组织运动二尖瓣环位移技术评估急性前壁心肌梗死患者左心室收缩功能的价值

目的探讨组织运动二尖瓣环位移技术评估急性前壁心肌梗死患者左心室收缩功能的价值。方法 32例择期接受冠状动脉介入(PCI)手术的急性前壁心肌梗死患者作为研究组,另选取32例健康志愿者作为对照组。术前1 w内、术后2个月分别进行左心室射血分数(LVEF)、左心室舒张末期容积(LVEDV)、左心室收缩末期容积(LVESV)、组织运动二尖瓣瓣环位移测量(TMAD)及二尖瓣环的收缩期位移峰值(Ds)测量,并进行相关性研究。结果研究组手术前、后LVEF较对照组显著降低,LVESV、LVEDV较对照组显著升高(P0.05),研究组手术后LVESV、LVEDV较术前降低,LVEF较手术前有所改善但差异尚无统计学意义(P0.05);研究组TMAD参数手术前后比较差异明显(P0.05),研究组患者手术前、后与对照组TMAD比较差异有显著意义(P0.05),TMAD参数与LVEF均存在显著正相关;研究组二尖瓣环收缩期位移峰值(Ds)手术前后比较差异明显(P0.05),研究组手术前、后与对照组二尖瓣环Ds比较差异显著(P0.05),研究组二尖瓣环6个位点平均Ds与LVEF亦呈正相关。结论TMAD各参数能早期反映急性前壁心肌梗死患者手术前、后左室收缩功变化,是一种快速可靠、简便的评价急性前壁心肌梗死患者左室整体收缩功能的方法。     

组织运动二尖瓣环位移自动追踪技术对急性心肌梗死患者左心室整体收缩功能的评价

目的:探讨组织运动二尖瓣环位移自动追踪技术(TMAD)在评价急性心肌梗死(AMI)患者左心室整体收缩功能中的临床应用价值。方法:选取AMI患者29例为AMI组,年龄匹配的健康志愿者31例为对照组,采用Philips IE33彩色超声诊断仪,行常规超声心动图检查,应用双平面Simpson法测量左心室舒张末容积、左心室收缩末容积和左心室射血分数(LVEF)。存储心尖四腔、三腔和两腔连续3～5个心动周期二维动态图像,用Qlab 7.0软件进行脱机分析,测量二尖瓣环6个位点收缩期最大位移(Ds)、瓣环连线中点最大位移(D-mid)和左心室长轴缩短率(FSL),分别计算其均值,并与简化双平面Simpson测量的LVEF做相关分析。结果:①与对照组相比,AMI组二尖瓣环6个位点Ds、D-mid、FSL及其均值显著降低,均差异有统计学意义(均P<0.001);②2组Ds均值、D-mid均值及FSL均值与LVEF均具有相关性(AMI组r分别为0.787、0.776和0.779,P<0.001;对照组r分别为0.662、0.706和0.759,P<0.001);③重复性检验:AMI组Ds均值、D-mid均值及FSL均值观察者内...     

超声斑点追踪成像技术对扩张型心肌病患者左心室同步性的初步研究

目的探讨斑点追踪成像技术(STI)评价扩张型心肌病患者左心室收缩同步性的临床应用价值。方法选择30例扩张型心肌病(DCM)患者及20名正常人,应用二维超声测量其左心室舒张末期内径(LVEDd)、舒张末期容积(LVEDV)、收缩末期容积(LVESV)和左室射血分数(LVEF)。应用STI技术测量左室长轴各节段及短轴切面(二尖瓣、乳头肌、心尖),各节段从心电图QRS波起始至收缩期峰值的纵向应变(Tssl)、径向应变(Tssr)、环向应变的达峰时间(Tssc)。并计算位于同一平面的所有节段达收缩期峰值纵向应变、径向应变、环向应变的时间标准差(Tssl-SD、Tssr-SD、Tssc-SD),及测量同一平面任意两节段最大达峰时间差值(Tssl-diff、Tssr-diff、Tssc-diff),并进行分析。结果 DCM组与正常组相比,LVEDd、LVEDV、LVESV均显著增加(P<0.05),LVEF显著减低(P<0.05);Tssl-SD、Tssr-SD、Tssc-SD、Tssl-diff、Tssr-diff、Tssc-diff显著增加(P<0.05)。结论 DCM患者左室心肌存在收缩不同步运动,超声二维斑点追踪技术为定量评价DCM患者左室收缩同步性提供了一种新方法。     

实时三平面超声心动图与双平面Simpson's法评价心肌梗死患者左心室收缩功能的相关性分析

目的 探讨实时三平面超声心动图(RT-3PE)与二维超声心动图(2DE)双平面Simpson,s法测量心肌梗死患者左室容积和左心室射血分数(LVEF)的相关性.方法 应用RT-3PE和二维超声心动图(2DE)双平面Simpson's法同期测量30例心肌梗死患者的左室舒张末期容积(LVEDV)、左室收缩末期容积(LVESV)和LVEF,并将两种方法的测值进行相关性分析.结果 RT-3PE法和2DE双平面法所测的LVEDV、LVESV和LVEF之间均无统计学意义(P＞0.05),且相关性良好(r分别为0.89、0.96和0.86,P＜0.01).结论 实时三平面超声心动图可以实时在线测定心肌梗死患者左心室容积和左室射血分数,为临床上定量分析心肌梗死患者左心室容积和左室射血分数提供了一种检查快速、简便和无创的新方法.     

组织运动二尖瓣环位移自动追踪技术评价冠心病患者左心室功能

目的探讨组织运动二尖瓣环位移自动追踪技术（TMAD）评价冠心病患者左心室收缩及舒张功能。方法经冠状动脉造影证实的冠心病患者（CHD组）27例及年龄匹配的对照组30例，连续测量3个心动周期二尖瓣环4个位点的收缩期峰值位移（Ds）、瓣环连线中点最大位移（Mid）、Mid与左心室舒张期末最大纵径比值（Mid%）、收缩期达峰时间（T）、舒张早期位移（De）及舒张晚期位移（Da），求均值，计算Da/Dt（Dt＝De＋Da），并将Ds均值、Mid均值、Mid%均值与双平面Simpson法计算出的左心室射血分数（LVEF）及将Da/Dt与二尖瓣口血流频谱A/E峰值比作相关性分析。结果（1）与对照组相比，CHD组4个位点Ds、Mid、Mid%及其均值均降低（P<0.01），4个位点达峰时间及其均值均延长（P<0.05或P<0.01）；（2）与对照组相比，CHD组4个位点De及其均值均降低（P<0.01），侧壁、前壁、下壁Da及4个位点Da均值均增高（P<0.05或P<0.01），Da/Dt增高（P<0.01）；（3）对照组、CHD组Ds均值、Mid均值及Mid%均值与LVEF呈正相关（对照组：r＝0.697，r＝0.711，r＝0.779，P<0.01；CHD组：r＝0.707，r＝0.703，r＝0.789，P<0.01）；（4）对照组、CHD组Da/Dt与A/E峰值比呈正相关（r＝0.739，r＝0.666，P<0.01）。结论TMAD新技术可以客观、方便地评价冠心病患者左心室功能。     

组织运动瓣环位移追踪技术定量评估左心室收缩功能的研究

目的探讨组织运动瓣环位移追踪技术(TMAD)定量评估左心室收缩功能的价值。方法随机选择150例观察对象,其中健康对照组30例,心功能不全患者120例。于心尖四腔切面,应用TMAD技术获取二尖瓣环室间隔(TMAD1)、侧壁(TMAD2)及此2位点连线中点处TMADmid相对于心尖的位移值,同时Simpson’s法测得左心室射血分数(LVEF)。测定血浆N末端脑钠肽值(NT-proBNP)。结果对照组TMADmid均值为(12.59±2.71)mm,与异常组均值(7.09±3.11)mm比较差异有统计学意义(P<0.01),并与LVEF相关(r=0.88,P<0.01)。TMADmid与LVEF异常例数在心功能不全各组中的分布差异有统计学意义(χ2=81.06,P<0.01)。TMADmid与NYHA心功能分级、NT-proBNP高度相关(r=0.90,r=-0.82,均P<0.05)。结论 TMAD能快速、客观地反映左心室收缩功能,是诊断心功能不全的有效指标。     

血清cTnIAAb与急性心肌梗死患者左心室重构的关系

目的探讨血清抗心肌肌钙蛋白Ⅰ自身抗体(cTnIAAb)在急性心肌梗死患者中的表达水平及其与左心室重构的关系。方法选取2016年1月至2018年3月于北京安贞医院收治的143例急性心肌梗死患者为研究对象,根据美国纽约心脏病协会(NYHA)制定的心功能分级标准将其分为NYHAⅡ级(n=62)、NYHAⅢ级(n=47)、NYHAⅣ级(n=34),并于同期随机选取40例健康体检者为对照组(n=40),采用酶联免疫吸附法检测入院时各组血清c Tn IAAb A 450 nm值,超声心动图检查各组左心室重构指标,包括左心室舒张末期直径(LVEDD)、左心室收缩末期直径(LVESD),M型超声检测左心室舒张末期容积(LVEDV)、左心室收缩末期容积(LVESV)、左心室射血分数(LVEF),并计算左室心肌质量指数(LVMI)。结果不同NYHA分级急性心肌梗死患者血清cTnIAAbA 450 nm值均高于对照组,且随着NYHA分级越高,血清c Tn IAAb A 450 nm值呈升高趋势,差异均有统计学意义(P0.05)。不同NYHA分级急性心肌梗死患者心室重构参数LVEDD、LVESD、LVEDV、LVESV、LVMI水平均大于对照组,LVEF水平低于对照组,且随着NYHA分级越高,患者心室重构参数LVEDD、LVESD、LVEDV、LVESV、LVMI越大,LVEF越小,差异均有统计学意义(P0.05)。Pearson积矩相关分析显示,急性心肌梗死患者血清cTnIAAb与心室重构参数LVEDD、LVESD、LVEDV、LVESV、LVMI均呈正相关性(r=0.637、0.598、0.517、0.562、0.632,P0.05),与LVEF呈负相关性(r=-0.622,P0.05)。结论血清cTnIAAb升高与急性心肌梗死左心室重构密切相关,早期检测可作为评估患者病情严重程度的重要指标。     

CT定量评估经导管主动脉瓣置换术前患者心肌应变的可行性研究

目的 以心脏磁共振(CMR)为参考标准,探讨CT评估经导管主动脉瓣置换术(TAVR)术前患者心肌应变的可行性。方法 回顾性收集2022年6至12月首都医科大学附属北京安贞医院行心脏CT检查的TAVR术前患者43例,采集心脏CT和CMR数据,测量心肌应变参数。将基于心脏CT的心功能和应变参数与CMR进行比较,包括LVEF、左心室舒张末期容积(LVEDV)、左心室收缩末期容积(LVESV)、舒张期心肌质量(MASS)、心排血量、整体纵向应变峰值(GPLS)、整体周向应变峰值(GPCS)和整体径向应变峰值(GPRS)。结果 基于心脏CT获得的LVEF、心排血量与CMR参数接近,差异无统计学意义(P>0.05),而基于心脏CT获得的LVEDV、LVESV、MASS明显高于CMR,GPLS、GPCS、GPRS绝对值明显低于CMR,差异有统计学意义(P<0.01)。Pearson相关性分析显示,基于心脏CT的LVEF、LVEDV、LVESV、MASS、GPCS、GPRS与CMR参数呈较强正相关(r=0.908,r=0.917,r=0.947,r=0.954,r=0.856,r=0.86...     

AMI患者血浆脑钠肽水平测定及其与左室重构的关系

测定对68例急性心肌梗死(AM I)患者发病后48 h内(早期)血浆脑钠肽(BNP)水平;于发病后28~30 d行超声心动图检查,测量左心室收缩末期容积(LVESV)、左心室舒张末期容积(LVEDV)和左心室射血分数(LVEF)。对血浆BNP水平与LVESV、LVEDV、LVEF进行相关性分析。结果LVEF≤40%者血浆BNP水平显著高于LVEF>40%者,P<0.05;血浆BNP水平与LVESV、LVEDV呈正相关,与LVEF呈负相关。认为AM I早期血浆BNP水平升高与其28~30 d左室重构程度密切相关,应积极进行干预治疗。     

组织运动瓣环位移技术评价老年双腔起搏器患者不同部位起搏与预后关系

目的 探讨右心室中位间隔面及心尖部起搏下组织运动瓣环位移（TMAD）及N末端B型利钠肽（NT-proBNP）水平与患者预后的关系.方法 2009年3月至2012年1月植入DDD起搏器老年患者148例为研究对象,选择右心室中位间隔部起搏患者（RVMSP组）56例、右心室心尖部起搏患者（RVAP组）42例,观察2组患者术前、术后6、18个月心电图QRS时限,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NT-proBNP、测量左心室舒张末期容积（LVEDV）以及出现心血管事件包括心室高频事件（VHR）等指标.结果 所有患者均顺利完成手术,按期随访.2组心血管事件发生率比较,RVAP组最高（P＜0.05）,2组VHR差异无统计学意义（P＞0.05）;与术前比较,RVMSP组患者术后6、18个月NT-proBNP、LVEF、LVEDV等均无变化,RVAP组NT-proB-NP、LVEF、LVEDV无变化,二尖瓣环各位点MAD以及二尖瓣环MADgloba降低,TAS-POST增加（P＜0.05）.术后18个月RVAP组NT-proBNP增加,LVEDV值增加（P＜0.05）,差异有统计学意义（P＜0.05）,LVEF无变化.结论 RVMSP心血管事件发生率较低,不影响患者心功能,为较理想起搏部位,TMAD可早期监测心功能受损,为起搏器患者早期心功能异常的检测提供新的方法.     

Left atrial transport function in myocardial infarction. Importance of its booster pump function.

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.     

Accurate estimates of absolute left ventricular volumes from equilibrium radionuclide angiographic count data using a simple geometric attenuation correction

To simplify and clarify the methods of obtaining attenuation-corrected equilibrium radionuclide angiographic estimates of absolute left ventricular volumes, 27 patients who also had biplane contrast cineangiography were evaluated. Background-corrected left ventricular end-diastolic and end-systolic counts were obtained by semiautomated variable and hand-drawn regions of interest and were normalized to cardiac cycles processed, frame rate and blood sample counts. Blood sample counts were acquired on (d degree) and at a distance (d') from the collimator. A simple geometric attenuation correction was performed to obtain absolute left ventricular volume estimates. Using blood sample counts obtained at d degree or d', the attentuation-corrected radionuclide left ventricular end-diastolic volume estimates using both region of interest selection methods correlated with the cineangiographic end-diastolic volumes (r = 0.95 to 0.96). However, both mean radionuclide semiautomated variable left ventricular end-diastolic volumes (179 +/- 100 [+/- 1 standard deviation] and 185 +/- 102 ml, p less than 0.001) were smaller than the average cineangiographic end-diastolic volume (217 +/- 102 ml), and both mean hand-drawn left ventricular end-diastolic volumes (212 +/- 104 and 220 +/- 106 ml) did not differ from the average cineangiographic end-diastolic volume. Using the blood sample counts obtained at d degree or d', the attenuation-corrected radionuclide left ventricular end-systolic volume estimates using both region of interest selection methods correlated with the cineangiographic end-systolic volumes (r = 0.96 to 0.98). Also, using blood sample counts at d degree, the mean radionuclide semiautomated variable left ventricular end-systolic volume (116 +/- 98 ml, p less than 0.05) was less than the average cineangiographic end-systolic volume (128 +/- 98 ml), and the other radionuclide end-systolic volumes did not differ from the average cineangiographic end-systolic volume. Therefore, it is concluded that: 1) a simple geometric attenuation-correction of radionuclide left ventricular end-diastolic and end-systolic count data provides accurate estimates of biplane cineangiographic end-diastolic and end-systolic volumes; and 2) the hand-drawn region of interest selection method, unlike the semiautomated variable method that underestimates end-diastolic and end-systolic volumes, provides more accurate estimates of biplane cineangiographic left ventricular volumes irrespective of the distance blood sample counts are acquired from the collimator.     

Right and left ventricular volume characteristics in children with transposition of the great arteries after Mustard's procedure

With use of biplane cine-angiocardiograms, the measurements of right and left ventricular volume were determined in 11 children with transposition of the great arteries following Mustard's procedure. Right ventricular end-diastolic volume (RVEDV) ranged from 124 to 264 percent of the normal right ventricular volume with an average of 188 +/- 40 (SDM) percent, and left ventricular end-diastolic volume (LVEDV) ranged from 57 to 181 (122 +/- 43) percent of the normal (p less than 0.01, vs. RVEDV). Right ventricular ejection fraction (RVEF) ranged from 0.26 to 0.66 (0.42 +/- 0.11), and left ventricular ejection fraction (LVEF) ranged from 0.51 to 0.79 (0.66 +/- 0.09) (p less than 0.001, vs RVEF). Left ventriculography showed a deviation of the interventricular septum toward the left ventricle in patients with simple transposition of the great arteries not associated with left ventricular hypertension. The left to right ventricular systolic pressure ratio ranged from 0.22 to 1.02 (0.48 +/- 0.28), and the left to right ventricular end-diastolic volume ratio ranged from 0.43 to 1.00 (0.63 +/- 0.18). There was a high correlation between the left to right ventricular systolic pressure ratio and the left to right ventricular end-diastolic volume ration (r = 0.94, p less than 0.001). The left to right ventricular systolic pressure ratio also correlated well with the right ventricular ejection fraction (r = 0.90, p less than 0.001). Deviation of the interventricular septum was considered to result in a diminished ejection fraction of the right ventricle, in patients with simple transposition of the great arteries not associated with left ventricular hypertension, after Mustard's procedure.     

房间隔缺损封堵术后心功能的变化

目的 评价左、右室功能及左房收缩功能在房间隔缺损（ASD）封堵治疗术后及随访中的变化。方法 对成功施行经皮穿刺ASD封堵术的20例患进行研究。所有患于封堵治疗术前、术后及术后3个月行超声心动图检查,左、右室容积采用单平面面积-长度法计算,以左室晚期充盈数作为反映左房收缩功能的指标。结果 ASD填充堵治疗术后,左室舒张末期前后径及及左室舒张末期容积增大,而左室收缩末期容积则未见明显改变,左室每搏量、左室射血分数及短轴缩短率增大。左客观存在偏心率及长径/短径比值均较术前缩小,左室前负荷、收缩功能及几何构型在随访中持续改善。ASD封 堵治疗术后右室舒张末期前后径、右室舒张末期容积、右室收缩末期容积、右室每搏量及右室射血分数（RVEF）均减小;随访中上述指标除RVEF外均进一步减小,而RVEF未见显改变,置入封堵器后及随访左室晚期充盈分数,差异无显性。结论 ASD封堵治疗既减轻了右室的容量铅荷,也改善了左室的收缩功能及几何构型,在短期随访中,左室功能及几何构型持续改善,右室功能维持于正常水平,置入封堵器对左房收缩功能未产生显影响。     

Significance of the pericardium in human subjects: effects on left ventricular volume, pressure and ejection

To assess the effect of the pericardium, left ventricular systolic function and diastolic compliance were studied in 15 patients before and after pericardiotomy during coronary artery surgery. Using first pass radionuclide angiography, curves for left ventricular systolic function (stroke work versus end-diastolic volume) and a measure of diastolic compliance (pulmonary capillary wedge pressure versus end-diastolic volume) were generated by changing body position to alter venous return. Left ventricular end-diastolic volume ranged from 41 to 111 ml/m2 and pulmonary capillary wedge pressure from 0 to 24 mm Hg. No significant changes were found in blood pressure (150/83 to 148/82 mm Hg), heart rate (66.7 to 67.1 beats/min), cardiac index (2.38 to 2.41 liters/min per m2), ejection fraction (0.56 to 0.54), end-systolic volume index (31.4 to 32.2 ml/m2), end-diastolic volume index (65.9 to 69.5 ml/m2) or pulmonary capillary wedge pressure (7.5 to 7.3 mm Hg). The pericardium did not affect the curves relating stroke work and end-diastolic volume or those relating pulmonary capillary wedge pressure and end-diastolic volume. Thus, when filling pressure and volume are normal or only moderately elevated, the pericardium does not appear to affect left ventricular systolic function or diastolic compliance in patients.     

Ventricular interaction during mechanical ventilation in closed-chest anesthetized dogs

The cardiac effects of positive pressure ventilation and positive end-expiratory pressure are incompletely understood. External constraint due to increased intrathoracic pressure decreases left ventricular end-diastolic volume; the effects on venous return and ventricular interaction are less clear. Phasic changes in inferior vena caval flow, end-diastolic ventricular dimensions and output were measured in seven anesthetized, ventilated normal dogs. During inspiration, caval flow, right ventricular diameter and output decreased; end-diastolic transseptal pressure gradient, septum-to-left ventricular free wall diameter, left ventricular area (ie, left ventricular volume index) and output increased despite the decreased sum of the septum-to-free wall diameters. The reverse occurred during expiration. Increased positive end-expiratory pressure decreased the left ventricular area, but the end-expiratory right ventricular diameter was unchanged. At given airway pressures, right ventricular diameter was greater at higher positive end-expiratory pressures, suggesting that a leftward septal shift (direct ventricular interaction) added to the effect of external constraint on left ventricular end-diastolic volume. In conclusion, positive pressure ventilation reduced right ventricular end-diastolic volume during inspiration and increased the transseptal pressure gradient, which shifted the septum rightward, increasing left ventricular end-diastolic volume and output. The reverse occurred during expiration. Positive end-expiratory pressure constrained left ventricular filling and decreased left ventricular end-diastolic volume further by a leftward septal shift.     

Left ventricular volume characteristics in children with tricuspid atresia before and after surgery

Left ventricular volume variables (left ventricular end-diastolic volume, ejection fraction, mass and systolic output) were quantified in (1) 13 patients with tricuspid atresia preoperatively (type Ia, 3 patients; type Ib, 9 patients; type IIb, 1 patient), (2) 4 patients after a shunt procedure (Blalock-Taussig, 3; Glenn, 1), and (3) 1 patient after corrective surgery. Cardiac catheterization and angiography were performed at age 1 month to 5.8 years (mean 1.4 years). All patients had decreased pulmonary blood flow. The results were compared with data in 15 patients with no significant heart disease. Left ventricular end-diastolic volume was significantly greater than normal in 12 of the 13 patients. Left ventricular mass was significantly greater than normal, but ejection fraction was significantly less than normal. There was a positive correlation between ejection fraction and systemic oxygen saturation. Left ventricular systolic index was normal in 9 of the 13 patients preoperatively. After a shunt procedure, left ventricular end-diastolic volume and systolic index increased significantly in all four patients, and ejection fraction improved greatly in three of the four. After corrective surgery, left ventricular end-diastolic volume and left ventricular systolic index returned to the normal range and left ventricular ejection fraction improved. These findings suggest that patients with tricuspid atresia have impaired left ventricular function.     

Radionuclide analysis of right and left ventricular response to exercise in patients with atrial and ventricular septal defects

In patients with ventricular or atrial septal defect, the ventricle which is chronically volume overloaded might not appropriately respond to increased demand for an augmentation in output and thereby might limit total cardiac function. In this study we simultaneously measured right and left ventricular response to exercise in 10 normal individuals, 10 patients with ventricular septal defect (VSD), and 10 patients with atrial septal defect (ASD). The normal subjects increased both right and left ventricular ejection fraction, end-diastolic volume, and stroke volume to achieve a higher cardiac output during exercise. Patients with VSD failed to increase right ventricular ejection fraction, but increased right ventricular end-diastolic volume and stroke volume. Left ventricular end-diastolic volume did not increase in these patients but ejection fraction, stroke volume, and forward left ventricular output achieved during exercise were comparable to the response observed in healthy subjects. In the patients with ASD, no rest-to-exercise change occurred in either right ventricular ejection fraction, end-diastolic volume, or stroke volume. In addition, left ventricular end-diastolic volume failed to increase, and despite an increase in ejection fraction, left ventricular stroke volume remained unchanged from rest to exercise. Therefore, cardiac output was augmented only by the heart rate increase in these patients. Right ventricular function appeared to be the major determinant of total cardiac output during exercise in patients with cardiac septal defects and left-to-right shunt.     

Pronounced dependence of ventricular endocardial QRS potentials on ventricular volume.

To evalulate the relation between ventricular endocardial potentials (QRS amplitude) and ventricular dimensions, left and right ventricular endocardial potentials were recorded with hook electrodes in anaesthetised open-chest dogs during transfusion and withdrawal of blood. Left ventricular end-diastolic diameter was measured by ultrasonic crystals, and end-diastolic volume was determined by thermodilution. In each dog, left ventricular endocardial potentials, whether recorded from anterior or posterolateral walls, decreased linearly as left ventricular end-diastolic diameter or volume increased, and vice versa. With an average increase in left ventricular end-diastolic diameter from 40.1 +/- 1.7 to 44.6 +/- 1.8 mm, left ventricular endocardial potentials decreased from 32.8 +/- 2.5 to 23.5 +/- 2.3 mV (P less than 0.001); and for an increase in left ventricular end-diastolic volume from 1.36 "/- 1.25 to 3.43 +/- 0.58 ml/kg left ventricular endocardial potentials decreased from 36.2 +/- 6.6 to 14.9 +/- 4.3 mV (P less than 0.001). Changes in right ventricular endocardial potentials paralleled the changes in left ventricular endocardial potentials. These findings indicate that acute changes in ventricular dimensions influence endocardial potentials considerably, and suggest a potential clinical application for detecting acute changes in ventricular volume.     

Effects of right ventricular ischemia on left ventricular geometry and the end-diastolic pressure-volume relationship in the dog

We studied the effects of right ventricular ischemia on left ventricular three-dimensional geometry and the end-diastolic pressure-volume relationship in 16 open-chest dogs before and after pericardiectomy. Left ventricular volume was calculated from three internal dimensions measured with ultrasonic crystals. In one group of eight dogs, right coronary artery (RCA) occlusion for 2 min with the pericardium intact reduced aortic flow by 24 +/- 9% (p less than .001) and septal-lateral dimension by 8 +/- 5% (p less than .01), without changing anterior-posterior and apical-basal dimensions. However, parameters of left ventricular systolic function (aortic flow, left ventricular systolic pressure, peak dP/dt, and mean percent systolic shortening) were similar to those observed at a comparable level of left ventricular end-diastolic volume during inferior vena caval occlusion. In the other group of eight dogs, during RCA occlusion before pericardiectomy the left ventricular end-diastolic pressure-volume relationship determined during rapid blood transfusion shifted leftward and upward significantly from the preocclusion relationship. After pericardiectomy, RCA occlusion caused less significant changes in aortic flow and septal-lateral dimension as well as in the left ventricular end-diastolic pressure-volume relationship. We concluded that right ventricular ischemia causes a leftward shift of the interventricular septum in end-diastole and an alteration of the left ventricular end-diastolic pressure-volume relationship without changing left ventricular myocardial performance. These changes are enhanced by the intact pericardium.