二维斑点追踪成像评价右室心尖部起搏对左室收缩同步性和功能的影响

目的 采用二维斑点追踪成像(STE)检测右室心尖部起搏(RVAP)对左室(LV)收缩同步性和收缩功能的影响.方法 行DDDR模式起搏器植入的病窦综合征(SSS)患者64例,均为RVAP,在术前及术后(19±6)个月采用STE检测左室短轴乳头肌水平心肌节段收缩期达峰值径向应变的时间(TRS),并将前间壁/间壁和后壁/侧壁TRS的差值(TAS-POST)≥130 ms定义为左室收缩不同步.结果 根据术后STE结果,分为同步组(42例)和不同步组(22例),RVAP导致左室收缩不同步的发生率为34%.同步组左室射血分数(LVEF)无明显变化,不同步组LVEF则显著减低,且TAS-POST和LVEF呈负相关(r=-0.81).结论 长期RVAP可导致左室收缩不同步和收缩功能减低,STE是准确评价左室收缩同步性的新方法.     

超声二维斑点追踪技术评价右心室不同部位起搏对左心室功能的影响

目的采用二维斑点追踪技术(STE)评价右心室心尖部起搏(RVAP)和右心室流出道起搏(RVOP)对左心室心肌功能及同步性的影响。方法选择行DDDR模式起搏器植入的高度或Ⅲ度房室传导阻滞(AVB)患者61例,根据右心室电极位置分为右心室心尖起搏(RVAP)组31例及右心室流出道起搏(RVOP)组30例,在术前及术后(21±5)个月采用STE测量左心室同步性指标(TAS-POST),将TAS-POST≥130ms定义为左心室收缩不同步。结果术后2年,RVAP组有12例(39%)患者发生左心室不同步,RVOP组有6例(19%)患者发生左心室不同步。尽管RVOP组及RVAP组术后前间壁及间壁TRS均较术前缩短,后壁及侧壁较术前延长(P0.05),但RVAP组术后较RVOP组更明显,术后左心室射血分数减低(P0.05)。增加的TAS-POST是LVEF减低的独立预测因素。结论 RVOP组较RVAP组更接近心室正常的激动顺序,获得更好的血流动力学收益。STE可以准确评价心室激动顺序,检测心肌收缩同步性。     

二维斑点追踪成像评价急性心肌梗死后左心室收缩同步性

目的 采用超声二维斑点追踪成像(STE)评价急性心肌梗死(AMI)后左心室收缩同步性及其影响因素.方法 65例QRS宽度正常的AMI患者在AMI发作72 h之内及60名正常人行STE检查,检测心肌峰值纵向应变(LSpeak)代表心肌收缩功能,并测量左心室短轴水平心肌节段收缩期达峰值径向应变的时间(TRS),将前间壁和后壁TRS的差值(TAS-POST)≥130 ms定义为左心室收缩不同步.以心肌室壁运动评分指数(WMSI)代表AMI面积(MIS).结果 AMI患者左心室射血分数(LVEF)和LSpeak减小,TAS-POST延长.AMI导致左心室收缩不同步的发生率为64.62%(42/65).TAS-POST 与LVEF、LSpeak和MIS(WMSI)显著相关,与QRS宽度无相关性.MIS(WMSI)是TAS-POST最有力的独立预测因素.结论 QRS宽度正常的AMI患者可出现左心室收缩不同步,且MIS是收缩不同步的主要影响因素.STE能够准确评价左心室收缩同步性.     

实时三维超声心动图与二维斑点追踪成像技术共同评价冠心病患者左心室收缩功能与同步性及二者相关性初探

目的 探讨实时三维超声心动图(RT-3DE)与二维斑点追踪成像技术(2D-STI)评价冠心病患者左心室收缩功能与同步性的应用价值,并初步研究2种技术的相关性.方法 55例患者根据冠状动脉造影结果分3组,对照组25例,分别进行2D-STI和RT-3DE.分析心肌收缩期峰值纵向应变(LS)、径向应变(RS)和圆周应变(CS),并测量左心室短轴水平心肌节段收缩期达峰值径向应变的时间(TRS)及前间壁和后壁TRS的差值(TAS-POST);分析17节段时间一容积曲线,获得左室舒张末期容积(EDV)、收缩末期容积(ESV)、射血分数(EF)及左心室16节段达到最小收缩容积时间差的标准差校正值(Tmsv-16SD％),并对Tmsv16-SD％与TAS-POST行相关性分析.结果 病例组各参数与对照组对应参数比较,差异均有统计学意义(P＜0.05),病例组间比较,多支病变组EDV、ESV及TAS-POST高于LCA组与RCA组(P＜0.05),多支病变组、LCA组LS与Tmsv16-SD％与RCA组有明显差异.Tmsv16-SD％与TAS-POST呈显著正相关(r=0.794,P＜0.001).结论 RT-3DE与2D-STI均能较好地评价不同冠状动脉狭窄的冠心病患者左心室的收缩功能与同步性变化情况,并且2种技术的在评价左心室同步性上存在一定的相关性.     

实时三维超声心动图评价右心室心尖部起搏对左心室收缩同步性的早期影响

目的 评价右心室心尖部起搏(RVAP)对左心室收缩同步性的早期影响.方法 53例起搏器植入(均为RVAP)的患者和30位正常人,在术前及术后1个月采用实时三维超声心动图(RT3DE)检测左心室16个心肌节段达收缩末最小容积时间的差值(Tmsv 16-Dif) 和标准差(Tmsv 16-SD)作为同步性参数,同时测量左心室射血分数(LVEF).结果术后Tmsv 16-Dif和Tmsv 16-SD 显著延长(P＜0.001),20.75%～22.64%患者出现左心室收缩不同步,而LVEF呈减低趋势(P＞0.05).Tmsv 16-Dif和Tmsv 16-SD与LVEF负相关(r=-0.40和r=-0.52).结论 RVAP早期即可导致左心室收缩不同步,且其可能是收缩功能减低的主要原因.RT3DE可准确评价左心室收缩同步性.     

组织运动瓣环位移技术评价右心室心尖部起搏对左心室收缩功能的早期改变

目的：采用组织运动瓣环位移技术（TMAD）检测长期右心室起搏（RVAP）对左心室整体与节段收缩功能的影响,为左心室早期心功能受损检测提供新的方法。方法入选行DDDR模式起搏的患者53例为研究对象,均为RVAP,在术前以及术后1年采用TMAD技术检测二尖瓣环六个位点二尖瓣环位移（MADseg）、整体位移（MADglobal）,采用M型超声检测左心室收缩期同步性指标TAS-POST以及双平面法测量左心室射血分数（LVEF）,实验室检查 N 末端 B 型利钠肽原（NT-proBNP）,根据起搏器程控检查计算心室累计起搏比例（Cum%VP）。同期选择性别、年龄相匹配的健康人60例作为对照组。结果与术前以及健康对照组比较,术后DDDR组LVEF、NT-proBNP无显著改变（P＞0.05）,然而其二尖瓣环各位点MAD以及二尖瓣环MADglobal均减低（P＜0.05）;与术前比较,DDDR组术后TAS-POST增加（P＜0.05）。相关性分析显示,MADglobal与Cum%VP显著负相关（r＝-0.646,P＝0.000）。结论长期RVAP左心室纵向整体与节段收缩功能以及同步性减低,TMAD可早期监测心功能受损,为长期RVAP患者早期心功能异常的检测提供新的方法。     

二维斑点追踪应变成像对冠心病患者左心室同步性的定量研究

目的 探讨二维斑点追踪应变成像技术评价冠心病患者左室同步性的临床价值.方法 42例急性心肌梗死患者、39例冠心病心肌缺血患者和32例对照者接受二维超声检查,用二维应变软件分析心尖长轴观、心尖两腔观和四腔观以及左室短轴观基底水平、乳头肌水平、心尖水平的图像,测量自心电图QRS波起点至左室在心尖长轴观上的收缩期纵向应变达峰时间(Tssl)及胸骨旁短轴观上的收缩期径向和环向应变达峰时间( Tssr,Tssc).计算左室各节段达峰时间标准差(Tssl-SD,Tssr-SD,Tssc-SD)及节段达峰时间最大差值(Tssl-Dif,Tssr-Dif,Tssc-Dif),以左室短轴观乳头肌水平前室间隔和后壁的径向应变的达峰时间之差(TAS-POST)≥130 ms作为左室收缩不同步标准,同时测量18个心肌节段纵向应变峰值与收缩末应变的差值之和作为纵向应变延迟指数(LSDI),LSDI≥25％作为左室不同步标准.结果 急性心肌梗死组同步性参数较对照组增加(P ＜0.001或P＜0.05);心肌缺血组同步性参数较对照组增高(P＜0.05); LSDI与TAS-POST呈正向线性相关(r=0.676,P＜0.05);急性心肌梗死组中,LSDI检测左室不同步敏感性高于TAs-POST(P＜0.05).结论 二维斑点追踪应变成像技术能准确评价左室不同步性,LSDI与TAS-POST可定量评价冠心病患者左室不同步性.     

超声二维应变成像观察冠心病患者缺血心肌收缩功能异常

目的 应用超声二维应变成像技术检测冠心病患者左心室缺血心肌在不同方向上收缩运动的变化特点。方法 收集接受冠状动脉造影检查患者83例,其中52例造影证实为冠心病(冠心病组),31例造影未见异常(对照组)。超声采集左心室短轴及心尖长轴切面的高频二维动态图像,应用二维应变分析软件测量左心室各节段心肌的收缩期纵向应变(LS)、径向应变(RS)、圆周应变(CS)和旋转角度(RA)。结果 二维应变技术对冠心病组缺血心肌的测量成功率为95.26%(402/422);缺血心肌的LS、RS显著低于对照组正常心肌(P＜0.05);除乳头肌水平前壁及后壁RA外,两组心肌CS、RA的差异无统计学意义(P＞0.05)。结论 二维应变技术所测LS、RS可敏感反映缺血所致局部心肌收缩功能异常;而CS、RA对于观察缺血心肌收缩功能损害不够敏感。     

超声组织追踪成像评价右心室不同位点房室顺序起搏左心室心肌力学状态差异性

目的应用二维超声组织追踪成像(two-dimensional ultrasound tissue tracking imaging,2DTT)评价右心室室间隔起搏(right ventricular septal pacing,RVSP)和右心室心尖起搏(right ventricular apical pacing,RVAP)左心室心肌力学状态差异性。方法 60例有症状缓慢性心律失常并接受永久双腔房室顺序起搏器植入术后患者,根据起搏部位不同分为RVSP组25例及RVAP组35例。均行超声心动图检查,分别获取心尖四腔、心尖三腔及心尖两腔二维图像,测量收缩期左心室节段纵向应变(longitudinal strain,LS)及节段纵向应变率(longitudinal strain rate,LSr)、左心室整体纵向应变(global longitudinal strain,GLS)、整体纵向应变率(global longitudinal strain rate,GLSr)及节段纵向应变达峰时间(peak time of longitudinal strain,Tsl),计算间隔-后壁延迟比率,比较两种右心室起搏位点左心室心肌力学状态差异。结果两组间临床特征及常规超声心动图测量参数差异无统计学意义(P0.05)。RVAP组LS值以及GLS值低于RVSP组,差异有统计学意义(P0.05)。RVAP组节段纵向应变达峰时间较RVSP组明显延长(P0.05),间隔-后壁延迟比率差异无统计学意义(P0.05)。结论与RVSP相比,RVAP造成了明显的左心室收缩不同步和左心室纵向收缩功能减低,RVSP是房室顺序心脏起搏较好的心室位点。     

组织多普勒成像评价DDD型右室心尖部起搏的左室收缩同步性和收缩功能的关系

目的 采用组织多普勒成像(TDI)检测右室心尖部起搏(RVAP)对于左室同步性和收缩功能的影响,并探讨两者的关系.方法 57例因病窦综合症(SSS)行RVAP治疗患者,在术前及术后(17±6)个月采用TDI检测左室12节段收缩期达峰时间的标准差(Ts-SD)作为同步化参数,并测量左室收缩功能.结果 根据术后TDI结果,分为同步组(36例)和不同步组(21例).同步组左室收缩末容积小于不同步组,射血分数则大于不同步组.且Ts-SD和射血分数显著负相关.结论 长期RVAP可导致左室收缩不同步和收缩功能减低,且前者是后者的主要原因.TDI技术可以准确评价左室收缩同步性.     

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 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 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 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.