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.     

不同起搏方式左心室收缩同步性超声评价的对比研究

目的：应用二维斑点追踪显像(2D-STI)和组织多普勒成像(TDI)技术对比分析直接希氏束起搏(direct His-bundle pacing,DHBP)与右室心尖部起搏(right ventricular apical pacing,RVAP)时左室收缩同步性,并探讨2D-STI 和 TDI 在评价左室收缩同步性中的应用价值。方法24例植入有 DHBP 和RVAP起搏方式的永久起搏器患者,分别在 DHBP 和 RVAP 状态下,采用2D-STI 测量左室18节段收缩期径向应变达峰时间,计算其标准差(Trs-SD)及最大差(Trs-Dif)、左室短轴乳头肌水平的前间隔与左室后壁收缩期径向应变达峰时间的差值(Tas-post);采用TDI测量左室12节段收缩期速度达峰时间,计算其标准差(Ts-SD)及最大差(Ts-Dif)。结果与 RVAP 相比,DHBP 状态下各左室收缩同步性参数均明显缩短,差异有统计学意义(均P <0.01)。DHBP时2D-STI对左室收缩同步性检出率优于TDI,RVAP时2D-STI对左室收缩不同步检出率亦优于TDI,差异均有统计学意义(均P <0.05)。结论 DHBP时左室收缩同步性及心功能均优于 RVAP;RVAP可能会引起左室收缩不同步;2D-STI 和 TDI 均能定量评价左室收缩同步性,2D-STI较TDI检出率更高。     

组织多普勒成像评价右心室心尖部及右室流出道起搏的同步性

目的采用组织多普勒成像（TDI）检测右室心尖部起搏（RVAP）、右室流出道起搏（RVOTP）对于左室同步性的影响与比较。方法 2008年3月2010年3月20例安置RVAP患者及20例安置RVOTP患者术后3个月行TDI检测,将左室12节段收缩达峰时间的标准差（TS-SD）、6个基底段收缩达峰时间差值、左室12个节段中任意两个节段收缩达峰时间最大差值作为同步化参数。结果 TDI结果显示,两组之间同步性参数比较,有统计学意义（P〈0.01）。结论 RVAP会导致左室内收缩不同步,TDI技术可以准确评价左室收缩同步性。     

二维斑点追踪成像评价长期右心室心尖部起搏对左心室心肌收缩功能的影响

目的 采用二维斑点追踪成像(STE)检测长期右心室心尖部起搏(RVAP)对左心室(LV)心肌收缩功能的影响.方法 行DDDR模式起搏器植入的高度或Ⅲ度房室传导阻滞患者47例,均为RVAP,在术前3d及术后1年采用STE检测左心室收缩同步性指标TAS-POST、左心室射血分数(LVEF)、心肌纵向二维应变(LS)和径向应变(RS).将TAS-POST≥130 ms定义为左心室收缩不同步.62例年龄和性别匹配的正常人作为对照组.结果 术后TAS-POST延长,心肌LS减低,RS则无显著变化.9例患者TAS-POST＞130 ms,长期RVAP导致左心室收缩不同步的发生率为19.15％.结论 长期RVAP可导致左心室心肌局部纵向收缩功能减低,且收缩同步性下降,STE 可以准确评价左心室心肌收缩功能和收缩同步性.     

实时三维超声心动图技术评估心衰患者左室收缩不同步的临床应用价值

目的 探讨实时三维超声心动技术(RT-3DE)评估慢性心力衰竭(心衰)患者左室收缩不同步性的临床价值.方法 选择32例慢性心衰患者和32例正常对照,应用RT-3DE和组织多普勒技术(tissue doppler imaging,TDI)分别获取两组的心尖四腔观、两腔观、左室长轴观的TDI图像和左心室的RT-3DE全容积图像,应用Qlab软件分别计算出RT-3DE全容积图像的QRS起点到16节段最小收缩容积时间标准差(Tmsv16-SD)的百分数标准差(Tmsv16-SD%)和TDI图像心室壁基底段和中间段12节段的收缩达峰时间(Ts)的标准差(Ts-SD).结果 患病组的Tmsv16-SD%明显高于对照组(8.6±4.5 vs 1.3±1.6,P<0.01),患病组的T16-SD%与左心室射血分数(left ventricular ejection fraction,LVEF)成负相关(r=-0.89,P<0.01).患病组的Ts-SD明显高于对照组(31.6±5.1 vs 14.5±5.3,P<0.01),患病组的Ts-SD与LVEF呈负相关(r=-0.69,P<0.01).所有受检者Tmsv16-SD%和Ts-SD有很好的相关性(r=0.76,P<0.01);RT-3DE和Simpsons双切面法测量的LVEF呈高度相关性(r=0.93,P<0.001).结论 RT-3DE可以定量分析心衰患者左室收缩不同步性,为心肌再同步化治疗患者的筛选提供了一种新技术.     

超声心动图对乳腺癌不同化疗周期患者左室收缩功能的研究

目的:研究分析超声心动图对乳腺癌不同化疗周期患者左室收缩功能。方法:选取本院(在2018年2月-2019年2月)搜集的43例乳腺癌患者一般资料。应用三种不同检测方法分析乳腺癌患者在术前术后不同化疗周期的左室收缩功能。结果:M型超声心动图检测方法与二维双平面Simpson法检测乳腺癌患者术前与第六化疗周期射血分数比较有统计学意义(P<0.05),单心动周期实时全容积三维超声心动图检测方法与第五化疗周期射血分数比较有统计学意义(P<0.05);单心动周期实时全容积三维超声心动图检测方法和二维双平面Simpson法检测乳腺癌患者术前左室舒张末容积和术后各个不同化疗周期的左室舒张末容积比较未有统计学差异(P>0.05)。结论:随着用药剂量的不断递增,乳腺癌患者会出现左室收缩功能降低情况,单心动周期实时全容积三维超声心动图检测方法能够早日发现射血分数减低情况。     

实时三维超声预测心脏再同步化治疗短期疗效的研究

目的 探讨实时三维超声(RT3DE)评价左室收缩同步性,预测心脏再同步化治疗(CRT)短期疗效的价值.方法 接受CRT治疗的心力衰竭患者24例,在术前3 d及术后1个月采用RT3DE检测左室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,同时测量左室收缩末容积(LVESV)和射血分数(LVEF).将术后LVESV减小率ΔLVESV≥15%定义为CRT短期治疗有效.结果 14例患者(58.3%)为CRT短期治疗有效组(R组).术前R组Tmsv 16-Dif和Tmsv 16-SD长于无效组(NR组),其余参数无差异.术后与NR组比较,R组的LVESV减小,LVEF增高,Tmsv 16-Dif和Tmsv 16-SD缩短.Tmsv 16-SD是预测ΔLVESV≥15%的独立因素,Tmsv 16-SD＞3.9%预测CRT短期疗效的敏感性和特异性分别为82%和79%.结论 CRT短期疗效可改善左室收缩同步性和收缩功能.RT3DE能准确评价左室收缩同步性和收缩功能,预测CRT短期疗效.     

急性心肌梗死患者左室收缩不同步程度的定量研究

目的 应用组织速度成像(TVI)技术定量研究急性心肌梗死(心梗)患者左室收缩不同步性.方法 对46例心梗患者和36例正常者对照者,用超声标准测量左室舒张末容积(EDV)、收缩末容积(ESV)、射血分数(EF)、左室舒张末内径(EDD)、左室收缩末内径(ESD),用TVI测量左室12个节段的收缩达峰时间(Ts),计算它们之间最大差值(Ts-diff)和标准差(Ts-SD).结果 心梗组与对照组Ts-diff和Ts-SD[(202.3±55.5)ms、(94.9±19.5)ms和(85.2±11.0)ms,(32.2±8.2)ms,P＜0.001]比较有显著性差异.结论 心梗患者左室存在收缩不同步现象,组织速度成像可以定量评价心梗患者心肌的不同步程度.     

应用二维斑点追踪技术对完全性左束支传导阻滞患者左心室的功能及其同步性的评价

目的 运用二维斑点追踪技术(two-dimensional speckle tracking imaging,2DSTI)评价正常人、孤立性完全性左束支传导阻滞(complete left bundle branch block,CLBBB)患者以及合并有心力衰竭的CLBBB患者左心室的收缩功能和机械同步性,并进一步分析心脏的收缩功能和机械同步性之间的关系.方法 选取孤立性CLBBB患者29例(CLBBB1),合并有心力衰竭的CLBBB患者20例(CLBBB2),正常对照组16例:采用双平面Simpson法测量左室射血分数(LVEF),2D-STI技术测量左心室整体纵向应变值(GLPS-Avg)以及18节段纵向应变达峰时间,从而计算出左心室18节段应变达峰时间标准差(Ts-SD).结果 (1)与正常组比较,CLBBB1组GLPS-Avg降低(P＜0.05),Ts-SD延长(P＜0.01);(2)与正常组和CLBBB1组比较,CLBBB2组LVEF、GLPS-Avg明显降低(P＜0.000),Ts-SD明显延长(P＜0.000); (3) LVEF与GLPS-Avg均反映左心室的收缩功能,二者具有良好的相关性.结论 左室射血分数在正常范围内的孤立性CLBBB患者,左室整体纵向应变值降低,左心室内同步性轻度受损,而合并有心力衰竭的CLBBB患者左室收缩功能明显降低,左心室内明显不同步.     

组织多普勒成像技术对心脏再同步化治疗的评价

目的探讨应用组织多普勒成像(TDI)技术评价心脏再同步化治疗(CRT)慢性心力衰竭患者的临床应用价值。方法选择拟行CRT的慢性心力衰竭患者31例,应用TDI测量收缩速度达峰时间判断左室收缩延迟部位,根据左室电极的位置是否与收缩延迟部位相符,将患者分为电极位置和收缩延迟部位符合者20例(A组)和不符合者11例(B组)。应用常规超声心动图及TDI技术观察两组术前及术后1,3,6个月左室收缩功能指标和心脏同步性参数的变化,评价CRT治疗效果。结果所有患者术前TDI技术评估均提示存在左室内收缩不同步,TDI技术能够指导左室电极植入理想靶静脉。术后1,3,6个月,患者的纽约心脏病协会心功能(NYHA)分级、6min步行距离、左室射血分数(LVEF)、左室舒张末期内径(LVEDd)、二尖瓣反流(MR)程度及室间机械延迟(IVMD)、左室12节段达峰时间标准差(Ts-SD)、左室内最晚收缩-最早收缩(Ts max-min)均较术前明显改善,术后6个月各参数改变最明显(P<0.05)。术后6个月,A,B组间NYHA分级、6min步行距离、LVEF、MR程度、IVMD、Tsmax-min及Ts-SD比较,差异均有统计学意义(均P<0.05)。结论 TDI技术可以用于慢性心力衰竭患者接受CRT的筛选,并能指导左室电极植入位置和评价疗效。     

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.