Right ventricle-sparing heart transplant: promising new technique for recipients with pulmonary hypertension

Background. Right heart failure remains the leading early cause of mortality after heart transplantation, especially with antecedent pulmonary hypertension. Paradoxically, the discarded recipient right heart, acclimated to pulmonary hypertension, is often stronger than its nonconditioned donor replacement. Heterotopic (“piggy-back”) transplantation is plagued by problems related to the retained, dilated, hypocontractile left ventricle (lung compression, systemic emboli, arrhythmias). Were it possible to retain the recipient’s right heart, excising only the left ventricle, this could have important advantages, especially in severe pulmonary hypertension. This report describes such a technique.

Methods and Results. In four transplantation experiments (dogs), right ventricular-sparing transplantation proved technically feasible and hemodynamically successful. Bleeding after excision of the left ventricle was easily controlled. Back-bleeding from the native aortic valve (now open into the pericardial space) was not problematic. All atrial, aortic, and pulmonary arterial connections proved feasible. The preserved recipient right heart of all animals remained in stable sinus rhythm. All recipients were easily weaned from cardiopulmonary bypass, maintaining mean arterial pressures 60 to 110 mm Hg.

Conclusions. This investigation develops a technique for donor right ventricle sparing in cardiac transplantation, demonstrating technical and hemodynamic feasibility. This method holds promise for the unsolved clinical problem of right heart failure after orthotopic heart transplantation with antecedent pulmonary hypertension.     

Novel technique for isolated accessory right heart transplantation for congenital heart disease

BACKGROUND: Our prior laboratory work has permitted adding a whole donor heart to a preserved recipient right heart, producing a heart-and-a-half preparation able to cope with pulmonary hypertension in the recipient. The experiments in the present study explore the feasibility of the converse operation: adding an isolated donor right heart to an entire preserved heart. METHODS: Eight adult mongrel dogs (4 donors and 4 recipients) were used in 4 transplant operations performed through a right thoracotomy without cardiopulmonary bypass (using side-biting control of recipient vessels). The donor heart underwent resection of the left atrium and left ventricle, leaving an isolated donor right heart. Blood supply to the donor right ventricle was preserved from the donor ascending aorta. Through a right thoracotomy, the donor right heart was transplanted in parallel to the native right heart of the recipient by using the following anastomoses: (1) donor superior vena cava to recipient superior vena cava (end-to-side anastomosis); (2) donor pulmonary artery to recipient pulmonary artery (end-to-side anastomosis); (3) donor ascending aorta to recipient aorta (through a great vessel [end-to-end anastomosis] to provide arterial inflow to donor coronary arteries). Animals were euthanized within 1 hour after completion of transplantation. RESULTS: Isolation of the right ventricle by excision of the left chambers was technically feasible. Transplantation without cardiopulmonary bypass was feasible in all cases. The isolated right heart beat well after transplantation in all animals, demonstrating sinus rhythm. Three of 4 animals were able to sustain good hemodynamics on support with epinephrine. Bleeding from the septum or aortic valve of the donor (now open to the pericardial space) was not problematic. Mean arterial pressure was 85 mm Hg (mean) at a right atrial pressure of 6 mm Hg (mean). In 2 animals the recipient superior vena cava was ligated to obligate upper body flow to pass through the accessory ventricle; hemodynamics were preserved under these circumstances. CONCLUSION: Transplantation of an isolated right heart is feasible. Such a technique has potential as a novel therapeutic alternative for obstructive or hypoplastic lesions of the right heart in human children.     

Mechanisms of transplant right ventricular dysfunction.

OBJECTIVE: Right ventricular (RV) dysfunction remains the leading cause of early mortality after cardiac transplantation. The effect of brain death and subsequent hypothermic cardioplegic arrest and storage on subsequent post-transplant right ventricular function was examined. SUMMARY BACKGROUND DATA: Right ventricular dysfunction in the donor heart usually is attributed to failure of the donor right ventricle to adapt to the sudden increase in afterload (pulmonary vascular resistance) in the recipient. Strategies to improve ventricular mechanics in the postoperative period are aimed at reducing pulmonary vascular resistance with vasodilators or augmenting right ventricular contractility with inotropic agents. Events occurring in the donor heart (brain death, hypothermic cardioplegic arrest, and storage) also may be directly related to post-transplant RV dysfunction. METHODS: A canine model of brain death and orthotopic cardiac transplantation was used. A dynamic pressure-volume analysis of RV mechanics was performed using micromanometers and sonomicrometric dimension transducers. Systolic function was assessed by measurement of preload recruitable stroke work (PRSW). Brain death was induced in 17 dogs by inflation of an intracranial balloon. Right ventricular function then was assessed serially to 6 hours (PRSW). Right ventricular adrenergic beta receptor density and function was sampled at control and after 6 hours of brain death. The effect of cardioplegic arrest and hypothermic storage was assessed in a second group of 17 dogs, using the same instrumentation and method of RV analysis. RESULTS: A significant decrease in right ventricular PRSW occurred after brain death, with the average decrease being 37% +/- 10.4% from the control. The RV myocardial beta adrenergic receptor density did not significantly change (253 +/- 34 fmol/ng control vs. 336 +/- 54 fmol/ng after brain death). The adenylyl cyclase activity of the RV beta receptor was assessed and was not altered by brain death. Orthotopic transplantation after cardioplegic arrest and hypothermic storage significantly decreased RV PRSW from 23.6 +/- 2.0 x 10(3) erg to 13.5 +/- 1.4 x 10(3) erg. CONCLUSIONS: These data indicate that the donor right ventricle is exposed to factors significantly detrimental to its mechanical performance well before facing an increased afterload in the recipient. Strategies to reduce RV dysfunction associated with brain death and hypothermic storage could positively impact post-transplant survival.     

Improved right ventricular function after intracoronary administration of a C1 esterase inhibitor in a right heart transplantation model.

OBJECTIVE: Myocardial injury from ischemia can be augmented after reperfusion due to proinflammatory events including complement activation, leukocyte adhesion, and release of various chemical mediators. It has been shown that intracoronary administration of a C1 esterase inhibitor (C1 INH) significantly reduces myocardial necrosis in an experimental model of ischemia. Our study addresses the question whether the most susceptible region of the heart for ischemic injury, the right ventricle (RV), can benefit from the protective effects of C1 esterase inhibition after transplantation. METHODS: To precisely control RV volume in vivo an isovolumic model was used in which the RV volume was regulated using an intracavity high compliance balloon inserted into donor hearts of domestic pigs (34+/-4 kg). After 4 h of ischemia, donor hearts were transplanted into recipient pigs (44+/-4 kg). Treatment groups, each with six animals, consisted of C1 INH treatment or control. After opening the cross clamp, the C1 INH group animals received 20 IU/kg body weight of C1 INH intracoronary over a 5 min period. The control animals received no drug therapy. The hearts were reperfused for 60 min, and thereafter the RV balloon volume was increased in 10 ml increments until RV failure occurred. These measurements were repeated after 120 min of reperfusion. RESULTS: There was no significant difference in maximal RV developed pressure between the two groups (after 1 h, 35.7+/-5.9 vs. 40.6+/-12.7 mm Hg; after 2 h, 41.5+/-10.7 vs. 46.3+/-15.2 mm Hg; for C1 INH and control animals, respectively). However, the RV could be loaded with a significantly higher volume after both 1 h (60.0+/-20.0 ml (C1 INH) vs. 46.7+/-13.7 ml (control) balloon volume, P<0.05), and 2 h of reperfusion (70.0+/-8.9 ml vs. 60.0+/-6.3 ml; C1 INH and control animals, respectively; P<0.05). CONCLUSIONS: Intracoronary administration of a C1 INH significantly improves right ventricular function in an experimental transplant model. Thus, inhibition of the classic complement cascade may be a promising therapeutic approach for effective protection of myocardium from reperfusion injury after transplantation.     

Production and reversibility of right ventricular hypertrophy and right heart failure in dogs.

Combined heart-lung transplantation has been used for end-stage primary pulmonary hypertension. Experience with single-lung transplantation for other conditions suggested that associated severe right ventricular dysfunction resulting from increased afterload would recover after placement of a satisfactory lung allograft. Early experience with the application of single-lung transplantation for pulmonary hypertension supports this contention. We devised a reversible canine model of chronic progressive pressure-overloaded right heart failure by pulmonary artery banding to study the echocardiographic, hemodynamic, and pathological reversibility of the failing right heart. Clinical right heart failure was defined as the development of ascites and pleural effusions. Right heart failure developed in 23 dogs 67 to 348 days after banding, and they were divided into two groups to determine its early and long-term effects. Group 1 dogs (n = 11) were either sacrificed immediately after the onset of right heart failure (n = 5) or unbanded (n = 6); group 2 dogs (n = 12) were maintained in right heart failure for 3 months and then either sacrificed (n = 6) or unbanded. Unbanded dogs in both groups were observed for 4 additional months before sacrifice. A control group of 6 normal dogs was sacrificed for pathological comparisons. After unbanding, the right ventricular systolic pressure fell from 97 +/- 17 mm Hg (group 1) and 88 +/- 31 mm Hg (group 2) to 44 +/- 11 mm Hg and 47 +/- 13 mm Hg, respectively. Despite this persistent gradient across the pulmonary artery, echocardiographic and hemodynamic measures of right ventricular function returned to normal, albeit more slowly in the group 2 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Glycine application and right heart function in a porcine heart transplantation model

Glycine reduces ischemia-reperfusion injury after experimental liver transplantation. We hypothesized that glycine might also protect right heart function in an isovolumic cardiac transplantation model. In six domestic donor pigs 150 ml of a 300 mmol L-glycine solution were administered intravenously. The hearts were then arrested with histidine-tryptophan-ketoglutarate solution. Animals without prior glycine infusion served as controls (n = 6). After 4 h of ischemia, hearts were transplanted into recipients. An isovolumic model was used in which the right ventricular (RV) volume was controlled in vivo using an intracavitary high-compliance balloon. After 1 and 2 h of reperfusion the RV balloon volume was gradually increased and the developed pressures were recorded (P(developed) = P(systolic) - P(diastolic)). Right ventricular failure was defined as a decrease in developed intracavitary pressure. Glycine hearts could be loaded with a significantly increased volume after 1 h (glycine: 53 +/- 13.7 ml vs. control: 32 +/- 11.7 ml; P = 0.015) and after 2 h (67 +/- 18.6 ml vs. 43 +/- 8.2 ml; P = 0.018). Maximal RV developed pressures were not significantly different between groups. Postischemic RV end-diastolic compliance was significantly higher in glycine-treated animals (P = 0.04). Glycine protects early postischemic RV compliance, but has no important influence on maximal developed pressures.     

Pathophysiology of severe pulmonary hypertension in the critically ill patient

Pulmonary hypertension (PH) is a threatening condition that can be associated with a great variety of both pulmonary and extrapulmonary diseases. In all forms of severe PH the pulmonary vascular bed looses its physiological features of a "high flow-low pressure system", putting an increased afterload on the right ventricle (RV). Acute pulmonary hypertension in the intensive care unit often represents a clinical problem secondary to acute respiratory failure, left heart failure, pulmonary embolism, or decompensation of prior PH by concurrent pulmonary or cardiovascular disease. Right ventricular failure (acute cor pulmonale) occurs when relevant increases in pulmonary vascular resistance overwhelm its compensatory mechanisms, both abruptly on a previously normal RV, or gradually on a chronic cor pulmonale. This review addresses the main pathophysiological aspects of severe PH, focusing on the hemodynamic derangements occurring in the setting of acute cor pulmonale, and emphasizing the role of ventricular interdependence (the way right ventricular failure greatly affects diastolic and systolic function of the left ventricle), the risk of RV ischemia (the end stage of RV failure) and systemic organ hypoperfusion (caused by antegrade and retrograde heart failure). The understanding of the peculiar features of this type of cardiovascular insufficiency is necessary to both provide effective monitoring and adequate supportive therapy.     

Evolution of right cardiac pressures during the first year after heart transplantation

INTRODUCTION: Preoperative pulmonary hypertension is an adverse prognostic factor for early morbidity-mortality after heart transplantation (HT). The persistence of hypertension is likewise associated with a poorer patient prognosis. The present study investigated the evolution of right cardiac pressures in the first year after HT with respect to the background cardiac disease. METHODS: This study of 60 consecutive patients subjected to HT analyzed the baseline clinical characteristics and mean right atrial and right ventricle systolic and diastolic pressures in a pre-HT study and during biopsies performed in the first 2 weeks as well as at 1, 3, 6, 9, and 12 months after transplantation. The study excluded retransplantations, heart and lung transplantations, and pediatric patients, as well as patients not subjected to biopsy because of early mortality. RESULTS: The mean patient age was 50 years (83% males); 31.7% were diabetics, and 33% showed hypertension. The background heart disease was of ischemic origin in 35% of cases, and consisted of dilated myocardiopathy in 33%, with a mean left ventricle ejection fraction (LVEF) of 23% and a mean pulmonary artery systolic pressure of 50.1 mm Hg. During the postoperative course, an important decrease versus baseline was observed in right heart pressures as soon as 2 weeks post-HT, with a drop in right ventricle (RV) systolic pressure from 50.3 +/- 13.7 to 42.5 +/- 10.4 mm Hg (P = .013), and a drop in RV diastolic pressure from 17.4 +/- 5.8 to 14.2 +/- 4.1 mm Hg (P = .007). This decreased tendency continued to a more moderate extent to the third month, after which the pressures stabilized. The same behavior was observed in patients with diseases of ischemic origin and in those with dilated myocardiopathy. CONCLUSIONS: In our series, right cardiac pressures showed an important decrease in the first days after HT, with stabilization by the third month--though without returning to normal values and without modifications in the first year after transplantation. No differences in this evolutive trend were seen according to the type of background heart disease.     

Accuracy of Doppler Echocardiography in the Assessment of Pulmonary Hypertension in Liver Transplant Candidates

Pulmonary hypertension has been associated with poor outcome after liver transplantation. We assessed the diagnostic accuracy of Doppler echocardiography in detecting significant pulmonary hypertension. Seventy-four potential liver transplant candidates underwent Doppler echocardiography in which the systolic right ventricular pressure (RVsys) was used to estimate the systolic pulmonary artery pressure (PAsys). Group 1 included 39 consecutive patients with RVsys ≥50 mm Hg who underwent elective right heart catheterization. Group 2 consisted of 35 patients with RVsys <50 mm Hg in whom pulmonary artery pressures were measured at the beginning of the transplantation procedure. The accuracy of the estimates by Doppler echocardiography was assessed against measurements made by direct catheterization. Patients in groups 1 and 2 were comparable in their demographic and liver disease characteristics. There was a strong correlation between RVsys by Doppler echocardiography and PAsys by right heart catheterization (r = .78, P < .01). Of the 39 patients in group 1, 29 (72%) had at least moderate pulmonary hypertension (mean pulmonary artery pressure [MPAP] ≥35 mm Hg), including 12 (30%) with severe pulmonary hypertension (MPAP ≥50 mm Hg). Only 1 of the group 2 patients had MPAP ≥35 mm Hg. Thus, in the diagnosis of moderate to severe pulmonary hypertension, the sensitivity of echocardiography was 97% and specificity was 77%. Doppler echocardiography is an accurate screening test to detect moderate to severe pulmonary hypertension. We advise that liver transplant candidates with RVsys ≥50 mm Hg undergo right heart catheterization to fully characterize pulmonary hemodynamics. (Liver Transpl 2000;6:453-458.)     

心脏移植围术期右心衰的危险因素与治疗

目的 探讨临床心脏移植围术期发生移植心脏右心功能衰竭(右心衰)的危险因素及针对肺动脉高压的治疗效果。方法 回顾性分析经筛选出的96例心脏移植患者的临床资料,建立移植心脏右心衰诊断标准,采用logistic回归分析确定危险因素,建立风险模型。以术前肺动脉收缩压(SPAP)为标准分为A组(SPAP ＜40 mm Hg,1 mm Hg =0.133 kPa)和B组(SPAP≥40 mm Hg)。比较组间各临床数据之间的差异。结果 年龄、瓣膜病、心衰病史、术前SPAP是移植心脏右心衰的危险因素。术前SPAP的危险系数最高是6.725,其次是心衰病史1.712、瓣膜病1.351、年龄1.051;冠心病和术前应用5-PDEs-Ⅰ为保护性因素,危险系数分别为0.056和0.034。A组与B组患者的年龄、原发病(瓣膜病)、心衰病史存在显著差异,右心衰发生率虽差异无统计学意义,但B组明显较A组为高(67.6％对45.8％)。两组应用体外膜氧合(ECMO)和右心衰死亡的比例差异无统计学意义。结论 心脏移植受者术前的肺动脉高压是移植心脏右心衰的主要风险因素,而针对肺动脉高压的靶向性药物治疗和ECMO辅助循环,虽然缺乏循证医学证据,但临床取得了较好的疗效。     

Pulmonary artery balloon counterpulsation for right ventricular failure. An experimental evaluation

Right ventricular (RV) failure frequently occurs in patients undergoing correction of congenital cardiac defects, as well as in other clinical settings. RV hypertrophy was created in 10 neonatal lambs by pulmonary artery (PA) banding. Twelve months later RV hypertrophy was present (RV weight/body weight = 2.71 +/- 0.31 gm/kg); RV systolic pressures were elevated (65 +/- 9 mm Hg) and the average gradient across the PA band was 38 +/- 9 mm Hg. RV failure was produced in all animals by performing a right ventriculotomy. Four unassisted (control) animals died shortly after separation from bypass. Six experimental animals underwent pulmonary artery balloon counterpulsation (PABCP). A Dacron graft anastomosed to the proximal PA served as a reservoir for a 40 ml intra-aortic balloon pump system. PABCP effectively reversed RV failure, low cardiac output, and systemic arterial hypotension. Periods with PABCP on and off in each animal were compared. PABCP increased cardiac output from 1.45 +/- 0.16 to 2.03 +/- 0.13 L/min (p less than 0.0001) and increased aortic systolic pressure from 78 +/- 7 to 99 +/- 6 mm Hg (p less than 0.0004). PABCP produced a significant reduction in RV peak systolic pressure from 56 +/- 5 to 41 +/- 3 mm Hg (p less than 0.0001). PA peak pressure distal to the band increased from 31 +/- 2 to 40 +/- 1 mm Hg (p less than 0.0001). Right atrial pressure decreased from 14 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0001) with PABCP, and RV end-diastolic pressure fell from 15 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0001). RV stroke work index increased 49% from 0.081 +/- 0.011 to 0.121 +/- 0.017 gm X m/kg/beat (p less than 0.01), and RV systolic pressure time index decreased 38% from 1140 +/- 79 to 710 +/- 65 mm Hg sec/min (p less than 0.0001). Thus PABCP in the presence of RV dysfunction can produce substantial improvement in RV function and in overall cardiac function and may prove clinically useful in managing patients in refractory RV failure.     

Management of pulmonary hypertension in the operating room

Pulmonary artery hypertension is defined as persistent elevation of mean pulmonary artery pressure > 25 mm Hg with pulmonary capillary wedge pressure < 15 mm Hg or elevation of exercise mean pulmonary artery pressure > 35 mm Hg. Although mild pulmonary hypertension rarely impacts anesthetic management, severe pulmonary hypertension and exacerbation of moderate hypertension can lead to acute right ventricular failure and cardiogenic shock. Knowledge of anesthetic drug effects on the pulmonary circulation is essential for anesthesiologists. Intraoperative management should include prevention of exacerbating factors such as hypoxemia, hypercarbia, acidosis, hypothermia, hypervolemia, and increased intrathoracic pressure; monitoring and optimizing right ventricular function; and treatment with selective pulmonary vasodilators. Recent advances in pharmacology provide anesthesiologists with a wide variety of options for selective pulmonary vasodilatation. Pulmonary hypertension is a major determinant of perioperative morbidity and mortality in special situations such as heart and lung transplantation, pneumonectomy, and ventricular assist device placement.     

Improved right heart function after myocardial preservation with 2,3-butanedione 2-monoxime in a porcine model of allogenic heart transplantation.

BACKGROUND: Right heart dysfunction is a major cause for early morbidity and mortality after heart transplantation. Experiments were designed to evaluate the influence of the calcium-desensitizing drug 2,3-butanedione 2-monoxime (BDM) on right heart function in a porcine model of heart transplantation. METHODS: Donor hearts of domestic pigs were arrested with BDM in Krebs solution (n = 7) and with BDM in Bretschneider's histidine-tryptophan-ketoglutarate (HTK) solution (n = 6). There were 2 control groups: University of Wisconsin (UW, n = 6) and HTK (n = 6). An isovolumic model was used in which the right ventricular volume was precisely controlled in vivo with an intracavitary high-compliance balloon. After 4 hours of ischemia, hearts were transplanted into recipients. After 1 and 2 hours of reperfusion, the right ventricular balloon volume was increased in 10-mL increments until right ventricular failure occurred and the developed pressures were recorded. RESULTS: Maximal right ventricular developed pressures were significantly different after 2 hours of reperfusion (UW: 35 +/- 13 mm Hg; HTK: 47 +/- 8 mm Hg; Krebs+BDM: 49 +/- 9 mm Hg; HTK+BDM: 50 +/- 6 mm Hg; P =.04). Hearts subjected to BDM could be loaded with a significantly increased volume after 1 hour and after 2 hours (UW: 57 +/- 10 mL vs HTK: 43 +/- 8 mL vs Krebs+BDM: 70 +/- 10 mL vs HTK+BDM: 67 +/- 15 mL; P =.002). Postischemic right ventricular enddiastolic compliance was significantly increased in groups treated with BDM after 1 hour (P =.02) and after 2 hours (P =.039). CONCLUSIONS: The drug BDM significantly improves right ventricular function in a heart transplantation model. The increase in volume load and developed right ventricular pressure achieved by BDM application would translate into a decreased risk of right ventricular failure after clinical transplantation.     

The hemodynamic effects and mechanism of action of pulmonary artery balloon counterpulsation in the treatment of right ventricular failure during left heart bypass

The efficacy of pulmonary artery balloon counterpulsation (PABC) was evaluated in improving right ventricular (RV) output during left heart bypass for global cardiac failure. In 13 pigs, a 40-ml balloon was positioned within a graft anastomosed to the pulmonary artery distal to the pulmonary valve, and left heart bypass was instituted from the left atrium to the carotid artery. Global myocardial failure was produced by an infusion of propranolol (range, 25 to 78 mg). In this model, RV output decreased despite volume loading to a right atrial pressure of 15 mm Hg and atrioventricular sequential pacing at 100 beats per minute. Pulmonary artery balloon counterpulsation increased both RV output (from 519 +/- 76 to 1,117 +/- 110 ml/min; p less than 0.01) and RV systolic stroke work (from 1.3 +/- 0.4 to 2.3 +/- 0.6 gm-m; p less than 0.01). Right atrial pressure decreased (from 15.5 +/- 0.9 to 10.7 +/- 1.0 mm Hg; p less than 0.01) in 8 of the pigs studied during RV failure. In 5 pigs, ventricular fibrillation occurred without a stable model of RV failure, and there was no cardiac output before or after counterpulsation. The mechanism of action of PABC was studied by placing a flow probe around a large branch of the right pulmonary artery. During RV failure, balloon inflation caused flow through the pulmonary circulation, and ventricular systole resulted in filling of the graft. During ventricular fibrillation, balloon inflation and deflation produced only a to-and-fro movement of blood in the pulmonary artery branch without net forward flow.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right ventricular dysfunction after cardiac transplantation: primarily related to status of donor heart

BACKGROUND: It is unclear whether right ventricular dysfunction after transplantation is due to donor brain death-related myocardial injury or recipient pulmonary hypertension. METHODS: A canine donor model of brain death and a monocrotaline pyrrole-induced chronic pulmonary hypertension recipient model were established, and used for 30 orthotopic bicaval cardiac transplantations divided into three groups: Controls (group A, normal donor/recipient), group B (brain-dead donors/normal recipient), and group C (normal donor/recipients with pulmonary hypertension). Right ventricular function was measured before transplant and brain death, 4 hours after brain death, and after transplant (1 hour off bypass) by load-independent means plotting stroke work versus end-diastolic volume during caval occlusion. Right ventricular total power and pulmonary vascular impedance were determined by Fourier analysis. RESULTS: In comparison to the control group right ventricular preload-recruitable stroke work and total power decreased significantly after brain death and transplant in group B (from 22.7 x 10(3) erg (+/-1.2) at baseline to 15.6 x 10(3) (+/-0.9) after brain death and to 11.3 x 10(3) (+/-0.9) after transplant). In group C there was a significant increase in pulmonary artery pressure, impedance, right ventricular preload-recruitable stroke work, total power after transplant. CONCLUSIONS: Normal donor hearts adapt acutely to the recipient's elevated pulmonary vascular resistance by increasing right ventricular power output and contractility. Brain death caused significant right ventricular dysfunction and power loss, which further deteriorated after graft preservation and transplantation. The effects of donor brain death on myocardial function contribute to right ventricular dysfunction after cardiac transplantation.     

Echocardiographic evidence of right ventricular remodeling after transplantation

Right ventricular (RV) failure is a significant source of mortality after cardiac transplantation. The use of RV assist devices (RVAD) as a bridge to recovery has been reported. However, early changes of RV structure and anatomy after RVAD implantation have yet to be described. We report a case of RV failure after transplantation requiring RVAD implantation. After 3 weeks of gradual weaning of inotropic and RVAD support, the device was explanted successfully. Transesophageal echocardiography documents RV hypertrophy and remodeling between RVAD implantation and removal, suggesting a rapid adaptive response of the right ventricle in the presence of pulmonary hypertension.     

Anesthetic concerns in lung transplantation for severe pulmonary hypertension

Lung transplantation has become a consolidated treatment for patients with severe pulmonary hypertension (PH). Several difficulties are encountered during the procedure in such candidates, who are still recognized as more severely affected by perioperative morbility and mortality than those undergoing lung transplantation for other diseases. Right ventricular (RV) enlargement with tricuspid regurgitation, small left ventricle (LV) with an asymmetric hypetrophic wall, interventricular septal shift toward the left, with ventricular stiffness and diastolic incompetence, are typical preoperative echocardiographic findings of end-stage PH. A smooth induction and tracheal intubation will help prevent hypertensive crisis in highly susceptible candidates. Uncompensated vasodilatation or myocardial depression caused by anesthetics and mechanical ventilation may be responsible for acute RV dysfunction associated with low systemic blood pressure. Resuscitation and emergency adoption of cardiopulmonary by-pass (CPB) has been described for near-fatal anesthesia induction. Cardiovascular instability can develop after institution of one-lung ventilation and pulmonary artery clamping. An acute increase in pulmonary pressure results in a decrease in RV ejection fraction and then in acute RV failure. Interdependence of the right and left ventricles occurs such that RV function can alter LV function. Early detection of impending circulatory and/or respiratory deterioration is warranted to prevent an irreversible decline in cardiac output, resulting in hazardous cardiac arrest. Inhaled nitric oxide represents the first choice for treatment of PH and RV failure associated with systemic hypotension during lung transplantation. Intraoperative situations requiring CPB must be identified before development of systemic shock, which represents a late ominous sign of RV failure.     

A Right Ventricular Hemopump Restores Right Ventricular Function with Pulmonary Artery Banding

Abstract: We investigated the ability of the Hemopump to support the right ventricle during acute, partial, pulmonary artery obstruction. In 6 pigs, a 14 Fr size Hemopump was placed through the pulmonary artery into the right ventricle. Control measurements were made. A band around the pulmonary artery proximal to the outflow port of the Hemopump was tightened, and measurements were repeated with the Hemopump at minimum and then maximum speed. With banding, right ventricular stroke volume and output decreased (43 [SD,7] to 28 [SD,8] ml, p < 0.001; 4.9 [SD,0.8] to 3.7 [SD,1.0] L/min, p < 0.01 respectively), but they were restored with the Hemopump (38 [SD,5] ml and 4.5 [SD,0.6] L/min; both p = NS vs control). Increases in right ventricular peak systolic (28 [SD,10] to 42 [SD,17] mm Hg; p < 0.01) and end-diastolic pressure (2 [SD,1] to 12 [SD,6] mm Hg; p < 0.02) were reversed by the Hemopump (29 [SD,8] and 4 [SD,2] mm Hg; both p = NS vs control). Right ventricular pressure rate product almost doubled with banding (3,199 [SD,1,252] to 5,962 [SD,2,796] mm Hg; p < 0.01), but it decreased with the Hemopump (3,368 [SD,767] mm Hg; p = NS vs control). With acute partial pulmonary artery banding, a right ventricular Hemopump restores output from and offloads the right ventricle.     

Right ventricular failure after heart transplantation: relationship with preoperative haemodynamic parameters

The prevalence of right ventricular failure after orthotopic heart transplantation, evaluated in 196 patients, was 11.7%, as assessed by the presence during the first postoperative month of right atrial pressure > 10 mm Hg. Two deaths, related to refractory right ventricular failure, were observed within the first month, both in subjects with preoperative pulmonary arteriolar resistances > 5 Wood Units. The haemodynamic profile after heart transplantation showed a significant decrease (P < 0.01) and an early normalization of pulmonary arterial pressure, pulmonary wedge pressure and pulmonary arteriolar resistances, while right atrial pressure slowly decreased until the third month. In a long-term analysis of survival (death within 1 year) the probability of death was significantly related to the values of right atrial pressure and cardiac index during the first month after heart transplantation. Otherwise, the presence of elevated values of right atrial pressure did not show a significant correlation with the echocardiographic right ventricular end-diastolic diameter nor with the presence of right bundle branch block. The careful selection of patients referred for the cardiac transplantation (mean value of pulmonary arteriolar resistances in the evaluated subjects was 2.5 ± 1.5 Wood Units) improves the probability of avoiding the appearance of severe right ventricular failure in the post-operative period in most cases. The best predictor of right ventricular failure remains to be clearly identified.     

Right ventricular assistance for experimental right ventricular dysfunction

Right ventricular dysfunction frequently occurs in patients undergoing correction of congenital cardiac defects, as well as in other clinical settings. The purpose of the present study was to surgically induce right ventricular dysfunction and then provide circulatory support with a right ventricular assist device. Right ventricular hypertrophy was created in 13 neonatal lambs by pulmonary artery banding. Right ventricular dysfunction was produced in all animals by performing a right ventriculotomy with the animal supported by cardiopulmonary bypass. In four unassisted animals the circulation failed after separation from bypass. Seven experimental animals underwent the insertion of a pneumatically activated ventricular assist device between the proximal pulmonary artery and the right ventricular apex. Periods with the right ventricular assist device on and off in each animal were compared. The right ventricular assist device increased cardiac output from 0.72 +/- 0.15 to 2.24 +/- 0.23 L/min (p less than 0.0002), increased left atrial pressure from 7 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0005), and increased aortic systolic pressure from 53 +/- 9 to 85 +/- 9 mm Hg (p less than 0.0001). Right ventricular assistance significantly reduced the right ventricular end-diastolic pressure from 19 +/- 3 to 12 +/- 1 mm Hg (p less than 0.0001). Pulmonary artery peak pressure distal to the band increased from 27 +/- 3 to 52 +/- 5 mm Hg (p less than 0.0001). The results indicate that right ventricular dysfunction can be produced by a vertical cardiotomy in a hypertrophied right ventricle with persistent outflow tract obstruction. Right ventricular dysfunction can be effectively reversed by a right ventricular assist device, which may prove clinically useful in managing patients with refractory right ventricular failure.