心室压力-容量环评价非体外循环冠状动脉旁路移植术患者术中右心室功能的变化

目的 采用心室压力-容量环(P-V环)评价非体外循环冠状动脉旁路移植术(OPCABG)患者术中右心室功能的变化.方法 择期行OPCABG的三支病变冠心病患者28例,年龄53～76岁,ASAⅡ或Ⅲ级.经右颈内静脉穿刺,置入肺动脉导管,于切皮前(T1)、心脏前壁、侧壁、后壁血管搭桥并放置心肌固定器后5 min(T2-4)、术毕缝皮(T5)时记录血液动力学指标;记录舒张末期、等容收缩末期、射血峰压期、收缩末期、等容舒张末期右心室压力及容量数据,绘制右心室P-V环(以A点代表舒张末期,A'点代表收缩末期),并计算右心室收缩末期弹性(EES)及舒张末期僵硬度(EED).结果 T1-5,时右心室P-V环大致向坐标轴左上方移动,其中A点向左上方移动,A'点未见明显移动.与T1时比较,T2-5时EED功升高(P<0.05);EES各时点间差异无统计学意义(P>0.05).结论 右心室P-V环结果分析显示:OPCABG患者术中右心室功能抑制与右心室壁顺应性降低有关,与心肌收缩力无关.     

静脉麻醉药对去甲肾上腺素预收缩兔肺动脉环的作用

本研究采用兔离体肺动脉环作为实验标本 ,观察了静脉麻醉药硫喷妥钠(ＳＴＰ)、氯胺酮 (ＫＥＴ)、异丙酚 (ＰＲＯ)对张力正常及去甲肾上腺素 (ＮＥ)预收缩肺动脉环的作用 ,以及肺动脉内皮完整性对药物作用的影响材料与方法一、离体肺动脉环的制备、张力测定和去内皮试验[1] 。二、药物对张力正常肺动脉环的直接作用　将ＰＲＯ以累积剂量 0 0 3ｍｍｏｌ/Ｌ、0 1ｍｍｏｌ/Ｌ、 0 3ｍｍｏｌ/Ｌ、 1 0ｍｍｏｌ/Ｌ、3 0ｍｍｏｌ/Ｌ分别加入浴槽 ,每剂量作用5ｍｉｎ ,观察每种药物对肺动脉环的直接作用。三、药物对去甲肾上腺素 (ＮＥ)预收缩肺…     

应用心室压力-容量关系探讨肝移植术中右心室收缩和舒张功能的变化

目的 用容量性肺动脉导管收集右心室收缩末期和舒张末期的压力、容量数据,并计算心室收缩末期弹性(end-systolic elagtance,Ees)、舒张未僵硬度(end-diastolic stiffness,EED)、有效动脉弹性(arterial effective elastance,Ea)、Ees/Ea,借以评价肝移植术中右心室收缩和舒张功能的变化.方法 12例拟行同种异体原位肝移植术的终末期肝病患者.ASA Ⅱ-Ⅳ级;无心脏病史,心功能Ⅰ或Ⅱ级;不合并肺动脉高压[以插入漂浮导管后平均肺动脉压(MPAP)25 mm Hg为标准]及其他肺部疾病.全麻后行右侧颈内静脉穿刺,放置容量性肺动脉导管.于切皮前麻醉稳定时、无肝期10 min、新肝期10 min、术毕缝皮时,4个时点收集数据,包括①记录右心血流动力学参数;②计算Ees、EED、Ea、Ees/Ea.结果 与切皮前相比,无肝期心指数(cardiac index,CI)、右心室舒张末期容积指数(RV ejection fraction,RVEF)、右心室作功指数(fight ventricular stroke work index,RVSWI)、肺动脉楔压(pulmonary artery wedge pressure,PAWP)、中心静脉压(central verous pressure,CVP)、MPAP、每博指数(stroke volume index,SVI)、右心室舒张末期容积指数(RV end-diastolic volume index,RVEDVI)、平均动脉压(mean arterial blood pressure,MAP)等指标均明显下降(P<0.05),新肝期均相应增加.术毕时恢复至切皮前水平.Ees在4个时期未见明显变化(P0.05).EED无肝期显著下降(P<0.05),新肝期显著升高(P<0.05),术毕时恢复至切皮前水平.PVRI与Ea变化趋势一致,无肝期和新肝期增加,但没有显著性.与切皮前相比,无肝期的Ees/Ea比下降(P<0.05).结论 不合并肺动脉高压的肝移植患者术中无肝期和新肝期RVEF下降与前负荷剧降及后负荷增加有关,不代表心肌收缩能力降低.新肝期右心室舒张功能下降,表现为室壁僵硬度增加,EED下降.术毕时,右心室收缩和舒张功能均可恢复至术前水平,并且右心室功能与肺循环的状态能够匹配.     

实时三维超声心动图评价法洛四联症患者手术前后右心室收缩功能

目的应用实时三维超声心动图（RT-3DE）评价法洛四联症（TOF）患儿术前及术后右心室收缩功能变化。方法应用RT-3DE测量29例TOF患儿术前及术后1周、6个月的右心室舒张末期容积（RVEDV）、右心室收缩末期容积（RVESV）、右心室每搏输出量（RVSV）及右心室射血分数（RVEF）。结果 29例TOF患儿中,12例术前RVEF低于50%（12/29,41.38%）。术后1周RVESV较术前增加,RVEF较术前减小,术后6个月RVEDV、RVESV较术前增加,RVEF值较术前减低（P均〈0.05）。随着心功能降低,三维右心室容积曲线（RVVC）逐渐低平、收缩峰值后移。结论 RT-3DE可准确、定量评价TOF患儿术前、术后右心室功能变化。     

静脉麻醉药对去甲肾上腺素积累剂量致兔肺动脉环收缩量—效…

目的：通过硫喷妥钠，异丙酚，氯胺酮对去甲肾上腺素（ＮＥ）收缩肺动脉量－效关系的影响，了解三种药物对肺血管平滑肌的直接作用，以及内上细胞完整性对其作用的影响。方法：制备免疫离体肺动脉环，应用ＤＣ－００１型离体器官测定仪，观察三种药物（１ｍＭ）对ＮＥ累积剂量量－效曲线的影响，结果：与ＮＥ对照组比较，完整内皮时，硫喷妥钠可加强肺动脉环对低浓度ＮＥ（１０＾－１０Ｍ）收缩反应，高剂量ＮＥ（１０＾－３，１０＾     

瓣膜病围术期左心收缩功能的研究

为用不受左室负荷影响的心肌收缩性能指标—收缩末弹性模量（Ｅｅｓ）—研究瓣膜病围术期左心功能，选择风心瓣膜病（ＲＨＤ）组１４例；先心对照（ＣＨＤ）组６例病人。以心外膜超声测左室容积、左室压，暂阻下腔静脉以绘出不同前负荷的左室压—容积环求得手术前后Ｅｅｓ。术中取部分病人乳头肌作电镜检查。结果示术前ＣＨＤ组Ｅｅｓ为０．６５７±０．１０１ｋＰａ／ｍｌ（４．９４±０．７６ｍｍＨｇ／ｍｌ），ＲＨＤ组０．２５４±０．０８９ｋＰａ／ｍｌ（１．９１±０．６７ｍｍＨｇ／ｍｌ）；术后ＣＨＤ组０．８１３±０．０８４ｋＰａ／ｍｌ（６．１１±０．６３ｍｍＨｇ／ｍｌ），ＲＨＤ组０．２７９±０．０５５ｋＰａ／ｍｌ（２．１０±０．４１ｍｍＨｇ／ｍｌ）。电镜显示ＲＨＤ组病人心肌纤维变性、坏死。结论：ＲＨＤ病人手术前后心肌收缩性能均减退且低于ＣＨＤ组（Ｐ＜０．０５）。心肌超微结构改变是心肌收缩性能下降的重要因素     

二尖瓣瓣下结构的心肌力学功能研究

以离体兔心灌注模型研究二瓣瓣环一乳头肌连续中断，腱索“牵拉”作用丧失后左室收缩及舒张特性的改变以及对左室过度充盈耐受性的影响，结果显示，连续中断后Ｅ ｍａｘ和ｄｐ／ｄｔ ｍａｘ减小，ＰＰＶＲ曲线右移，受过度充盈后，上述各项指标出现进下步的类似变化，结论：（１）二尖瓣及其瓣下结构具有不可忽视的心肌力学功能，即瓣膜一室协同作用。（２）瓣环－乳头肌连续连续中断后，左室收缩性减退，压力负荷耐受性削弱；主动     

非停跳冠脉搭桥术中病人心脏形态和功能的变化

目的观察非停跳冠脉搭桥术（OPCAB）中病人心脏形态和功能的变化。方法择期行OPCAB病人30例，ASAll或Ⅲ级。麻醉诱导后气管插管，经右侧颈内静脉放置CCO／SVO，／CEDV导管，连续监测血液动力学参数，经口放人多平面经食管彩色超声诊断仪探头，监测食管超声心动图（TEE）参数。分别于打开心包时（基础值）、前降支（LAD）搭桥、回旋支（LCX）搭桥、右冠状动脉（RCA）搭桥、吻合完毕时测定TEE参数及血液动力学参数。结果与基础值比较，LAD搭桥时二尖瓣血流E波减速时间（DL）缩短，经过二尖瓣口的左心流量（Q；）降低，MAP、HR下降，CVP升高；LCX搭桥时左心室舒张末直径（LVEDD）、右心室舒张末直径（RVEDD）、三尖瓣环直径（TVD）、射血分数（EF）、Q，、经过中尖瓣口的右心流量（Q2）、左心室流出道舒张变化率[（DDL—SDL）／DDL]、三尖瓣血流E／A比值（E2／A2）、TVD降低，二尖瓣血流E／A比值（E1／A1）升高，DL、三尖瓣血流E波减速时间（DT2）缩短，HR、MAP、每搏量（sV）、混合静脉血氧饱和度（蹄01）、右心室舒张末容积（RVEDV）、右心室收缩末容积（RVESV）、右心室射血分数（RVEF）、右心室舒经末容积指数（RVEDVI）降低，CVP升高；RCA搭桥时LVEDD、LVESD、二尖瓣环直径、Q，、E2／A2、HR、MAP、平均肺动脉压、SV、SvO2、RVEVD、RVESV、RVEF、RVEDVI降低，CVP升高，DT1缩短，右心室流出道舒张直径（RVOTDD）、右心室流出道收缩直径（RVOTSD）增加（P＜0．05）；吻合完毕时各指标恢复到基础值水平（P＞0．05）。心脏形态学表明LAD、RCA搭桥时以左心室直接受压为主，LCX搭桥时以右心室受压为主。结论在OPCAB中LAD、LCX、RCA搭桥时左右心室同时受压，但左右心室受压的程度随着搭桥血管、心脏位置不同而不同；心功能呈一过性的损害，在完成血管搭桥后均能恢复。     

异丙酚对大鼠缺氧性肺血管收缩反应的影响

目的 观察异丙酚对大鼠缺氧性肺血管收缩(HPV)反应的影响及可能机制。方法 雄性 SD 大鼠，麻醉后取出心肺并制成肺动脉环，给予不同的悬挂初张力，以得到鼠肺动脉环收缩的最适初张力，在此最适初张力下测定肺动脉环的 HPV 反应强度；此后，分别给予不同浓度的异丙酚(1、3、10、30、100μmol/L)测量 HPV 反应强度的变化。测量60mmol/L KCI 引起的肺动脉环收缩强度，并比较异丙酚(10、30μmol/L)预先给药后收缩强度的改变；累计剂量式加入去氧肾上腺素(PE)测量肺动脉环收缩强度，并与异丙酚(10、30μmol/L)预先给药后进行比较。结果 小剂量异丙酚对 HPV 反应无明显影响(P>0.05)，随着剂量的增加对 HPV 的影响加大(P<0.05)。异丙酚呈剂量依赖性抑制肺动脉对 KCl 的收缩反应(P<0.05)。异丙酚抑制肺动脉对 PE 的收缩反应与剂量有关，不仅对 PE 引起的最大收缩反应具有抑制作用，且导致肺动脉对 PE 的敏感性降低。结论 异丙酚剂量依赖性抑制鼠肺动脉环的 HPV 反应，其可能机制是异丙酚对于肺动脉平滑肌细胞内钙的敏感性、内钙释放以及多种钙离子通道的抑制作用。     

左心衰竭后右心室急性压力超负荷模型的建立

目的观察左心衰竭后右心室过度压力负荷的血流动力学及心脏病理变化。方法将11只绵羊冠状动脉对角支结扎建立左心衰竭模型,采用肺动脉主干环缩造成右心室压力超负荷,并进行超声心动图、血流动力学、病理学检查。结果11只绵羊中6只存活。右心室收缩压/主动脉收缩压由左心衰竭后的0.23±0.09上升至0.31±0.09,心排血量由1.60±0.42L/m in上升至1.71±0.34L/m in,差别有统计学意义(P<0.05);肺动脉环缩1周时每搏量由基础对照值的44.08±14.11m l下降至29.17±6.89m l,左心室短轴缩短率由0.33±0.02下降至0.25±0.04,射血分数由0.68±0.07下降至0.53±0.04,差别有统计学意义(P<0.05);左心室舒张期末容积由基础对照值的65.97±18.42m l下降至51.06±17.19m l(P<0.05);病理学检查右心室心肌细胞肥大。结论在左心衰竭情况下,右心室可以耐受一定程度的急性压力负荷。     

左心室及双心室辅助装置对缺血心肌的影响

目的 比较左心室辅助装置（LVAD）和双心室辅助装置（BVAD）对缺血心肌再灌注后心脏血流动力学、心肌能量代谢物质和心肌超微结构中线粒体形态的影响。方法 将16只绵羊随机分为LVAD组和BVAD组,每组8只,常温阻断升主动脉25分钟,造成双心室缺血损伤的动物模型。结扎右颈内动脉远端,在心脏复跳后应用转子泵分别行LVAD（左心室－右颈内动脉径路）和BVAD（左心室－右颈内动脉和右心室－肺动脉径路）辅助循环120分钟,测定血流动力学,心肌三磷酸腺苷、磷酸肌酸、观察心肌超微结构变化。结果 施行BVAD或LVAD辅助循环的同时增加容量负荷能够显著改善心脏血流动力学,但LVAD组右心房压显著高于BVAD组（P＜0．05）;BVAD组右心室心肌三磷酸腺苷、磷酸肌酸含量和心肌线粒体比表面值均高于LVAD组（P＜0．05）。结论 BVAD与LVAD更有助于促进双心室缺血损伤心肌的功能恢复。     

Is there a correlation between brain naturietic peptide levels and echocardiographic and hemodynamic parameters in heart transplant patients?

BACKGROUND: Brain naturietic peptide (BNP) elevations have been reported in heart transplant patients both at baseline and during rejection. An association between BNP levels and certain echocardiographic and hemodynamic abnormalities has also been found in nontransplanted heart disease patients. We sought to determine whether BNP values were correlated with echocardiographic and hemodynamic parameters among a large cohort of heart transplant patients. MATERIALS AND METHODS: We studied 71 consecutive heart transplant patients, excluding combined grafts, retransplants, and pediatric cases. We performed 488 BNP determinations during catheterization and within 48 hours of echocardiography. Hemodynamic parameters included mean pulmonary artery pressure, right ventricular systolic and diastolic pressures. Doppler echocardiography parameters were wall thickness, ventricular mass, left and right ventricular end-diastolic and end-systolic diameters, isovolumic relaxation time, and mitral flow deceleration time. RESULTS: We observed significant correlations between BNP values and left ventricular size, ventricular mass, and a restrictive filling pattern. BNP levels were also significantly correlated with right ventricular size, mean pulmonary artery pressure, and right ventricular diastolic and end-diastolic pressures. CONCLUSIONS: In heart transplant patients, BNP levels positively correlated with ventricular diameters and a restrictive filling pattern. An increase in right ventricle and pulmonary artery pressures was associated with elevated BNP values.     

Early changes and rules of cardiac function and hemodynamics in rabbits with experimental myocardial contusion

Objective: To study changes and rules of the left ventricular functions in rabbits with myocardial contusion through parallel functional analysis by using echocardiography combined with cardiac catheter intervention. Methods : Thirty healthy rabbits were selected and impacted to make moderate or severe myocardial contusion by BIM-Ⅱ biomedical impact machine. The changes of bemodynamics and cardiac systolic and diastolic functions were respe~vely observed before injury and 1, 4, 8 and 24 hours after injury. Results: After myocardial contusion, the heart rate,systolic pressure, diastolic pressure and mean arterial pressure of rabbits decreased remarkably at 1-4 hours. The left ventricular end-systolic pressure ( LVESP ), the maximum increasing rate of the left intraventricular pressure ( dp/dtmax), isovolumic pressure (IP) and the maximum systolic vdocity of the left ventricle (Vmax) also decreased markedly. And then these parameters recovered to the levd of preinjury at 8-24 hours. The left ventricular end-diastolic pressure (LVEDP), the rate of the left intraventricular pressure ( - dp/dtmax ) and the decreasing time constant of the left intraventricular pressure (T) increased remarkably 1 hour after myocardial contusion,and did not decrease until 8 hours after myocardial contusion. Detection by echocardiography showed that ejection fraction of the left ventricle markedly decreased at 24 hours after myocardial contusion, while the systolic volume decreased obviously as early as 1 hour after myocardial contusion, at 4-8 hours it recovered a little and again decreased at 24 hours. The end systolic volume and end diastolic volume increased after myocardial contusion,but statistical sitmificance was only seen at 8 hours after myocardial contusion. Conclusions: Cardiac functions of the left and right ventricles are markedly injured after myocardial contusion with disorders of the left ventricle diabolic function and of the right ventricle systolic function as the dominant injury.While the systolic function of the left ventricle can recover.Echocardiography shows clinical importance in detection of early injuries of cardiac functions.     

Effects of acute left ventricular unloading on right ventricular function in normal and chronic right ventricular pressure-overloaded lambs

OBJECTIVE: Right ventricular pressure overload occurs in several types of (congenital) heart disease, as well as in pulmonary disease. Clinical outcome in some of these patient groups might in part be related to left ventricular loading conditions. The effects of left ventricular unloading on the function of the hypertrophic right ventricle have not been studied. We aimed to study the effects of left ventricular unloading on right ventricular hemodynamics and contractility in an animal model of chronic right ventricular pressure overload. METHODS: In lambs the pulmonary artery was chronically banded to increase right ventricular pressure to systemic levels. After 8 weeks, right ventricular contractility and hemodynamic function were assessed in these lambs, as well as in age-matched control animals, by using a combined pressure-conductance catheter in the right ventricle during baseline conditions and during complete bypass of the left ventricle. RESULTS: In both groups acute left ventricular unloading significantly decreased left ventricular pressure to low levels while aortic pressure was maintained. In the right ventricle of the control group, both end-systolic and end-diastolic volumes increased with left ventricular unloading (P <.01) while end-systolic pressure was maintained. Cardiac output was unchanged despite decreased right ventricular contractility. In the banding group acute left ventricular unloading also decreased right ventricular contractility but increased cardiac output. During acute left ventricular unloading, diastolic stiffness was unchanged in the control group, whereas it was significantly decreased in the banding group. CONCLUSIONS: Both in normal hearts and in hearts subject to chronic right ventricular pressure overload, acute left ventricular unloading decreases right ventricular contractility. Although no effects on cardiac output are encountered in normal hearts during left ventricular bypass, cardiac output is improved in right ventricular pressure-overloaded hearts, most likely related to improved right ventricular diastolic compliance.     

Effects of left heart bypass on right ventricular performance. Evaluation of the right ventricular end-systolic and end-diastolic pressure-volume relation in the in situ normal canine heart

Although left heart bypass has gained popularity as a powerful technique to assist the severely failed left heart, apparent right heart failure has often developed during the bypass procedure. We investigated whether the coexisting right heart failure is attributable to the left heart bypass in 16 open-chest dogs. We evaluated the effects of left heart bypass on the right ventricular systolic properties by the slope of the end-systolic pressure-volume relation and its effects on the diastolic properties by chamber compliance. Overall right ventricular performance was assessed by the end-diastolic pressure versus cardiac output relationship. The left heart bypass decreased the slope slightly when the assisted flow ratio exceeded 75% (-14% +/- 8% at the assisted flow ratio of 100%, p less than 0.02) and thus had a deleterious influence on right ventricular performance. The left heart bypass, on the other hand, had a counteracting beneficial influence on right ventricular performance through the increase in chamber compliance (38% +/- 5%, p less than 0.01) and the decrease in pulmonary arterial input resistance (-15% +/- 12%, p less than 0.01). The net effect of the left heart bypass was the increase in cardiac output (20% +/- 2%, p less than 0.05) for any given right ventricular end-diastolic pressure. We conclude that in normal hearts the left heart bypass augments right ventricular performance. We ascribe these beneficial effects to diastolic ventricular interdependence and afterload unloading.     

Efficacy of an endothelin-A receptor antagonist in heart transplantation from asphyxiated canine non-heart-beating donors

Objective Hypoxic perfusion before arrest, an indeterminate period of warm ischemia, and subsequent reperfusion are major causes of cardiac allograft dysfunction in non-heart-beating donors (NHBDs). The present study was undertaken to elucidate the cardioprotective effects of ET_A receptor antagonist FR139317 for hearts obtained from asphyxiated NHBDs in a canine transplantation model. Methods Hypoxic cardiac arrest was induced in 17 donor dogs. FR139317 (10 mg/kg) was given to 7 of the dogs over a period of 10 min before disconnecting the ventilator. The hearts were preserved with FR 139317-supplemented cardioplegic solution (FR group). The remaining 10 did not receive FR 139317 at any time during the experiment (control group). Orthotopic transplantation was performed after a mean myocardial ischemic time of 4 h. Results During the agonal period, the highest systolic pulmonary artery pressure in the FR group was lower than that in the control group (47 ± 14 vs. 58 ± 27 mmHg). All animals in the FR group were weaned from cardiopulmonary bypass, whereas only five of the controls were weaned, two of which were identified to have dominant right ventricular failure. After transplantation, recovery rates of the left ventricular end-systolic pressure-volume ratio (Emax) and the maximum first derivative of pressure measured over time (max dP/dt) were not significantly different between the groups, but recovery rates of the cardiac index, left ventricular minimum dP/dt and exponential time constant of LV relaxation (tau) in the FR group were higher than those in the control group. Conclusions The ET_A receptor antagonist FR 139317 reduced pressure overload on the right ventricle by decreasing the peak pulmonary artery pressure before donor arrest. Cardioprotective effects of this agent for heart transplantation from NHBDs are manifested by preserved diastolic properties of the left ventricle.     

Experimental study on the hemodynamic effects of veno-arterial extracorporeal membrane oxygenation with an automatically driven blood pump on puppies.

Hemodynamics, mainly the pressure of the heart, was studied while performing veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) on 16 puppies between the right atrium and the right carotid artery with a unique ECMO circuit using an automatically driven blood pump. The resulting decrease in the mean pulmonary arterial pressure indicated a definite support of VA-ECMO on the volume work of the right heart. The right and left ventricular end-diastolic pressures decreased during the low flow bypass, but increased significantly with flow over 50 ml/min/kg. The results indicated biventricular pressure strain due to the increase in afterload. The left ventricular systolic pressure gradually increased despite the steady decrease in the systemic arterial systolic pressure when bypass flow exceeded 60 ml/min/kg. The findings were similar to those in peripheral circulatory insufficiency. The authors concluded that VA-ECMO flow should be kept as low as possible, in view of undesirable hemodynamic effects on both ventricles.     

Pulmonary artery counterpulsation to improve right ventricular function after heart transplantation

The effectiveness of pulmonary artery counterpulsation in improving right ventricular function after heart transplantation was evaluated in a pig model. The balloon catheter was introduced through the anterior wall of the pulmonary artery distal to the pulmonary valve. A Millar catheter with a distal high-fidelity pressure transducer was placed in the right ventricle, where the peak rate of pressure rise, dP/dT, was measured. Pulmonary artery counterpulsation significantly improved right ventricular function, increasing both dP/dT and systolic pressure. A diastolic dip in pulmonary artery pressure and a fall in the early portion of the right ventricular pressure curve were seen. Inflation of the balloon caused a second (suprasystolic) wave in that curve. Improved right ventricular function was also seen when normal pig hearts were counterpulsated after occlusion of the right coronary artery and following increased afterload due to occlusion of a main pulmonary artery. There were no changes in central venous or systemic pressure. The results indicate that pulmonary artery counterpulsation may be valuable when the transplanted heart has a poorly functioning right ventricle.     

Atriopulmonary shunt

A new alternative to cavopulmonary anastomosis or systemic pulmonary arterial shunt in the treatment of tricuspid valve atresia, pulmonary valve atresia, single ventricle, and underdeveloped right ventricle was studied experimentally in dogs. Complete diversion of all the systemic venous return from the right atrium directly to the pulmonary circulation was possible using a pulmonary valve homograft. The congenital lesions were simulated by surgical closure of the tricuspid valve. Four long-term survivors were studied by serial angiocardiography and cardiac catheterization, which demonstrated complete bypass of the right ventricle and normal hemodynamics. These experimental results support cautious clinical application of the operation provided pulmonary artery pressure is normal and flow through the left side of the heart is not obstructed.     

Effects of acute right ventricular ischemia on ventricular interactions during prosthetic left ventricular support

Systolic ventricular interactions may be partially responsible for right ventricular failure that sometimes occurs during clinical use of prosthetic left ventricular assist devices. In this hypothesis, it is proposed that the left ventricular assist device reduces left ventricular pressure and its contribution to right ventricular performance, thus impairing right ventricular output. On the other hand, these effects may be small compared with other causes of right ventricular failure such as ischemia. To test the systolic interaction hypothesis in the normal and ischemic right ventricle, we used a left ventricular assist device to pressure unload the left ventricle of anesthetized pigs, and we compared its effect on right heart function before and after 2 minutes of acute right coronary artery occlusion as a model of right heart failure. Pigs were instrumented for measurements of septal to left ventricular and right ventricular free wall dimensions with ultrasonic crystals, ventricular chamber pressures, and cardiac output with a pulmonary artery blood flow probe. Without right ventricular ischemia, the left ventricular assist device produced an 80% +/- 6% reduction in left ventricular pressure-time integral while maintaining aortic pressure. This resulted in a leftward septal shift with an 11.6% +/- 1.8% decrease in left ventricular septal-to-free wall dimension and a 12.5% +/- 2.4% increase in right ventricular septal-to-free wall dimension, with no changes in right ventricular cardiac output or stroke work. In contrast, right coronary artery occlusion alone produced right heart failure, with a 50% +/- 6% reduction in right ventricular global stroke work and 26% +/- 6% and 27% +/- 3% reductions in cardiac output and right ventricular peak systolic pressure, respectively. This right heart failure persisted during left ventricular unloading with the left ventricular assist device, which resulted in further leftward septal shifting and unchanged but still depressed stroke work and flow output. These findings support the hypothesis that a preexisting pathologic condition is the dominant factor in determining right ventricular function during prosthetic left ventricular support and that direct anatomic interactions play a minor role.