实时三维超声心动图评价轻度肺动脉高压患者右室功能的研究

目的 探讨应用三维超声心动图测量右室容积及射血分数评价轻度肺动脉高压患者右室功能的变化.方法 应用三维超声心动图及常规二维超声心动图测量40例轻度肺动脉高压患者以及20例正常人的右室收缩末期容积(RVESV)、右室舒张末期容积(RVEDV)、右室每搏量(RVSV)、右室射血分数(RVEF).结果 正常组与肺动脉高压组二维超声测量RVESV、RVEDV、RVSV、RVEF进行比较,无统计学差异(P>0.05);正常组与肺动脉高压组三维超声测量RVESV、RVEDV、RVSV相比较有统计学差异(P<0.05);RVEF较对照组无统计学差异(P>0.05).结论 实时三维超声心动图能通过测量右室容积及射血分数来评价轻度肺动脉高压患者右室功能的变化.     

体表超声测量RVEF值监测肺栓塞及溶栓的动物实验

目白；为深入研究肺栓塞的诊断和治疗，用中国试验小型猪制备急性肺栓塞的人工动物模型。方法：选用脲激酶30万单位，在栓塞后1-2h行溶栓治疗，为了掌握这一全过程的病理变化和治疗结果，采用ECG，UCG进行常规监测，肺动脉造影，核医学等检查方法多次进行了观察，应用了专用的计算机软件，通过体表2-D超声方法测量RVEF值。结果：栓塞前RVEF为53.2%-64.9%。属正常范围；栓塞后RVEF均降低10%以上，为35.3%-51.1%；溶栓后逐渐恢复到正常范围，整个变化过程符合临床病理变化，也证实了体表2-D超声方法在观测肺动脉栓塞和肺动脉高压方面的实用性，结论：急性肺栓塞可使右室功能降低，及时溶栓治疗可使右室功能迅速恢复，通过2-D超声测量RVEF可为明确诊断，观察疗效提供重要信息。     

ET-1与肺动脉高压右室功能相关关系的研究

目的:探讨内皮素-1(ET-1)在肺动脉高压(PH)右室功能损害、右室重塑病理生理过程中的作用和相关关系.方法:PH组58例,非PH组23例,对照组20例.超声心动图分别测量三尖瓣前向血流及反流频谱、肺动脉前向血流频谱;ET-1的测定采用非平衡法.结果:PH组与非PH组及正常对照组相比,E、E/A显著降低,A增加,PV显著降低,IRT、ICT显著延长,Tei指数显著增加(P<0.001);血浆ET-1浓度显著增高,与肺动脉收缩压正相关.ET-1与E/A、PV负相关,与A、IRT、ICT正相关.结论:ET-1参与了肺动脉高压及右室功能减退的病理生理过程.     

超声心动图急性肺栓塞溶栓治疗的评估

目的应用超声心动图技术观察急性肺栓塞患者溶栓抗凝治疗前后肺动脉栓子、右心结构及收缩功能的改变。方法前瞻性非随机对照研究,对2002年12月至2006年4月间经肺动脉CT或肺血管造影证实的30例急性肺栓塞患者行溶栓治疗,应用经胸超声心动图观察治疗前、治疗后24～30h、1个月的肺动脉栓子、主肺动脉及其分支内径、右房室内径,右室前壁运动幅度、右室舒张末期容积、右室射血分数,三尖瓣返流、肺动脉收缩压等指标。结果30例急性肺动脉栓塞患者溶栓治疗24～30h后右房室结构明显改善,表现为右房长径及横径、右室前后径及横径、主肺及右肺动脉内径、右室舒张末期容积与治疗前比较明显回缩(P<0.01),右室前壁运动幅度、右室射血分数有所增加(P<0.01),肺动脉收缩压明显下降(P<0.01);治疗后1个月后右房室大小、主肺及右肺动脉内径、右室舒张末期容积、右室前壁运动幅度及肺动脉收缩压等仍有恢复(P<0.05或P<0.01)。5例患者主肺动脉和/或右、左肺动脉内检出栓子,溶栓后栓子逐渐消失。结论超声心动图可动态、实时、无创评价急性肺动脉栓塞溶栓治疗效果,尤对血栓的溶解、右房室结构、右室超负荷及肺动脉高压的变化有独到的价值。     

Tei指数评价系统性红斑狼疮右室功能的变化

目的探讨超声心动图测定右室Tei指数评价系统性红斑狼疮(SLE)患者右室功能的价值。方法对30例正常对照者及56例SLE患者进行超声心动图右室功能检测。结果与对照组相比,SLE患者组的右室等容收缩时间与等容舒张时间之和(ICT IRT)延长,右室射血时间(ET)及肺动脉血流加速时间(AT)缩短,右室Tei指数显著增高(P<0.01)。结论SLE患者在右心构型尚无明显改变时,右室功能及肺动脉血流已出现异常。多普勒超声心动图检测右室Tei指数有可能为SLE患者的早期病情判断与诊治提供重要信息。     

脉冲多普勒估测高原健康成人肺动脉压及其与右室的相关性

应用脉冲多普勒超声心动图，通过分析肺动脉血流频谱估测了７５例高原（３６５８ｍ）地区健康世居、移居成人的肺动脉压及其与右室的关系．结果表明：高原健康世居成人的肺动脉压及右室内径与平原健康成人无差异。高原健康移居成人的肺动脉压及右室内径较健康世居成人差异显著，并随移居时间的延长而增高，短期移居者两者间呈良好的相关性（ｒ＝０．７６９）．肺动脉压升高的原因由移居早期的肺血管收缩为主转为晚期肺循环血量增加为主。移居时间５年以内者，其空间隔厚度与世居健康成人无差异；超过５年者，其室间隔增厚，两者相差非常显著．     

结缔组织病合并肺动脉高压患者的右室功能:多普勒组织成像技术研究

目的采用多普勒组织成像技术分析结缔组织病（CTD）合并肺动脉高压（PAH）患者右室功能和各项指标之间的关系。方法34例CTD合并PAH患者以及32例无PAH的对照者进行超声心动图检查,评价右室大小和功能。同时采用多普勒组织成像（DTI）评价右室侧壁、室间隔和左室侧壁的应变曲线及三尖瓣环的运动速度。结果DTI结果显示与对照组相比,CTD合并PAH患者的右室应变峰值、三尖瓣环收缩速度和舒张早期速度显著降低,同时存在右室不同步。结论DTI技术可以反映CTD合并PAH患者的右室功能状况。     

定量组织速度成像评价急性心肌梗死后的右室功能

目的 应用QTVI技术测定三尖瓣环的运动速度和幅度评价初次急性心肌梗死后的右室功能。方法 研究对象分为急性下壁心梗组20例。急性前壁心梗组16例和对照组20例，用QTVI技术中的时间速度积分测定三尖瓣环右室收缩期，舒张早期与晚期运动幅度；应用QTVI技术中的组织速度成像测量右室收缩期，舒张早期与晚期的运动峰速度。结果 下壁心梗组和前壁心梗组右室游离壁三尖瓣环Vs,VE,VE/VA,SD与DED均显著低于对照组，下壁心梗组患者降低尤为显著。下壁心梗组和前壁心梗组LVEF均显著低于对照组。前壁心梗组LVEF减低更明显。结论 应用QTVI测量右室游离壁三尖瓣环运动速度和幅度可作为评价心肌梗死患者右室舒缩功能的新指标。有助于指导治疗和随访观察。心肌梗死患者左、右室功能相互影响。     

20例右室双流出口伴主动脉瓣下型室间隔缺损患儿的术后护理

报告了20例右室双流出口伴主动脉辩下室间隔缺损患儿的术后护理.术后密切监测循环功能的变化.防治低心排综合'征的发生;对术前合并肺动脉高压的患儿.术后持续监测肺动脉压力,积极预防和处理肺高压危象;密切观察,及早发现.及时处理全身毛细血管渗漏综合征;同时加强呼吸道管理,防治肺部并发症;及时行床边二维超声心动图,及早发现和处理左或右室流出道梗阻.本组死亡2例,其余18例经积极治疗和护理治愈出院.随访2个月至5年,心功能均恢复良好.     

组织多普勒成像技术对肺动脉高压患者右心室功能的评价

目的运用右室侧壁三尖瓣环组织多普勒TDI-Tei指数评价肺动脉高压患者右心室功能。方法 30例健康者作为对照组,90例肺动脉高压患者依肺动脉压程度分为轻、中、重度3个亚组,各30例,超声常规测量右心室横径、右心房横径、肺动脉主干内径,下腔静脉呼吸动度,并测量三尖瓣前叶瓣环的组织多普勒频谱,测量其右室Tei指数,进行比较分析。结果肺动脉高压轻、中、重组患者右心结构及肺动脉出现渐进性重构,右心室Tei指数敏感地反映肺动脉压力及右心功能变化。结论肺动脉高压患者右心室Tei指数升高,右心室整体功能降低,且与肺动脉收缩压相关。TDI-Tei指数可以灵敏地反映肺动脉高压患者右心室功能的变化,是评价其右心室整体功能的较好指标。     

Right Ventricular Tachycardia with Left Bundle Branch Block and Inferior Axis Morphology: Clinical and Arrhythmological Characteristics in 15 Patients

Fifteen patients (mean age 30) presenting with right ventricular tachycardia (VT) of the outflow tract type (left bundle branch block with inferior axis morphology), in the absence of obvious organic heart disease, were studied. Seven patients had palpitations, one presyncope and seven were asymptomatic. The echo and/or angiographic findings were normal in 11 patients (73%), suggesting arrhythmogenic right ventricular dysplasia (ARVD) in three (20%) and dubious in one (7%). The VT was sustained in three patients (20%), nonsustained (11 +/- 6 beats) in twelve (80%), inducible during exercise in two out of 15 patients (13%) and with ventricular stimulation in one out of eight (12.5%). Four patients were treated with sotalol, three with Class IC drugs and one with amiodarone. At follow-up of 36 +/- 30 months, only three patients had VT recurrences due to drug withdrawal. In conclusion: (1) abnormal echo and/or angiographic findings suggested that ARVD was observed in a minority of the patients (22%); (2) the low inducibility of VT and the good response to sotalol suggested a possible mechanism of abnormal automaticity; and (3) at a 3-year follow-up the prognosis appeared to be good in both patients with or without echo-angiographic signs suggestive of right ventricular dysplasia.     

Acute and Chronic Hemodynamic Impact of Total Right Ventricular Disarticulation

Right ventricular disarticulation is a radical operation to control ventricular arrhythmias in patients with arrhythmogenic right ventricular dysplasia. This report describes the acute and chronic hemodynamic impact of the procedure based on our experience of five patients with life-threatening arrhythmias unresponsive to medical therapy who have undergone total disarticulation of the right ventricle. Although all patients suffered acute postoperative hemodynamic problems, all survived and returned to an excellent functional class. Right ventricular disarticulation should be considered in patients with drug refractory ventricular tachycardias due to arrhvthmogenic right ventricular dysplasia when the arrhythmia either poses a life threat or results in chronic morbidity.     

Evaluation and course of an unusual case of arrhythmogenic right ventricular dysplasia

We report a case of a 42-year-old Caucasian man who presented with isolated right ventricular failure and atrial fibrillation without ventricular arrhythmia. In this report, we describe accurate evaluation by MR imaging confirmed by histopathologic findings as well as imaging progression of this unusual case of arrhythmogenic right ventricular dysplasia.     

A Comparison of Ventricular Function During High Right Ventricular Septal and Apical Pacing after His-Bundle Ablation for Refractory Atrial Fibrillation

This study compares LV performance during high right ventricular septal (RVS) and apical (RVA) pacing in patients with LV dysfunction who underwent His-bundle ablation for chronic AF. We inserted a passive fixation pacing electrode into the RVA and an active fixation electrode in the RVS. A dual chamber, rate responsive pulse generator stimulated the RVA through the ventricular port and the RVS via the atrial port. Patients were randomized to initial RVA (VVIR) or RVS (AAIR) pacing for 2 months. The pacing site was reversed during the next 2 months. At the 2 and 4 month follow-up visit, each patient underwent a transthoracic echocardiographical study and a rest/exercise first pass radionuclide ventriculogram. We studied nine men and three women (mean age of 68 +/- 7 years) with congestive heart failure functional Class (NYHA Classification): I (3 patients), II (7 patients), and III (2 patients). The QRS duration was shorter during RVS stimulation (158 +/- 10 vs 170 +/- 11 ms, P < 0.001). Chronic capture threshold and lead impedance did not significantly differ. LV fractional shortening improved during RVS pacing (0.31 +/- 0.05 vs 0.26 +/- 0.07, P < 0.01). RVS activation increased the resting first pass LV ejection fraction (0.51 +/- 0.14 vs 0.43 +/- 0.10, P < 0.01). No significant difference was observed during RVS and RVA pacing in the exercise time (5.6 +/- 3.2 vs 5.4 +/- 3.1, P = 0.6) or the exercise first pass LV ejection fraction (0.58 +/- 0.15 vs 0.55 +/- 0.16, P = 0.2). The relative changes in QRS duration and LV ejection fraction at both pacing sites showed a significant correlation (P < 0.01). We conclude that RVS pacing produces shorter QRS duration and better chronic LV function than RVA pacing in patients with mild to moderate LV dysfunction and chronic AF after His-bundle ablation.     

Demonstration of Entrainment and Presence of Slow Conduction During Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

During VT in two cases with arrhythmogenic right ventricular dysplasia, entrainment criteria, constant fusion beats except for the last entrainment beat, progressive fusion, and a localized conduction block associated with interruption of VT, were demon strated with rapid ventricular pacing performed during VT. Furthermore, a long conduction interval was present during entrainment from the pacing site to the earliest activation site during VT. indicating the presence of a slow conduction area. VT in these cases was, thus, due to reentry with an area of slow conduction within the circuit.     

Cardiac function in open-chest dogs after left to right ventricular shunting and right coronary artery occlusion

Summary. Patients with acquired ventricular septal defect (VSD) after myocardial infarction have a particularly bad prognosis if right ventricular function is severely impaired. The significance of an ischaemic right ventricular free wall on cardiac function during interventricular shunting was examined in open-chest dogs. An external interventricular shunt could be opened and closed at will, and by occlusion of the right coronary artery (RCA), a part of the right ventricular free wall was rendered ischaemic. Aortic flow decreased by 8±2% when the shunt was opened in the presence of a normal right ventricle, and by 16±2% (difference: P<0.05) in the presence of right ventricular ischaemia. Aortic flow fell by 19±3% when the RCA was occluded. Right ventricular dyskinesia was demonstrated after occlusion of RCA, by recording segment lengths in the right ventricular free wall. The dyskinesia was aggravated when the shunt was opened. The left ventricle exerted a ‘negative’ work on the ischaemic right ventricular free wall. Retention of blood in the right ventricle, with a subsequent decline in left ventricular filling and an almost unchanged interventricular shunting of blood, explain why aortic flow fell more when the shunt was opened in the presence of right ventricular ischaemia.     

Distinctive Response of Arrhythmogenic Right Ventricular Disease to High Dose Isoproterenol

HAISSAGUERRE, M., ET AL.: Distinctive Response of Arrhythmogenic Right Ventricular Disease to High Dose Isoproterenol. Arrhythmogenic right ventricular disease is a potential cause of ventricular arrhythmias. Diagnosis is important due to the risk of sudden death, particularly as first symptom. Diagnosis is based on the angiographic demonstration of abnormal right ventricular morphology and function, while the sensitivity of noninvasive tests is relatively low. Following a particular observation studied in 1984, we prospectively assessed the diagnostic value of high dose isoproterenol infusion in 44 patients with an angiographically determined arrhythmogenic right ventricle. A continuous infusion of isoproterenol (8–30 µg/min) was administered during a 3-minute period, regardless of the obtained heart rate. In a control group of 50 patients without structural heart disease, isoproterenol induced a monomorphic ventricular tachycardia salvo in only one patient (2%). In patients with an arrhythmogenic right ventricle, isoproterenol induced one or more ventricular tachycardia runs in 39/44 cases (88%): one triplet in three patients, several runs in 23 patients and a sustained ventricular tachycardia in 13 patients. Arrhythmia was polymorphous in 85% of cases, but left bundle branch block morphelogy was the predominant pattern. In conclusion, high dose isoproterenol is a highly sensitive test for the diagnosis of arrhythmogenic right ventricular disease.     

Activation of the Right Ventricular Apical Electrogram during Ventricular Tachycardia: Suitahility for Synchronizing Intracavitary Cardioversion

An intravascular catheter positioned in the right ventricular apex has been used for intracavitary cardioversion in patients with recurrent ventricular tachycardia. We examined the timing of the right ventricular apical electrogram during sinus rhythm and ventricular tachycardia (VT) in order to determine if this signal could be used to synchronize the delivery of a countershock. Sixty-three distinct morphologies of VT were observed in 33 patients undergoing electrophysiologic testing with programmed stimulation. Regardless of VT morphology or site of origin, the bipolar right ventricular electrogram always occurred within the peripheral QRS complex during ventricular tachycardia. Relative timing occurred within the QRS ranging from the initial 13% of the QRS to the last 12%. When all episodes of VT were examined, the timing of the right ventricular electrogram did not correlate linearly with the peak of the ECG, but the right ventricular electrogram occurred within 60 ms of the peak ECG in 83% of episodes of ventricular tachycardia. In one case of arrhythmogenic right ventricular dysplasia, the right ventricular electrogram occurred 160 ms after the peak ECG in ventricular tachycardia, a time when delivery of a countershock may have precipitated ventricular fibrillation. Six of these patients underwent cardioversion utilizing an intracavitary catheter and external generator. Acceleration of VT, or conversion to ventricular fibrillation, occurred following two of 27 shocks (7.4%). The right ventricular electrogram occurred the latest within the QRS complex in the two patients who developed acceleration of the tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)