人左,右心室阻抗微分心动图的比较研究

作者利用Ⅱ导心电图、心音图、颈动脉搏动图、右（或左）心室阻抗微分心动图同步描记的方法，对人左、右心室阻抗微分心动图进行了比较分析。结果显示：人的左、右心室阻抗微分心动图图形相似，波形稳定，转折明显，均有清晰的生理标志点。两种图形各相应生理标志点在时相上存在着区别，且人的左、右民室阻抗微分心动图能分别反映人的左、右心室收缩和舒张过程。说明利用人的左、右心室阻抗微分心动图能分别测定人的左、右心室收缩时     

狗右心室阻抗微分心动图波形及其产生原理的研究

本研究用健康狗12条,采用我们设计的右心室阻抗微分心动图的导联方法,描记了稳定的右心室阻抗微分心动图。实验结果显示:右心室阻抗微分心动图波形的各生理标志点与同步描记的右心室内压（或其微分）曲线图及心音图的相应变化相吻合(Ae-S_1b:0.083±0.0075s,E_b-d-RVP_p1和 Ej-RVP_p1:0.0300±0.0000s,y-A₂:0.0205±0.0035s)。本文还根据生物电阻抗原理和心动周期中左、右心室、左、右心房、近心大血管血流和心脏位置的交化,探讨了右心室阻抗微分心动图各波、点的形成原理,说明右心室阻抗微分心动图各波形成有其生理学、物理学基础,符合已知的生理学规律,可用于右心室 STI 与右心室 DTI 测定。     

高血压病患者静息状态左心室舒张间期的分析

高血压病随着病情的进展，心脏功能会受到一定程度的影响，有关此病时心脏收缩功能的变化已有不少报道。高血压病左室舒张功能的变化国内虽有少数报道，但未见采用无创性心前区阻抗微分图方法的研究报道过。我们采用王鹏巨，臧益民的无创性心前区阻抗微分图(LVIG)方法，对高血压病患者左室舒张间期进行了临床探讨。     

甲苯二异氰酸酯对右心室收缩时间间期的影响

本文利用同步记录心电图(ECG)、心音图(PCG)和肺血流图(Δz)及其一阶微分图形(da/dt),测定了185名正常人和65名经常接触甲苯二异氰酸酯(TDI)工人的右心室收缩时间间期(RSTI)。测出了正常人RSTI 指标的正常值,并分析了年龄、性别等对 RSTI 指标的影响,最后评定了经常接触 TDI 工人的 RSTI.结果表明,经常接触 TDI 的男性工人的右心室收缩时间间期指标中 RPEP 明显延长,QB/T 和 RPEP/RVET 显著性增大和 RVET 明显缩短;而 TDI 对女性工人的右心室收缩时间间期则无明显影响。     

超声心动图评价双腔起搏器不同房室间期设置时心功能变化

目的采用超声心动技术评价双腔起搏器设置不同房室间期（AVD）时的急性血流动力学和心脏收缩舒张功能改变。方法36例高度或Ⅲ度房室传导阻滞安装双腔起搏器的患者,在常规设置AVD和根据体表心电图优化设置AVD的情况下分别进行超声心动图检查。结果与常规设置AVD相比,AVD优化后左室舒张末期容积、左室每搏量、左室射血分数和心排量显著增加,左室充盈时间延长,二尖瓣血流速度时间积分显著增加,Tei指数显著减小。此外,AVD优化后组织多普勒指标室间隔、左室前壁、下壁基底段收缩期峰值速度（Sm）显著增高,左、右心室壁基底段舒张晚期峰值速度（Am）显著增高,右室游离壁基底段的Sm、舒张早期峰值速度和Am均显著高于左室壁各基底段。结论双腔起搏器最佳AVD设置能改善患者的血流动力学指标和心脏功能,这些变化可用超声心动图来评价。     

高血压病患者静息状态左心室舒张间期的分析

<正> 高血压病随着病情的进展,心脏功能会受到一定程度的影响,有关此病时心脏收缩功能的变化已有不少报道。高血压病左室舒张功能的变化国内虽有少数报道,但未见采用无创性心前区阻抗微分图方法的研究报道过。我们采用王鹏巨、臧益民的无创性心前区阻抗微分图（LVIG）方法,对高血压病患者左室舒张间期进行了临床探讨。     

左间隔分支阻滞患者的左室收缩间期测定

应用心阻抗图的方法测定30例有症状的左中隔支阻滞患者及16例无症状的左中隔支阻滞患者的左室收缩间期,并与50例正常人进行了对照分析。结果显示:有症状组的左中隔支阻滞患者比正常组QS_1、PEP、ICT延长,LVET缩短,P/L值增大,无症状组比正常组PEP也延长,LVET缩短,P/L比值增大,但其程度不如有症状组,说明不论有无心血管病的症状,心电图表现为左中隔支阻滞者,其左室收缩间期与某些缺血性心脏病患者的收缩间期的变化是一致的,存在左心功能受损的情况。     

应用多普勒超声心动图评价糖尿病患者的左右心室功能

应用脉冲多普勒超声心动图对比观测84例有、无并发症的非胰岛素依赖型糖尿病（NIDDM）患者及50例正常人的左、右心室功能。结果显示：NIDDM患者的左、右心室舒张及收缩功能均减退，早期以舒张功能减退为著，继之，收缩功能受损。高血压、冠心病、微血管病变等并发症可进一步加重损害，且左、有心室舒张功能参数间有显著相关关系，而收缩功能参数相关性较差。     

心阻抗图和心机械图测定心脏收缩时间间期的比较

心阻抗图和心机械图测定心脏收缩时间间期的比较王沙京１李琳琳２（１同济医科大学附属梨园医院心内科武汉４３００７３２湖北省直属机关门诊部）关键词心动描记术，阻抗心缩间期对比研究心脏收缩时间间期（ＳＴＩ）测定已较普遍被认为是估计心脏功能首选的非侵入性方法...     

健康成人右心收缩间期及其影响因素

对比分析了左右心收缩间期的差异及相关关系，探讨右心收缩间期的生理变异，特别是其增龄性变化的规律性，提供改善其临床应用价值和可靠性的理论及实践依据。研究对象:经严格筛选的健康成人１２９例（男７２，女５７），年龄２１～８１（平均４９．１±１４．８）岁。方法:以多普勒超声心动图检测左右心收缩间期指标，分析其间差异显著性和相关关系。并分别以右心收缩间期各项指标为应变量，以可能对其有影响的生理因素为自变量，进行多元逐步回归及直线相关分析，以筛选对右心收缩间期有独立影响的因素。结果提示，左右心室大多数心缩间期指标间差异有显著性，同时也存在显著性相关关系，反映了左右心室解剖结构、功能及血液动力学的相互联系和差别；随年龄增长，ＲＰＥＰ延长，ＲＶＡＴ缩短，ＲＰＥＰ／ＲＶＥＴ比值增大，而ＲＶＥＴ变化不大。对右心收缩间期有显著性独立影响的其他因素还有性别、体格大小、肥胖程度、心脏径限、体循环血压水平。结论:在以右心收缩间期作为评估右心功能或肺动脉压的指标时，应制定考虑性别、年龄、体格大小等影响因素的衡量标准。     

Non-invasive assessment of left ventricular function after correction of severe aortic regurgitation.

Twenty patients were studied with simultaneous left ventricular cavity echocardiograms and apex cardiograms during the first two weeks after correction of severe aortic regurgitation. Endocardial echoes and apex cardiograms were digitized, so that left ventricular dimensions, their rates of change, and echo dimension-apex cardiogram relations could be studied. After aortic valve replacement, there was an early reduction in end-diastolic dimension, within 2 days, from 7-0 +/- 0-8 cm to 5-7 +/- 1-0 cm (P less than 0-001), while peak normalized shortening rate (peak Vcf) dropped from 1-9 +/- 0-6 to 1-4 +/- 0-6 S-1 (P less than 0-01), and remained unchanged for the remainder of the study. Immediately after operation, striking abnormalities of isovolumic contraction and, to a lesser extent, of early relaxation, could be seen, which regressed over 4 to 7 days, except in 2 patients who developed a low output state. These changes in left ventricular dimension, Vcf, and isovolumic contraction could not have been described by an single "measure" of left ventricular function.     

Relation of filling pattern to diastolic function in severe left ventricular disease

M mode and Doppler echocardiograms, apex cardiograms, and phonocardiograms were recorded in 50 patients with severe ventricular disease of varying aetiology to examine how left ventricular filling is disturbed by cavity dilatation. The size of the left ventricular cavity was increased in all with a mean (SD) transverse diameter of 7.2 (0.8) cm at end diastole and 6.3 (0.8) cm at end systole. All were in sinus rhythm and 35 had functional mitral regurgitation. In nine patients, in whom filling period was less than 170 ms, transmitral flow showed only a single peak, representing summation. In the remainder there was a strikingly bimodal distribution of filling pattern. In 12 the ventricle filled dominantly with atrial systole (A fillers). Isovolumic relaxation was long (75 (35) ms) and wall motion incoordinate; mitral regurgitation was present in only one. In most (29) the left ventricle filled predominantly during early diastole (E fillers). Mitral regurgitation, which was present in 26, was much more common than in the A fillers, while the isovolumic relaxation time (10 (24) ms) was much shorter and the normal phase relations between flow velocity and wall motion were lost. In 24 E fillers no atrial flow was detected. In four there was no evidence of any mechanical activity, suggesting "atrial failure". In 20, either the apex cardiogram or the mitral echogram showed an A wave, implying that atrial contraction had occurred but had failed to cause transmitral flow, showing that ventricular filling was fundamentally disturbed in late diastole. A series of discrete abnormalities of filling, beyond those shown by Doppler alone, could thus be detected in this apparently homogeneous patient group by a combination of non-invasive methods. The presence and nature of these abnormalities may shed light on underlying physiological disturbances.     

Relation of filling pattern to diastolic function in severe left ventricular disease.

M mode and Doppler echocardiograms, apex cardiograms, and phonocardiograms were recorded in 50 patients with severe ventricular disease of varying aetiology to examine how left ventricular filling is disturbed by cavity dilatation. The size of the left ventricular cavity was increased in all with a mean (SD) transverse diameter of 7.2 (0.8) cm at end diastole and 6.3 (0.8) cm at end systole. All were in sinus rhythm and 35 had functional mitral regurgitation. In nine patients, in whom filling period was less than 170 ms, transmitral flow showed only a single peak, representing summation. In the remainder there was a strikingly bimodal distribution of filling pattern. In 12 the ventricle filled dominantly with atrial systole (A fillers). Isovolumic relaxation was long (75 (35) ms) and wall motion incoordinate; mitral regurgitation was present in only one. In most (29) the left ventricle filled predominantly during early diastole (E fillers). Mitral regurgitation, which was present in 26, was much more common than in the A fillers, while the isovolumic relaxation time (10 (24) ms) was much shorter and the normal phase relations between flow velocity and wall motion were lost. In 24 E fillers no atrial flow was detected. In four there was no evidence of any mechanical activity, suggesting "atrial failure". In 20, either the apex cardiogram or the mitral echogram showed an A wave, implying that atrial contraction had occurred but had failed to cause transmitral flow, showing that ventricular filling was fundamentally disturbed in late diastole. A series of discrete abnormalities of filling, beyond those shown by Doppler alone, could thus be detected in this apparently homogeneous patient group by a combination of non-invasive methods. The presence and nature of these abnormalities may shed light on underlying physiological disturbances.     

A new look at diastole

The isovolumic period following systolic ejection is associated with untwisting of the apex that follows systolic torsion of the left ventricle, with simultaneous generation of negative pressures in the left ventricle. Previous studies have described this period as isovolumic relaxation, and have regarded the untwisting as entirely caused by restoring elastic forces. However, evidence from several sources indicates that some ventricular muscle is still contracting during this period, and that this muscle is subepicardial muscle or the ascending spiral segment of the ventricular myocardial band that extends from the apex up along the left ventricular epicardium and the right ventricular side of the septum to the root of the aorta. It is possible that diastolic dysfunction is due to defective incoordination of muscle contraction between the ascending and descending segments of this band rather than to defective passive restoring forces.     

等容收缩期心肌加速度评价心室收缩功能的研究进展

组织多普勒显像获得的等容收缩期心肌加速度是一个敏感的心室收缩功能指标,相对不依赖生理范围内前、后负荷改变。等容收缩期心肌加速度与有创方法获得的最大心室压力变化速率（心室内压力变化的最大速率）及射血分数密切相关。等容收缩期心肌加速度是无创评价各种先天性及获得性心脏病患者左、右心室整体或局部收缩功能的有用工具。     

The 'rapid filling wave' of the apex cardiogram. Its relation to echocardiographic and cineangiographic measurements of ventricular filling.

In order to study the relation between the 'rapid filling wave' of the apex cardiogram and left ventricular filling, simultaneous apex cardiograms, phonocardiograms, and echocardiograms were recorded in 57 patients. Continuous measurements of left ventricular dimension were derived from the echocardiograms by digitization using manual tracing and a computer. Possible errors in the use of a single dimension to assess left ventricular filling were investigated by frame-by-frame analysis of cineangiocardiograms in 37 patients, and the timing of changes in transverse diameter found to correlate closely with those in cavity area. Mitral valve opening, shown as the initial separation of the valve cusps by echocardiography, preceded the 'O' point of the apex cardiogram in all except 3 patients, the 'O' point appearing to correlate more closely with the time of peak rate of outward wall movement. A third heart sound was present in 29 patients, and in 25 of these it occurred later than the peak rate of wall movement (ment interval 51 ms). The end of rapid filling derived from the dimension trace occurred in relation to the third heart sound after a mean interval of 9 ms, with a range from 50 ms before to 80 ms after the third sound. Peak rates of wall movement were similar in patients with and without third heart sounds. The results show that outward left ventricular wall movement begins with a period of acceleration, with peak rates occurring synchronous with the 'O' point of the apex cardiogram and thus with the nadir of the ventricular pressure trace. Outward wall movement becomes less rapid thereafter, so that the rapid filling wave of the apex cardiogram does not reflect the time of rapid filling of the left ventricle. The 'O' point is not related to mitral valve movement nor does the third heart sound bear a consitent relation to any aspect of left ventricular wall movement.     

Comparison of subclinical left and right ventricular systolic dysfunction in non-dipper and dipper hypertensives: impact of isovolumic acceleration

Objectives: To evaluate subclinical left ventricular and right ventricular systolic impairment in dipper and non-dipper hypertensives by using isovolumic acceleration.

Methods: About 45 normotensive healthy volunteers (20 men, mean age 43?±?9 years), 45 dipper (27 men, mean age 45?±?9 years) and 45 non-dipper (25 men, 47?±?7 years) hypertensives were enrolled. Isovolumic acceleration was measured by dividing the peak myocardial isovolumic contraction velocity by isovolumic acceleration time.

Results: Non-dippers indicated lower left ventricular (2.2?±?0.4?m/s² versus 2.8?±?1.0?m/s², p?2 versus 3.5?±?1.0?m/s², p?=?0.012) compared with dippers. Left ventricular mass index (p?=?0.001), interventricular septal thickness (p?=?0.002) and myocardial performance index (p?p?=?0.002), mass index (p?=?0.001) and right ventricular myocardial performance index (p?Conclusion: The present study demonstrates that non-dipper hypertensives have increased left and right ventricular subclinical systolic dysfunction compared with dippers. Isovolumic acceleration is the only echocardiographic parameter in predicting this subtle impairment.     

The 'rapid filling wave' of the apex cardiogram. Its relation to echocardiographic and cineangiographic measurements of ventricular filling.

In order to study the relation between the 'rapid filling wave' of the apex cardiogram and left ventricular filling, simultaneous apex cardiograms, phonocardiograms, and echocardiograms were recorded in 57 patients. Continuous measurements of left ventricular dimension were derived from the echocardiograms by digitization using manual tracing and a computer. Possible errors in the use of a single dimension to assess left ventricular filling were investigated by frame-by-frame analysis of cineangiocardiograms in 37 patients, and the timing of changes in transverse diameter found to correlate closely with those in cavity area. Mitral valve opening, shown as the initial separation of the valve cusps by echocardiography, preceded the 'O' point of the apex cardiogram in all except 3 patients, the 'O' point appearing to correlate more closely with the time of peak rate of outward wall movement. A third heart sound was present in 29 patients, and in 25 of these it occurred later than the peak rate of wall movement (ment interval 51 ms). The end of rapid filling derived from the dimension trace occurred in relation to the third heart sound after a mean interval of 9 ms, with a range from 50 ms before to 80 ms after the third sound. Peak rates of wall movement were similar in patients with and without third heart sounds. The results show that outward left ventricular wall movement begins with a period of acceleration, with peak rates occurring synchronous with the 'O' point of the apex cardiogram and thus with the nadir of the ventricular pressure trace. Outward wall movement becomes less rapid thereafter, so that the rapid filling wave of the apex cardiogram does not reflect the time of rapid filling of the left ventricle. The 'O' point is not related to mitral valve movement nor does the third heart sound bear a consitent relation to any aspect of left ventricular wall movement.     

Isovolumic contraction time of right ventricle in d-transposition of great arteries.

The pre-ejection period of the right ventricle in d-transposition of the great arteries is known to be prolonged, compared with the same interval of the left ventricle of normal subjects. In the present study, the echocardiographic measurement of the components of the pre-ejection period of the right ventricle of 14 patients with d-transposition of the great arteries shows that the isometric contraction time of the right ventricle in d-transposition of the great arteries is similar to the same interval calculated on the left ventricle of 76 normal children of comparable age. On the other hand, the electromechanical delay was significantly greater for the right ventricle of d-transposition of the great arteries than for the left ventricle of the normal subjects. It is concluded that the prolonged pre-ejection period of the right ventricle in d-transposition of the great arteries is not the result of right ventricular dysfunction but solely of a longer electromechanical delay.     

Changes in the pressure-volume relation of the right ventricle when its loading conditions are modified

Ventricular pressure-volume diagrams were obtained from the right ventricle in patients before and after relief of right ventricular pressure load, in patients with volume loaded right ventricles, and from the left ventricle in patients after the Mustard procedure for transposition of the great arteries. The patterns of ejection during pressure development and decline were similar in patients after relief of pressure load and in those with isolated volume load. A right ventricular pressure load, however, reduced ejection during the two "isovolumic" periods, and the overall shape of the pressure-volume loop resembled that of the normal left ventricle. Pressure-volume diagrams obtained from the left ventricle after the Mustard procedure were indistinguishable from the normal right ventricle, which accords with the hypothesis that the normal right ventricular contraction pattern is a consequence of loading conditions rather than a reflection of an intrinsic property of the myocardium.