实时三维超声对室间隔缺损的直视效果及影响因素分析

目的探讨实时三维超声（RT3DE）对室间隔缺损（VSD）全貌的直视效果及其影响因素。 方法应用RT3DE对238例VSD患者进行检查，其中包括法洛四联症（TOF）36例、完全型心内膜垫缺损（TECD）2例和十字交叉心2例。获取并切割“全容积三维”图像，寻找最佳视角显示病变结构全貌。 结果RT3DE对中型和大型VSD（直径≥5mm）的直视效果优于小型VSD（〈5mm）。可显示缺损的形状、部位及毗邻结构。胸骨旁四腔位和心底短轴位RT3DE图像效果最佳，胸骨旁长轴位及心尖五腔位次之。 结论VSD的大小、部位及三维图像质量是决定RT3DE观察效果的主要因素。RT3DE可清晰直视中型及大型VSD的全貌。     

实时三维超声心动图在先天性心脏病诊断中的应用

目的探讨实时三维超声心动图(RT-3DE)对先天性心脏病的诊断价值.方法选取56例先天性心脏病患者分别行二维超声心动图及RT-3DE检查,采集二维、实时三维及全容积三维图像,分析比较3种超声显像技术对心血管解剖结构的显示能力,并对20例室间隔缺损(VSD)、房间隔缺损(ASD)患者缺损最大直径的二维及三维超声测值与手术测值进行比较.结果RT-3DE可以:(1)实时显示心脏的立体结构;(2)实时显示室间隔或房间隔缺损的空间位置、形态,测量的缺损最大直径与手术测值无显著差异(P>0.05);(3)完整显示先天性心脏瓣膜病的瓣叶位置、数目、狭窄口面积及功能状态,清晰显示心内膜垫缺损的共同房室瓣形态及数目,并清晰显示肺动脉瓣病变患者的肺动脉瓣发育情况;(4)清晰显示法乐四联症患者病变的复杂结构,尤其在主动脉根部的短轴观方位显示室间隔的骑跨程度;(5)清晰显示部分动脉导管未闭患者的导管走行及形态.结论 RT-3DE能实时显示先天性心脏病的立体结构及功能状态,为外科手术提供更多信息.     

曲线M型组织速度图与应变率图评价右心室起搏时心室收缩顺序的对照研究

目的　评价组织多普勒曲线M型 (CMM )技术检测右心起搏时心室肌的收缩起源和顺序的可行性 ,并比较其组织速度图 (TVI)和应变率图 (SRI)两种成像模式的特点。方法　应用CMM的TVI和SRI成像模式 ,结合同步记录的心电图 ,分别在心尖四腔观、左室两腔观以及心尖左室长轴观评价 2 5例安装右心起搏器患者与 2 0例健康成人局部心肌收缩 (或形变率 )的先后次序。结果　①正常心肌的收缩起源位于室间隔中部 ,室间隔中部早于心尖部收缩的显示率为 90 %;而右心起搏心律组则显示室间隔心尖部最先收缩 ,TVI图和SRI图显示室间隔心尖早于中部、基底部心肌收缩的比例为 84%和 92 %;正常心肌和右心起搏心肌间的差异有显著意义 (P <0 .0 0 1)。②右心起搏心肌的心室收缩顺序与正常心肌迥异。右室游离壁心尖部和室间隔心尖最早除极收缩 ,右室游离壁较室间隔中部、基底部心肌收缩早 ;左室的侧壁、前壁和左室后、下壁心肌的收缩明显延迟 (P <0 .0 5～ 0 .0 0 5 ) ,并呈现由心尖至心底方向依次收缩减慢的特点。结论　高帧频的组织多普勒曲线M型的速度和应变率曲线 ,为超声准确客观地评估心肌电活动状态提供了全新的定量工具 ,具有广阔的临床应用前景。     

实时三维超声心动图在室间隔缺损评价中的应用价值

目的 探讨实时三维超声心动图(RT3DE)评价室间隔缺损的价值.方法 应用超声心动图诊断仪采集35例室间隔缺损(VSD)患者的三维数据,应用QLab软件显示室缺切面图,逐帧对其进行测量及动态观察,并与二维超声和手术测值进行比较.结果三维超声心动图所测室缺最大径值较二维心动图所测数值与手术结果有更好的相关性(γ=0.91 vs γ=0.84).室间隔缺损随心动周期呈动态变化.结论 实时三维超声心动图能够准确评估室间隔缺损的大小和形态,为临床治疗提供更全面的资料.     

实时三维超声心动图在主动脉瓣成形术中的应用价值

目的 初步探讨实时三维超声心动图在保留瓣叶的主动脉瓣成形术中的应用价值.方法 对11例主动脉瓣中重度关闭不全患者在术前、术后进行常规超声心动图、实时三维超声心动图(RT-3DE)及彩色实时三维超声心动图(color RT-3DE)检查.结果 11例患者术前及术后RT-3DE、color RT-3DE均能立体观察主动脉瓣的形态及对合情况,5例患者术前color RT-3DE能立体观察室间隔缺损部位、形态、大小及空间关系,而且RT-3DE测量主动脉瓣环直径、窦部直径、窦干部直径、升主动脉直径及室间隔缺损大小基本上与手术中的测值呈线性相关.结论 RT-3DE能快速、准确地测量主动脉瓣环、窦部、窦干部及升主动脉的直径,同时能立体显示主动脉瓣的形态和功能及主动脉瓣反流的程度.     

实时三维超声心动图在先天性心脏病介入封堵治疗中的临床价值

目的评价实时三维超声心动图(RT-3DE)在先天性心脏病介入封堵术前及术后的应用价值。方法RT-3DE检测21例先天性心脏病患者(包括8例房间隔缺损、8例室间隔缺损和5例动脉导管未闭),分析缺损口和未闭导管的空间位置、大小和形态;并于封堵术后RT-3DE评估封堵器的位置及其距主动脉瓣、二尖瓣和三尖瓣等周围组织和血管的距离。结果RT-3DE能实时动态地显示房间隔缺损、室间隔缺损和动脉导管未闭及其封堵器的位置、形态及其与周围组织的关系,其中1例室间隔缺损和2例房间隔缺损因缺损处周边没有足够的边缘组织,改行外科手术。结论RT-3DE在明确先天性心脏病病变的解剖位置,观察封堵器释放后的形态结构,明确残余分流的性质及原因等方面较二维超声心动图具有明显优势。     

实时三维超声心动图评价房间隔缺损患者右室整体及局部容积与功能

目的 应用实时三维超声心动图(RT3DE)技术评价房间隔缺损(ASD)患者右室整体及局部容积与功能.方法 对32例ASD患者及32例正常对照者行三维容积成像,应用实时三维右室定量法(3D RVQ)测量并比较两组右室各局部舒张、收缩末期容积及局部射血分数,并将上述方法与长轴八平面法(LA 8-plane)测量的右室整体容积及射血分数行相关分析.结果 ASD患者右室局部及整体舒张、收缩末期容积较正常对照组明显增加(P<0.05),右室心尖部及整体射血分数较正常对照组减低(P<0.001).3D RVQ法与LA 8-plane法测量的右室整体舒张、收缩末期容积及射血分数相关良好.结论 RT3DE能准确评价右室局部及整体容积与功能,ASD患者右室局部及整体容量负荷较正常人显著增加,右室心尖部和整体收缩功能均有降低.     

急性心肌梗塞合并室间隔破裂的2DE和PDE诊断

6例急性心肌梗塞(AMI)并发室间隔破裂(VSR),2DE均能直接显示VSR的位置与大小。前壁AMI VSR发生在前室间隔或室间隔近心尖部,下壁AMI VSR在后室间隔。PW的取样容积在室间隔右室侧都可探及收缩期左向右分流频移信号,1例偶尔可探及舒张晚期左向右分流信号,5例能根据分流频移信号的方向判断VSR部位。全组无MR。5例经手术1例经尸检证实2DE和PW判断VSR部位同     

经食管实时三维超声心动图在伴房间隔缺损的房间隔膨胀瘤中的应用

目的 探讨经食管实时三维超声心动图(RT3D-TEE)在伴房间隔缺损(ASD)的房间隔膨胀瘤(ASA)中的应用。方法 回顾性分析于我院接受RT3D-TEE检查、伴ASD的ASA患者31例,观察ASA发生的部位、形态、大小及与ASD的毗邻关系。结果 2例ASA累及整个房间隔组织;余29例ASA均位于房间隔中部的卵圆窝;5例ASA为3RL型,26例ASA为1R型;经RT3D-TEE检查17例患者合并双孔及以上的筛孔型ASD;1例ASA合并单纯卵圆孔未闭;13例ASA合并单孔型ASD。结论 RT3D-TEE可清晰显示ASA的形态、大小、部位及与伴发ASD的空间位置关系,可为临床治疗方式的选择提供准确的诊断信息。     

外伤性室间隔缺损1例

患者男,15岁,主因"竹签刺入前胸"入院.二维超声心动图于心尖四腔心切面显示室间隔肌部缺损,宽度约0.56～0.82 cm,将肌部间隔分为两部分,下部间隔游离端偏向左心室侧(图1A),多普勒探及左向右分流,峰值流速4.00 m/s.实时三维超声心动图显示室间隔肌部中央见一梭形缺损,呈右下至左上斜行左右心室通道.     

Aberrant Ventricular Conduction Resembling Ventricular Premature Beats

Patients who complain of gaseous indigestion may be more sensitive to an underlying intestinal motor abnormality than are others with similar dysfunctbn. Modifications in living and eating habits are basic steps that can be taken to relieve the problem; drugs that alter intestinal activity or responses may be effective.     

Ventricular Activation Onset-Triggered Left Ventricular Pacing:

Ventricular activation onset-triggered (VAOT) left ventricular pacing modalities synchronize left ventricular paced activation with existing intrinsic ventricular activation, in patients with complete LBBB and adequate rate. The purpose of this study was to evaluate the safety and feasibility of VAOT pacing with one left ventricular pacing lead, during temporary pacing in the postoperative period following open heart surgery. VAOT pacing was studied in five patients with LBBB and two patients with previously implanted right ventricular pacemakers. The VAOT pacing system used was assembled by modifying the function of existing equipment and its programming is described in detail. Comparative ECGs are reported, documenting the changes in ventricular activation produced by VAOT pacing. Stability of surface ECG acquisition was found to be essential to the success of temporary VAOT pacing and inappropriate pacing due to ECG instability is described. Patients were studied at rest and none experienced congestive heart failure. In the comparison of cardiac output, with and without VAOT pacing, no significant differences were found in LBBB patients or those with right ventricular pacemakers. In the comparison of arterial pressure, with and without VAOT pacing, no significant differences were found in six patients, however, in one LBBB patient with intrinsic predominant ventricular trigeminy, VAOT pacing was observed to have an antiarrhythmic effect resulting in suppression of ventricular ectopy and stabilization of arterial pressure. All patients survived VAOT pacing and the postoperative period without complications requiring additional intervention or treatment. (PACE 2004; 27[Pt. I]:730–739)     

Ventricular remodeling

Ventricular remodeling is an extremely complicated process that is not well understood. There seem to be multiple feedback loops that respond to mechanical events as well as to neurohormonal stimulation, cytokine release, and other, yet unidentified, agents. The progression of ventricular remodeling after the index event includes: Myocyte slippage and thinning of infarct area, chamber dilatation. Fibrosis and scar formation. Collagen strut dissolution and excessive accumulation of interstitial matrix. Increased wall stress. Myocyte hypertrophy. Neurohormonal activation. Cytokine release. Ongoing myocyte hypertrophy. Cell apoptosis and necrosis. Continued deterioration of cardiac function. It is impossible to place the sequence of events in order, because the multiple feedback systems create a complex interactive process. A basic awareness of the pathophysiology of ventricular remodeling can aid in understanding current and future treatments for heart failure. It is clear that therapeutic interventions solely aimed at improving cardiac pump function do not slow the progression of heart failure or reduce mortality. Drugs that block the neuroendocrine contribution to the remodeling process have been shown to have a greater impact. Current therapies with angiotensin-converting enzyme inhibition, beta blockade, and aldosterone antagonism are associated with significant reductions in morbidity and mortality in heart failure. Other therapeutic strategies suggested by knowledge of remodeling mechanisms, such as drugs to block cytokines, endothelins, and MMPs, may offer further benefit to patients with heart failure in the future.     

Ventricular arrhythmias

Sudden cardiac death remains a leading cause of death in the United States. It is usually due to ventricular arrhythmia, either ventricular tachycardia or ventricular fibrillation. The probability of life threatening ventricular arrhythmia correlates closely with underlying structural heart disease. In any patient presenting with a ventricular arrhythmia, a careful search for underlying causes is required, and treatment should be considered primarily if it will prolong survival. Treatment of patients without underlying heart disease who are experiencing ventricular ectopy, and/or nonsustained ventricular tachycardia, consists of reassurance and education. If symptoms are severe, a beta-blocker is an appropriate choice for drug treatment. Patients with ventricular arrhythmia and structural heart disease are generally best managed in conjunction with a cardiologist.     

Ventricular Tachycardia

Ventricular tachycardia most often is a manifestation of intrinsic heart disease or digitalis intoxication. Differential diagnosis is of utmost importance in planning treatment.

Intravenous administration of procaine amide hydrochloride is the treatment of choice. However, if the arrhythmia occurs without underlying heart disease and is well tolerated, orally administered therapy is preferable to that given intravenously. Digitalis is no longer contraindicated in ventricular tachycardia unless intoxication with this drug is suspected.

NaEDTA has proved effective in digitalis-induced ventricular tachycardia.