undergoing chronic supraventricular tachycardia exhibit systolic dysfunction in the absence of dilation. The depression in contractile protein calcium adenosine triphosphatase activity provides information at a subcellular level regarding the mechanism responsible for this cardiomyopathy.     

Immediate enhancement of left ventricular relaxation by coronary artery bypass grafting: intraoperative assessment

We investigated the effect of coronary artery bypass grafting on the rate of left ventricular relaxation as defined by the time constant for isovolumetric relaxation, T, measured in milliseconds. Completeness of relaxation at rapid heart rates was determined by comparison of the relationship between left ventricular pressure and echocardiographic left ventricular cross-sectional cavity area during rapid ventricular pacing with that obtained after a prolonged diastole when the ventricle was maximally relaxed. Twelve patients with coronary artery disease had significantly higher T values (94.5 +/- 6.2) than six patients without coronary artery disease who were undergoing other open heart procedures (39.5 +/- 5.0, p less than .001). T was significantly reduced after coronary artery bypass grafting (68.2 +/- 5.1, p = .007), but was unchanged in the six control patients after cardiopulmonary bypass (37.8 +/- 4.5, p = .54). Similar changes were found during rapid pacing to 100, 120, and 140/min. Incomplete relaxation was detected in three of 10 (heart rate 120 beats/min) and nine of 11 (heart rate 140 beats/min) patients with coronary artery disease and this decreased to 0 of 10 (heart rate 120 beats/min) and six of 11 (heart rate 140 beats/min) patients after coronary artery bypass. Incomplete relaxation before bypass at a heart rate of 120 beats/min averaged 0.9 +/- 0.3 mm Hg. At a heart rate of 140 beats/min, incomplete relaxation averaged 5.6 +/- 1.6 mm Hg before and 1.4 +/- 0.5 mm Hg after bypass. Intake of beta-blockers or calcium-channel blockers, body temperature, and systolic blood pressure were not found to be related to these changes. We conclude that immediately after coronary artery bypass relaxation of left ventricular muscle is enhanced and incomplete relaxation at rapid heart rates is less likely. The most probable cause of this improvement in ventricular relaxation after coronary artery bypass grafting is relief of ischemia.     

快速右心室起搏致充血性心力衰竭犬可控性动物模型的建立

目的 建立不同严重程度的心力衰竭动物模型。方法 35只犬随机分为5组,分别接受假手术,快速右心室起搏1周、2周、3周和4周,通过动物心衰症状的轻重和血液动力学指标评价心力衰竭的严重程度,RIA法测定血浆内皮素浓度。结果 随着起搏时间的延长,动物逐渐出现相应的症状,血液动力学参数显示心力衰竭严重程度逐步增加,血浆内皮素浓度逐渐上升并与心力衰竭严重程度明显相关。结论 快速起搏致充血性心力衰竭犬模型在病程上具有可控性的优点,是一种较为理想研究充血性心力衰竭的实验模型。     

比索洛尔对快速右室起搏犬心室重塑的影响

１９条犬随机分为心脏起搏组（Ｐ，ｎ＝７），起搏加比索洛尔干预组（ＰＢ，ｎ＝６）和对照组（Ｃ，ｎ＝６）。Ｐ与ＰＢ组动物均以２５０次／分钟频率持续右室起搏４周。起搏后Ｐ组动物均出现心力衰竭表现。组织病理学显示心肌细胞浊肿，质膜水肿，肌节排列紊乱，部分肌丝溶解、断裂。ＰＢ组起搏后肺楔压升高和心排量降低幅度以及心肌病理改变程度均显著轻于Ｐ组。以上表明，比索洛尔可以减轻这一心肌病模型的心肌损害程度。     

Reduced cardiac reserve in amiodarone-treated pigs after cardiopulmonary bypass and cardioplegic arrest.

An animal model was designed for blinded study to elucidate whether cardiac pump failure after heart surgery in amiodarone-treated patients is due to interference between the drug and the surgical procedures. Seventeen adult pigs were treated with amiodarone for 30 days (study animals, 1,400 mg/day, n = 9; untreated control animals, n = 8) followed by exposure to cardiopulmonary bypass and topical cold cardioplegic arrest (Bretschneiders solution) for 60 min. Apart from 1 g of calcium, no inotropic agents were administered. Cardiac reserve was tested by ventricular pacing (200 beats/min for 30 min or until exhaustion). No difference in hemodynamic status was observed between the treated and the untreated group before pacing. Pacing duration in the amiodarone-treated pigs was 10 +/- 3 versus 22 +/- 4 min in control pigs (p less than 0.05). Only one amiodarone-treated pig survived 30 min of pacing compared with five control pigs (11% vs. 63%, p less than 0.05). The following variables differed significantly in the two groups during pacing: cardiac output, left ventricular pressure, arterial pressure and peak positive and negative first derivative of left ventricular pressure (dP/dt). Most marked were the changes in peak positive dP/dt, indicating a compromised systolic function. The two groups did not differ in preload or afterload at any time during the experiments.     

Hemodynamic effects of left ventricular pacing site in an animal model of heart failure

BACKGROUND: This study investigates how different left ventricular epicardial and endocardial pacing sites influence hemodynamic performance in an animal model of heart failure (HF). METHODS: In six adult sheep, dilated HF was induced by rapid pacing. Subsequently, endocardial left ventricular stimulation was performed using a 64-electrode basket catheter. Epicardial pacing was achieved with temporary electrodes. RESULTS: Baseline cardiac output (CO) was 2.7 +/- 0.4 l/min and improved significantly with lateral wall epicardial and endocardial stimulation (3.6 +/- 0.7 and 3.8 +/- 0.65 l/min), whereas right ventricular pacing led to lower CO (2.1 +/- 0.5 and 2.0 +/- 0.9 l/min). In the optimal pacing location arterial pressure, pulmonary capillary wedge pressure (pcwp) and LV diameters improved significantly. Right ventricular pacing impaired hemodynamics, while no change was observed in the LV inferior wall and apex pacing. CONCLUSION: Endocardial and epicardial pacing of the lateral wall led to an improvement in LV function while right ventricular pacing induced a further reduction of LV performance. As this optimal pacing site cannot always be reached via the coronary sinus, surgical implantation of epicardial electrodes should be considered in all non-responding patients.     

Electrical Remodeling and Atrial Dilation During Atrial Tachycardia are Influenced by Ventricular Rate: Role of Developing Tachycardiomyopathy

INTRODUCTION: Atrial fibrillation (AF) and congestive heart failure (CHF) are two clinical entities that often coincide. Our aim was to establish the influence of concomitant high ventricular rate and consequent development of CHF on electrical remodeling and dilation during atrial tachycardia. METHODS AND RESULTS: A total of 14 goats was studied. Five goats were subjected to 3:1 AV pacing (A-paced group, atrial rate 240 beats/min, ventricular rate 80 beats/min). Nine goats were subjected to rapid 1:1 AV pacing (AV-paced group, atrial and ventricular rates 240 beats/min). During 4 weeks, right atrial (RA) and left ventricular (LV) diameters were measured during sinus rhythm. Atrial effective refractory periods (AERP) and inducibility of AF were assessed at three basic cycle lengths (BCL). After 4 weeks of rapid AV pacing, RA and LV diameters had increased to 151% and 113% of baseline, whereas after rapid atrial pacing alone, these parameters were unchanged. Right AERP (157+/-10 msec vs 144+/-16 msec at baseline with BCL of 400 msec in the A-paced and AV-paced group, respectively) initially decreased in both groups, reaching minimum values within 1 week. Subsequently, AERP partially recovered in AV-paced goats, whereas AERP remained short in A-paced goats (79+/-7 msec vs 102+/-12 msec after 4 weeks; P < 0.05). Left AERP demonstrated a similar time course. Inducibility of AF increased in both groups and reached a maximum during the first week in both groups, being 20% and 48% in the A-paced and AV-paced group, respectively. CONCLUSION: Nature and time course of atrial electrical remodeling and dilation during atrial tachycardia are influenced by concurrent high ventricular rate and consequent development of CHF.     

Short-term effects of right atrial, right ventricular apical, and atrioventricular sequential pacing on myocardial oxygen consumption and cardiac efficiency in patients with coronary artery disease.

OBJECTIVE--To investigate the short-term effects of atrial, atrioventricular, and ventricular pacing on myocardial oxygen consumption, myocardial blood flow, and cardiac efficiency in patients with coronary artery disease. DESIGN--Prospective study that started at the end of diagnostic coronary angiography in 13 patients and was performed during atrial, atrioventricular, and ventricular pacing for 5 min, in random order, at 20 beats/min more than the heart rate of the patient's positive exercise test. A Baim thermodilution catheter in the coronary sinus was used to measure myocardial blood flow and oxygen consumption and a pacing electrode at the right ventricular apex and a catheter in the pulmonary artery were used to estimate cardiac output. SETTING--Referral cardiology centre. PATIENTS--13 patients with coronary artery disease (mean (SD) age 53(5) years). All the patients had a positive exercise test and most of them (77%) had left anterior descending coronary artery disease. RESULTS--Mean (SD) cardiac output increased by 0.5(1.6) l/min during atrial pacing, increased by 0.1(1) l/min during atrioventricular pacing, and decreased by 0.8(1.2) l/min during ventricular pacing (P = 0.01 v atrial pacing, P = 0.03 v atrioventricular pacing). Diastolic pulmonary pressure increased by 6(4) mm Hg during atrial pacing, by 8.6(4) mm Hg during ventricular pacing (P = 0.02 v atrial pacing), and by 7.5(4.7) mm Hg during atrioventricular pacing. Changes in myocardial oxygen consumption and cardiac efficiency during the different pacing modes were similar. CONCLUSION--Atrial, atrioventricular, and ventricular pacing had similar short-term effects on myocardial oxygen consumption, myocardial blood flow, and cardiac efficiency in patients with coronary artery disease. Ventricular pacing, however, did not increase cardiac output.