犬急性缺血心肌非同步运动与左心功能的相关性研究

目的：探讨定量组织速度成像（QTVI）评价犬急性缺血心肌非同步运动与左心功能的相关性。方法：健康犬21只,暴露心脏,于左冠状动脉主干阻断前（对照组）、后（实验组）分别获取左心室12个节段的QTVI曲线,测量各点QRS波起点至心肌收缩期峰值速度和舒张早期峰值速度的时间（Ts和Te）,计算同一壁内3个节段Ts最大差值（Intra-△Ts）和Te最大差值（Intra-△Te）以及左心室12个节段Ts和Te的最大差值（Max-△Ts和Max-△Te）。心室间的不同步指标测量QRS波起点到主动脉瓣血流频谱起点时间（Q-A）,QRS波起点到肺动脉瓣血流频谱起点时间（Q-P）及其差值（Q-AP）。左室射血分数（LVEF）和Tei指数反映左心整体功能。结果：实验组缺血节段Intra-△Ts、Intra-△Te、Max-△Ts、Max-△Te、Q-A、Q-P及Q-AP较对照组明显延长（P＜0.01）,Max-△Ts与Tei指数呈正相关（P＜0.05）,与LVEF呈负相关（P＜0.05）。QRS与Max-△Te呈正相关（P＜0.05）。结论：犬急性缺血左心室内及心室间心肌存在明显非同步运动,且与心功能密切相关。     

定量组织速度成像技术对心力衰竭患儿心脏非同步运动的研究

目的 探讨定量组织速度成像(QTVI)评价充血性心力衰竭(CHF)患儿心室间及左心室内非同步运动的临床意义.方法 正常小儿40例,CHF患儿30例,左心室内非同步性指标检测采取标准心尖四腔和两腔观,获得左心室4个壁基底段、中间段和心尖段共12个位点的QTVI曲线,测量各位点QRS波起点至心肌收缩期峰值速度和舒张早期峰值速度的时限(Ts和Te).计算左心室同一壁内3个节段间Ts最大差值和Te最大差值(Intra-△Ts和Intra-△Te)以及左心室12个心肌节段Ts和Te的最大差值(Max-△Ts和Max-△Te).心室间的不同步指标测量QRS波起点到主动脉瓣血流频谱起点时间(Q-A)、QRS波起点到肺动脉瓣血流频谱起点时间(Q-P)及其差值(Q-AP).左室射血分数(LVEF)及Tei指数反映左心室整体功能.结果 CHF组Intra-△Ts和Intra-△Te、Max-△Ts和Max-△Te、Q-A、Q-P及Q-AP较正常组明显延长.Max-△Ts与LVEF负相关(r=-0.54,P＜0.05;),与Tei指数正相关(r=0.58,P＜0.01),与QRS不相关.Max-△Te与QRS正相关(r=0.57,P＜0.01),与LVEF及Tei指数不相关.结论 CHF患儿心室间及左心室内存在明显的非同步运动,且与心功能关系密切.     

定量组织速度成像技术对病毒性心肌炎患儿左室内非同步性的研究

目的探讨三平面基础上应用定量组织速度成像技术（QTVI）评价病毒性心肌炎（VMC）儿童左室内非同步运动的临床意义。方法正常儿童30例,VMC患者32例,每个受试者在实时三维成像的基础上获得标准的心尖四腔、两腔和三腔心切面,采集左心室6个壁的基底段、中间段、心尖段共18个位点的QTVI图像,测量各位点QRS波起点至收缩期峰值速度和舒张早期峰值速度的时限（Ts和Te）,计算左心室同一个壁内3个节段间Ts最大差值和Te最大差值（Intra-ΔTsI、ntra-ΔTe）以及同一个节段内6个壁之间Ts最大差值和Te最大差值（Inter-ΔTsI、nter-ΔTe）以及左心室18个节段Ts最大差值和Te最大差值（Max-ΔTs、Max-ΔTe）。结果 VMC组Intra-ΔTsI、ntra-ΔTe、Inter-ΔTsI、nter-ΔTe、Max-ΔTs、Max-ΔTe均较正常组延长。结论 VMC患儿左室内存在明显的非同步运动。     

组织追踪显像技术评价心力衰竭患者心脏非同步化运动

目的探讨组织追踪显像技术(TTI)评价充血性心力衰竭(CHF)患者心室间及左心室内非同步运动的临床价值。方法对照组35例及CHF患者30例,应用TTI获得左心室壁运动位移曲线,测量QRS波起始至左心室壁12节段收缩期位移达峰时间(Ts)及各点向心尖方向的最大位移(Ds),计算左心室12个心肌节段Ts的最大差值(Max-△Ts)及同一壁内2节段Ts的差值(Ts-diff);同时计算12个节段Ds的均值(mDs);并测量左右心室侧壁基底段Ts的差值作为左右心室间的延迟(L-RV-D)。左室射血分数(LVEF)及Tei指数反映左心室整体功能。结果与对照组相比,CHF组Max-△Ts、Ts-diff及L-RV-D明显延长(均P<0.01),mDs显著降低(P<0.01)。Max-△Ts与LVEF、mDs呈负相关(r=—0.68,P<0.01;r=—0.59,P<0.01),与Tei指数呈正相关(r=0.64,P<0.01),与QRS不相关,而mDs与LVEF呈正相关(r=0.61,P<0.01)。结论CHF患者心室间及左心室内存在明显的非同步运动,并且与左心功能关系密切。     

定量组织速度成像评价心肌梗死患者左心室舒张不同步性及整体舒张功能

目的探讨应用定量组织速度成像技术(QTVI)评价心肌梗死患者左心室非同步舒张运动的意义。方法获取60例心肌梗死患者及40例正常人的标准心尖部左室长轴、两腔和四腔观组织速度图像,离线分析左心室6个壁基底段、中间段和心尖段共18个位点及左心室各壁二尖瓣环的组织速度曲线,测量心电图QRS波起始点至各位点心肌舒张早期峰值速度(Ea)的时限(TQ-E)。计算同一节段6个壁间TQ-E的最大差值(Inter-ΔTQ-E)、同一壁内3个节段间TQ-E的最大差值(Intra-ΔTQ-E)及左心室18个位点间TQ-E的最大差值(Max-ΔTQ-E)。计算左心室各壁二尖瓣环Ea与舒张晚期峰值速度(Aa)比值的平均值(Ea/Aa′)。并利用常规超声心动图测定心肌梗死患者左室整体舒张末容积(EDV)、收缩末容积(ESV)、射血分数(LVEF)。结果与正常人相比,心肌梗死组EDV、ESV均明显升高,心肌梗死组EF明显降低,心肌梗死患者的Inter-ΔTQ-E、Intra-ΔTQ-E、Max-ΔTQ-E均明显延长,Ea/Aa′明显降低。心肌梗死患者中,Max-ΔTQ-E与Ea/Aa′均呈显著负相关;与EDV及ESV呈显著正相关;与EF呈显...     

心力衰竭患者左心室非同步运动对左心功能、心肌重构影响的超声心动图研究

目的 探讨充血性心力衰竭（CHF）患者左心室非同步运动与左心功能、心肌重构的关系及双心室起搏（DDD）对改善左心功能、逆转心肌重构的作用。 方法 CHF患者45例，正常人50例，利用定量组织速度成像（QTVI）测量左心室18个节段QRS波起始至心肌收缩期峰值速度的时限Ts及Ts的最大差值（Max-ΔTs）；左心功能、心肌重构指标包括左心室射血分数（LVEF）、Tei指数、左心室收缩末径（LVESD）、舒张末径（LVEDD）、球形指数（LVSI）。其中7例CHF患者实施DDD，分别于术后3d和3个月复查超声心动图各项指标。 结果 CHF患者Max-ΔTs与LVEF呈负相关；与LVESD、LVEDD、Tei指数、LVSI呈正相关。7例实施DDD治疗患者术后3d Max-ΔTs、LVEF、Tei指数较术前改善；LVESD、LVEDD、LVSI无明显变化。与术前及术后3d比较，术后3个月Max-ΔTs、LVEF、Tei指数进一步改善；LVESD、LVEDD、LVSI减小。 结论 CHF患者左心室非同步运动与左心功能、心肌重构关系密切，DDD可改善其左心功能并逆转重构。     

定量组织多普勒速度成像技术对正常人心肌同步性运动的研究

目的　探讨超声定量组织多普勒速度成像技术 (QTVI)评价正常人左、右心室间及左心室内各节段心肌同步性运动的价值。方法　获取标准心尖位左室长轴观、两腔观和四腔观 ,应用 QTVI获得 4 0例正常人右心室侧壁基底段及左心室各节段心肌的组织多普勒速度曲线 ,分别测量各节段自 QRS波起始至心肌收缩期峰值速度和舒张早期峰值速度的时限收缩期同步性指标 (Ts)和舒张期同步性指标 (Te)。结果　正常人左室内各节段心肌运动 Ts和 Te差异无显著性 (P>0 .0 5 ) ;右心室侧壁基底段心肌 Ts较左室 Ts延迟 2 7ms(P<0 .0 5 ) ,左右心室之间 Te无显著性差异 (P>0 .0 5 )。结论　正常人左室内各节段心肌舒缩运动是同步的 ;右心室收缩稍晚于左心室 ,舒张运动两心室之间无差异。 QTVI可快速、无创、定量地评价心肌的同步性运动 ,为临床提供可靠信息     

组织速度成像评估原发性扩张型心肌病右心室心肌舒缩协调性

目的探讨原发性扩张型心肌病(DCM)右室心肌舒缩协调性特点及其意义。方法35例DCM患者[单纯左室扩大组(A组)和双室扩大组(B组)]和18例正常人(C组)入选。常规测定、计算心脏结构和功能参数。分析右室3个壁基底段和中间段组织速度曲线,测量QRS波起点至6节段Sa、Ea时限,计算6节段间TQ-S、TQ-E最大差值(Max-ΔTQ-S、Max-ΔTQ-E)。依据公式计算右室整体心肌作功指数。结果与C组相比,A、B组Max-ΔTQ-S、Max-ΔTQ-E明显延长(B组最显著),且与心脏结构和功能参数具有相关性。结论DCM患者右室存在非同步运动(其中合并右室扩大者最差),且与心脏结构和功能关系密切。     

充血性心力衰竭患者左室心肌收缩性及非同步性组织速度成像研究

目的利用定量组织速度成像技术(QTVI)对充血性心力衰竭(CHF)患者左室心肌收缩功能评价及其非同步性分析。方法选择左室舒张末期内径(LVIDd)≥60mm,左室射血分数(LVEF)≤40%,NYHA心功能分级Ⅱ-Ⅳ级的CHF患者65例。二维超声采集心尖四腔心、二腔心和左室心尖长轴3个切面,左心6个室壁,利用QTVI分别测量各壁基底段、中间段和心尖段的18个节段收缩期峰值运动速度(Vs),以及6个壁基底段从心电图QRS波群起始到最大收缩峰值时限(Q-Ts),计算其最大差值(Max-△Ts)。与40例正常对照组进行对比研究。结果两组左室心肌各节段Vs规律均表现为基底段>中间段>心尖段(除CHF组后间隔心尖段>基底段>中间段外)。CHF组左室心肌各节段Vs均低于正常对照组,其中降低幅度最大的是基底段达57%,中间段次之为50%,心尖段最少是43%。18个节段中除后间隔的心尖段平均Vs下降值与对照组比较无统计学意义(P>0.05),其他17个节段两组对比均有统计学意义(P<0.05)和显著统计学意义(P<0.01)。CHF6个壁基底段Q-Ts均延长,Max-△Ts平均83.08±40.19ms,与对照组比较有显著统计学意义。结论QTVI技术能准确、同时显示CHF患者室壁多个节段的心肌运动速度和时相,从而了解心肌整体和局部功能,有效评估心肌运动协调性。     

心肌组织速度成像评价慢性心力衰竭患者心室收缩不同步性及其与QRS间期相关性的研究

目的应用心肌组织速度成像（TVI）评价慢性心力衰竭患者左心室收缩不同步性与心电图QRS间期的关系。方法选取心功能NYHAⅢ～1V级的扩张性心肌病（DCM）患者60例作为研究对象，依QRS间期分为DCMI组21例（QRS间期〈120ms）、DCMII组21例（QRS间期120～150ms）和DCMⅢ组18例（QRS间期〉150ms）；对照组为30例健康志愿者。分别测量QRS波起点到主动脉瓣血流频谱起始点时间（Q-AO）和到肺动脉瓣血流频谱起始点时间（Q-Pulm），采用两者的差值即心室间机械延迟参数（IVMD）评价左右心室间的同步性。获取左心室各节段心肌TVI曲线，测量各节段从心电图QRS波起点到TVI曲线S波起点的时间（Q-Sb），取18节段Q-Sb的标准差作为左心室内同步性指数（TSI），取各室壁基底段和心尖段Q-Sb的差值作为各室壁内的同步性指数（RSI）。结果以IVMD〉40ms为判定左右心室间不同步的截点值，在DCM Ⅰ、Ⅱ、Ⅲ组中观察到室间非同步性的患者分别为4、10和13例，发生率差异无统计学意义（P〈0．01），且IVMD与QRS间期密切相关（r=0．73，P〈0．01）。DCM组TSI和RSI较对照组显著延长（P〈0．01），但TSI和RSI与QRS间期无明显相关性。结论DCM患者心室间非同步性和QRS间期相关，左心室各室壁间与各室壁内非同步性和QRS间期无明显相关性。     

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.