Right Ventricle Dysfunction in Patients With Adult Cystic Fibrosis Enlisted for Lung Transplant

Knowledge of preoperative right heart function of adult patients with cystic fibrosis (CF) awaiting lung transplant (LUTX) is limited. The echocardiography of adult patients with CF enlisted for LUTX was retrospectively analyzed and compared with standards and invasive analyses (right heart catheterization, multigated radionuclide ventriculography). We included 49 patients (reported as mean ± standard deviation; 29 ± 9 years of age; forced expiratory volume in first second of expiration, 31% ± 11% predicted; lung allocation score, 36 ± 5; invasive mean pulmonary artery pressure, 17 ± 5 mm Hg; multigated radionuclide ventriculography right ventricle [RV] ejection fraction, 50% ± 9%). Patients had increased RV end-diastolic area, RV wall thickness, and increased pulmonary artery acceleration time with subnormal tricuspid annular plane systolic excursion, tissue Doppler positive peak systolic velocity, and fraction area change. Subnormal tricuspid annular plane systolic excursion (< 23 mm), tissue Doppler positive peak systolic velocity (< 14 cm/s), and fraction area change (< 49%) had high sensitivity and negative predictive value in predicting impaired RV.ejection fractionA good correlation between echocardiographic estimated and invasively measured systolic pulmonary artery pressure was observed (R² = 0.554, P < .001). Adults with CF awaiting LUTX have morphologic alterations of the right heart, with subclinical impairment of RV systolic function. Echocardiography may be used as a bedside, repeatable, and reliable noninvasive test to screen further deterioration in RV function while on the waiting list for LUTX. More prospective follow-up echocardiographic studies are necessary to confirm such a hypothesis.     

Right Ventricular Systolic Function Is Not Depressed In Morbid Obesity

Background: The increased pulmonary blood volume associated with the increased total blood volume in morbidly obese patients increases pulmonary artery pressure and pulmonary vascular resistance, resulting in increased right ventricular (RV) afterload. Thus, the morbidly obese may develop RV dysfunction owing to the increased RV afterload. We examined this possibility by assessing RV contractile function in morbidly obese patients, using RV end-systolic pressure-volume relationship and RV systolic time intervals. Methods: Included were 25 morbidly obese patients undergoing gastric bypass surgery under general anesthesia. Pulmonary artery pressure and RV end-systolic volume were measured with a thermodilution pulmonary artery catheter. Pulmonary arterial dicrotic notch pressure was used as an estimate of RV end-systolic pressure. Two data points were used to define RV end-systolic pressure-volume relationship. RV systolic time intervals were determined by simultaneous graphic display of the electrocardiograph, phonocardiograph, and pulmonary artery pressure curve, and were expressed as a pre-ejection period/RV ejection time ratio. Results: The mean slope of right ventricular end-systolic pressure-volume relationship line was 0.54 ± 0.13 and mean pulmonary vascular resistance 274 ± 80 dyne·sec·cm⁻⁵·m⁻². The mean pre-ejection period/RV ejection time ratio was 0.4 ± 0.11. There was an inverse correlation between the pre-ejection/RV ejection time ratio and the slope of RV end-systolic pressure-volume relationship line (R²=0.658, P<0.0001). Conclusion: Our data indicate that RV function is not depressed in morbid obesity despite increased RV afterload.     

Effects of Inhaled Nitric Oxide Following Lung Transplantation

Abstract Background: Lung transplantation offers an established therapeutic option for end‐stage lung disease. It is associated with several complications, and early allograft failure is one of the most devastating among all. Different studies are focused on an attempt to minimize these complications, especially transplant failure. We aimed to evaluate the effects of inhaled nitric oxide (iNO) treatment in patients receiving lung transplantation. Methods: Nine patients (six female, three male; mean age 42.9 ± 15.8) requiring lung transplantation for end‐stage pulmonary disease—chronic obstructive pulmonary disease (three patients), cystic fibrosis (three patients), scleroderma and systemic sclerosis (two patients), Eisenmenger's syndrome (one patient), and treated with iNO were included in this retrospective study. Hemodynamic data (mean arterial pressure, mean pulmonary arterial pressure, heart rate) and respiratory parameters were analyzed. Pretreatment data were compared with the post‐iNO treatment data at 6–8 hours and 12–14 hours. Results: The inhalation of nitric oxide was started with an initial dose of 40 parts per million (ppm) and the dose was gradually decreased until hemodynamic and pulmonary stability was achieved. Six patients underwent double‐lung transplantation and three single‐lung transplantations were performed. Cardiopulmonary bypass was used in seven patients. The iNO therapy was started before transplantation in five patients, after the procedure in four patients. Mean iNO therapy duration was 83.2 ± 74.4 hours. The administration of iNO resulted in a significant reduction in mean pulmonary arterial pressure (36.8 ± 15.8 mm Hg to 22 ± 6.8 mm Hg at 6–8 hours and 22.8 ± 7.96 mm Hg at 12–14 hours). Mean systemic arterial pressure slightly increased at 6–8 hours and significantly increased at 12–14 hours (70.2 ± 6.3 mm Hg to 90.1 ± 11.96 mm Hg). Heart rate was not significantly affected with the treatment. Arterial oxygenation improved with the treatment. All patients except one showed improvement of overall respiratory functions. The mean duration of mechanical ventilation was 12.8 ± 10.9 days. Mortality occurred in one patient due to neurologic injury. NO₂ and methemoglobin levels were closely monitored during the treatment. Methemoglobinemia did not occur and NO₂ levels remained between 0.1 and 0.4 ppm. Conclusion: Nitric oxide inhalation for the prevention and treatment of early allograft failure in lung transplant recipients is encouraging. It is superior to other vasodilators with its selectivity to the pulmonary vasculature, while having no significant side effects on systemic circulation. It appears to improve gas exchange and oxygenation properties. Further prospective randomized studies will aid to standardize inhalation nitric oxide therapy.     

Inhaled iloprost to control pulmonary artery hypertension in patients undergoing mitral valve surgery: a prospective, randomized-controlled trial

Background: Pulmonary hypertension (PHT) is common in patients undergoing mitral valve surgery and is an independent risk factor for the development of acute right ventricular (RV) failure. Inhaled iloprost was shown to improve RV function and decrease RV afterload in patients with primary PHT. However, no randomized‐controlled trials on the intraoperative use of iloprost in cardiac surgical patients are available. We therefore compared the effects of inhaled iloprost vs. intravenous standard therapy in cardiac surgical patients with chronic PHT. Methods: Twenty patients with chronic PHT undergoing mitral valve repair were randomized to receive inhaled iloprost (25 μg) or intravenous nitroglycerine. Iloprost was administered during weaning from cardiopulmonary bypass (CPB). Systemic and pulmonary haemodynamics were assessed with pulmonary artery catheterization and transoesophageal echocardiography. Milrinone and/or inhaled nitric oxide were available as rescue medication in case of failure to wean from CPB. Results: Inhaled iloprost selectively decreased the pulmonary vascular resistance index after weaning from CPB (208 ± 108 vs. 422 ± 62 dyn·s/cm⁵/m², P<0.05), increased the RV‐ejection fraction (29 ± 3% vs. 22 ± 5%, P<0.05), improved the stroke volume index (27 ± 7 vs. 18 ± 6 ml/m², P<0.05) and reduced the transpulmonary gradient (10 ± 4 vs. 16 ± 3 mmHg, P<0.05). In all patients receiving inhaled iloprost, weaning from CPB was successful during the first attempt. In contrast, three patients in the control group required re‐institution of CPB and had to be weaned from CPB using rescue medication. Conclusions: In patients with pre‐existing PHT undergoing mitral valve surgery, inhaled iloprost is superior to intravenous nitrogylycerine by acting as a selective pulmonary vasodilator, reducing RV afterload and moderately improving RV‐pump performance.     

Correlation of Echocardiographic and Hemodynamic Parameters in Pulmonary Hypertension Assessment Prior to Heart Transplantation

Introduction

Invasive assessment of pulmonary artery pressure (PAP), via right heart catheterization, is part of the usual protocol prior to heart transplantation. Echocardiography is considered a valuable technique to evaluate PAP. We sought to determine the reliability of measurements of PAP via a noninvasive technique, echocardiography, in relation to the estimated PAP via right catheterization. We also determined its safety when invasive procedures are restricted to just patients with pulmonary hypertension (PHT) according to echocardiographic parameters.

Materials and methods

We performed a retrospective study of 67 right catheterizations performed in our hospital, within the heart transplant study protocol, from January 2000 to December 2006. PAP parameters were estimated by echocardiography and right catheterization.

Results

Hemodynamically, 57.1% of the patients had severe PHT (more than 45 mm Hg mean PAP); 13.2% moderate PHT (between 35 and 45 mm Hg mean PAP); 12.1% had mild PHT (between 25 and 35 mm Hg mean PAP); and 17.6% of patients showed no PHT. Pearson correlation index with systolic PAP (estimated via echocardiography) and mean PAP (calculated via invasive method) was 0.69 (P < .001). PHT was considered significant when systolic PAP estimated via echocardiography reached more than 40 mm Hg and mean PAP estimated via right catheterization reached more than 35 mm Hg, the value from which the vasodilator test was carried out. According to these parameters, echocardiography showed a sensitivity of 89% to diagnose significant PHT and 46% specificity, with positive and negative predictive values of 70% and 76%, respectively.     

长期维持性血液透析患者并发的肺动脉高压

目的 研究长期维持性血液透析(MHD)患者肺动脉高压(PHT)的特征及相关因素.方法 参照2010年美国心脏超声协会右心检测指南,肺动脉收缩压(PASP)＞35 mm Hg诊为PHT.超声心动图和脉搏波传导速度(baPWV)于透析后次日集中检测.自体动静脉内瘘(AVF)流量采用超声稀释法检测.收集及评估患者的透析相关信息,取血检测血常规、钙、磷、甲状旁腺激素(iPTH)、肝肾功能等指标.结果 我院透析中心进行MHD 6个月以上,采用自体AVF并除外其他疾病引起并发PHT者,共111例,其中男性45例,女性66例,平均年龄( 57.32±12.49)岁,平均透析龄为(70.51±44.98)个月.28例诊为PHT,占25.23％,平均PASP为(45.68±10.83) mm Hg.PHT组的左室舒张功能不全明显较非PHT组常见(53.60％比6.02％,P＜0.01).PHT组左室射血分数(EF)值(62.06％±14.90％比69.72％±8.60％)、左室内径缩短分数(36.46％±10.04％比40.20％±7.86％)均低于非PHT组(均P＜0.01).EF＜50％者在PHT组和非PHT组分别占21.43％和3.61％.但PHT组和非PHT组在年龄、性别、透析龄、身高、体质量指数(BMl)、透析间期平均每日体质量增长、透析前血压、血红蛋白、血白蛋白、前白蛋白、血钙、血磷、iPTH、标准化蛋白分解率(nPCR)、Kt/V、baPWV以及AVF流量等差异均无统计学意义.结论 PHT是维持性血液透析常见的并发症,其发生与左室收缩和舒张功能下降密切相关;与钙磷代谢、AVF流量、血红蛋白、透析充分性及营养状态等无明显相关性.     

Intraaortic Balloon Counterpulsation Improves Right Ventricular Failure Resulting From Pressure Overload

Background. Right ventricular (RV) dysfunction is common after heart transplantation, and myocardial ischemia is considered to be a significant contributor. We studied whether intraaortic balloon counterpulsation would improve cardiac function using a model of acute RV pressure overload.

Methods. In 10 anesthetized sheep, RV failure was induced using a pulmonary artery constrictor. Baseline measurements included mean systemic blood pressure, RV peak systolic pressure, cardiac index, and RV ejection fraction. Myocardial and organ perfusion were measured using radioactive microspheres.

Results. After pulmonary artery constriction, there was an increase in RV peak systolic pressure (32 ± 2 to 60 ± 3 mm Hg; p < 0.01) and a decrease in mean systemic blood pressure (68 ± 4 to 49 ± 2 mm Hg; p < 0.01), RV ejection fraction (0.51 ± 0.04 to 0.16 ± 0.02; p < 0.01), and cardiac index (2.48 ± 0.04 to 1.02 ± 0.11; p < 0.01). Blood flow to the RV did not change significantly, but there was a significant reduction in blood flow to the left ventricle. The initiation of intraaortic balloon counterpulsation (1:1) using a 40-mL intraaortic balloon inserted through the left femoral artery resulted in an increase in mean systemic blood pressure (49 ± 2 to 61 ± 3 mm Hg; p < 0.01), cardiac index (1.02 ± 0.11 to 1.45 ± 0.14; p < 0.05), RV ejection fraction (0.16 ± 0.02 to 0.23 ± 0.02; p < 0.01), and blood flow to the left ventricle.

Conclusions. In a model of right heart failure, the institution of intraaortic balloon counterpulsation caused a significant improvement in cardiac function. Although RV ischemia was not demonstrated, the augmentation of left coronary artery blood flow by intraaortic balloon counterpulsation and subsequent improvement in left ventricular function suggest that left ventricular ischemia contributes to RV dysfunction, presumably through a ventricular interdependence mechanism. Therefore, study of the safety and efficacy of intraaortic balloon counterpulsation in the management of patients with acute right heart dysfunction is warranted.     

Prevention of Right Heart Failure After Left Ventricular Assist Device Implantation by Phosphodiesterase 5 Inhibitor

Right ventricular (RV) function immediately after left ventricular assist device (LVAD) implantation is a crucial prognostic factor. RV failure is linked to increased mortality and worse outcome. A phosphodiesterase 5 inhibitor, sildenafil, was shown to decrease pulmonary vascular resistance and pulmonary artery pressure post‐LVAD. We report on a series of heart failure patients, and the effect of sildenafil on the incidence of RV failure after LVAD implantation. We retrospectively analyzed the data of end‐stage heart failure patients who underwent LVAD implantation with pulmonary hypertension and RV dysfunction prior to surgery. Patients were divided into two groups; group 1: patients who received sildenafil perioperatively, and group 2: patients who did not receive sildenafil. Hemodynamic and echographic data were collected before and after surgery. Fourteen patients were included, 8 patients in group 1 and 6 in group 2. Sildenafil was administered with a mean dose of 56.2 ± 9.4 mg in group 1 and was able to significantly reduce right heart failure incidence, and to demonstrate a significant reduction in pulmonary vascular resistance, pulmonary artery pressure, transpulmonary gradient, and a significant increase in cardiac output. In conclusion, sildenafil seems to have a promising role perioperatively in preventing acute RV failure postsurgery in patients with RV dysfunction and pulmonary hypertension, requiring LVAD therapy.     

Pattern of resolution of pulmonary hypertension,long‐term allograft right ventricular function,and exercise capacity in high‐risk heart transplant recipients listed under oral sildenafil

Unresponsive pulmonary hypertension (PH) implies poor posttransplant outcomes. Data on late adaptation of the right ventricle (RV) are still few. This study evaluated three‐yr RV function and remodeling, exercise capacity, and hemodynamic data in a selected group of patients initially disqualified because of PH. Between May 2005 and December 2009, 31 consecutive patients were qualified for oral sildenafil because of unresponsive PH at baseline right heart catheterization (RHC). After a 12‐wk trial, RHC disclosed PH reversibility (mean PVR: 5.41 ± 3 Wood units, mean TPG 14.5 ± 5.6 mmHg, and mean systolic PAP 68.9 ± 15.1 mmHg), allowing listing even though as high‐risk procedures. All patients underwent heart transplantation. RV failure developed in three patients (9.6%), and hospital mortality was 3.2%. Protocol RHC disclosed pulmonary hemodynamic profile normalization within the third postoperative month, allowing weaning from sildenafil in the 30 hospital survivors. One‐ and three‐yr RHCs confirmed stable PH reversal (n = 26, all three‐yr survivors). Parameters of late RV function and remodeling proved satisfactory. Parameters of functional capacity (Vo₂ peak 19.7 ± 3.6 mL/kg/min and slope VE/Vco₂ 34.8 ± 2.7) proved homogeneous to those measured in transplant recipients with normal preoperative pulmonary artery pressure. Oral sildenafil is effective in allowing candidacy, safe transplantation, and long‐term survival in PH recipients initially disqualified.     

Pulmonary Hemodynamics and Perioperative Cardiopulmonary-Related Mortality in Patients With Portopulmonary Hypertension Undergoing Liver Transplantation

In the setting of moderate to severe pulmonary artery hypertension, orthotopic liver transplantation (OLT) may be complicated by pulmonary hemodynamic instability and cardiopulmonary mortality. We retrospectively studied the relationship between cardiopulmonary-related mortality and initial (untreated) pre-OLT pulmonary hemodynamics in 43 patients with portopulmonary hypertension who underwent attempted OLT. Thirty-six patients were reported in 18 peer-reviewed studies, and 7 patients underwent OLT at our institution since 1996. Transplantation procedure outcome, mean pulmonary artery pressure (MPAP), pulmonary vascular resistance (PVR), cardiac output, pulmonary capillary wedge pressure, and transpulmonary gradient (TPG) are summarized. Overall mortality was reported in 15 of 43 patients (35%). Fourteen of the 15 deaths (93%) were primarily related to cardiopulmonary dysfunction. Two deaths were intraoperative, 8 deaths occurred during the transplantation hospitalization, and 4 patients died of cardiopulmonary deterioration posthospitalization. In 4 patients, the transplantation procedure could not be successfully completed. Cardiopulmonary mortality was associated with greater pre-OLT MPAP (49 ± 14 v 36 ± 7 mm Hg; P < .005), PVR (441 ± 173 v 261 ± 156 dynes·s·cm⁻⁵; P < .005), and TPG (37 ± 13 v 22 ± 10 mm Hg; P < .005). MPAP of 50 mm Hg or greater was associated with 100% cardiopulmonary mortality. In patients with an MPAP of 35 to less than 50 mm Hg and PVR of 250 dynes·s·cm⁻⁵ or greater, the mortality rate was 50%. No mortality was reported in patients with a pre-OLT MPAP less than 35 mm Hg or TPG less than 15 mm Hg. Cardiopulmonary-related mortality in OLT patients with portopulmonary hypertension was frequent and associated with significantly increased pre-OLT MPAP, PVR, and TPG compared with survivors. Treated or untreated, we recommend intraoperative cancellation or advise against proceeding to OLT for an MPAP of 50 mm Hg or greater. Patients with an MPAP of 35 to less than 50 mm Hg and PVR of 250 dynes·s·cm⁻⁵ or greater appear to be at high risk for cardiopulmonary-related mortality after OLT. A prospective study is needed to define optimal pretransplantation treatments and pulmonary hemodynamic criteria that minimize OLT mortality associated with portopulmonary hypertension. (Liver Transpl 2000;6:443-450.)     

Impact of Residual Mitral Regurgitation on Right Ventricular Systolic Function After Left Ventricular Assist Device Implantation

Significant mitral regurgitation (MR) is thought to decrease after left ventricular assist device (LVAD) implantation, and therefore repair of mitral valve is not indicated in current practice. However, residual moderate and severe MR leads to pulmonary artery pressure increase, thereby resulting in right ventricular (RV) dysfunction during follow‐up. We examined the impact of residual MR on systolic function of the right ventricle by echocardiography after LVAD implantation. This study included 90 patients (mean age: 51.7 ± 10.9 years, 14.4% female) who underwent LVAD implantation (HeartMate II = 21, HeartWare = 69) in a single center between December 2010 and June 2014. Echocardiograms obtained at 3–6 months and over after implantation were analyzed retrospectively. RV systolic function was graded as normal, mild, moderate, and severely depressed. MR (≥moderate) was observed in 43 and 44% of patients at early and late period, respectively. Systolic function of the RV was severely depressed in 16 and 9% of all patients. Initial analysis (mean duration of support 174.3 ± 42.5 days) showed a statistically significant correlation between less MR and improved systolic function of RV (P = 0.01). Secondary echocardiographic analysis (following a mean duration of support of 435.1 ± 203 days) was also statistically significant for MR degree and RV systolic dysfunction (P = 0.008). Residual MR after LVAD implantation may cause deterioration of RV systolic function and cause right‐sided heart failure symptoms. Repair of severe MR, in selected patients such as those with severe pulmonary hypertension and depressed RV, may be considered to improve the patient's clinical course during pump support.     

Lung transplantation for pulmonary vascular disease

BACKGROUND: Pulmonary hypertension (PHT) is a lethal condition resulting in markedly diminished life expectancy. Continuous prostaglandin I2 infusion has made an important contribution to symptom management, but it is not a panacea. Lung or heart-lung transplantation remains an important treatment option for end-stage PHT patients unresponsive to prostaglandin I2. This study reviews the outcomes after transplantation for PHT in our program. METHODS: A retrospective chart review was performed for 100 consecutive patients with either primary PHT (48%) or secondary PHT (52%) transplants since 1989. Living recipients were contacted to confirm health and functional status. RESULTS: Fifty-five adult and 45 pediatric patients underwent 51 bilateral lung transplants, 39 single lung transplants, and 10 heart-lung transplants. Mean age was 23.7 years (range, 1.2 months to 54.8 years) and mean pre-transplant New York Heart Association class was 3.2. Pre-transplant hemodynamics revealed a mean right atrial pressure of 9.6+/-5.4 mm Hg and mean pulmonary artery pressure of 64+/-14.4 mm Hg. Hospital mortality was 17% with early death predominantly because of graft failure and infection. With an average follow-up of 5.0 years, 1- and 5-year actuarial survival was 75% and 57%, respectively. Mean pulmonary artery pressure on follow-up catheterization was 22+/-6.0 mm Hg, and mean follow-up New York Heart Association class was 1.3 (p < 0.001 for both compared with pre-transplant). Diagnosis and type of transplant did not confer a significant difference in survival between groups. CONCLUSIONS: Whereas lung or heart-lung transplant for PHT is associated with higher early mortality than other pulmonary disease entities, it provides similar long-term outcomes with dramatic improvement in both quality of life and physiologic aspects.     

Pulmonary Hypertension in Patients With End-Stage Renal Disease Undergoing Renal Transplantation

Introduction

Pulmonary hypertension (PHT) has been reported to occur in a considerable proportion of patients with end-stage renal disease (ESRD). It is a progressive condition of the pulmonary circulation that poses prognostic importance. In this study, we sought to investigate the prevalence and the predictors of PHT among ESRD patients undergoing renal transplantation.

Patients and methods

We retrospectively evaluated the records, clinical and demographic data as well as laboratory results of 500 adult patients who underwent renal transplantation at our institution. A comprehensive Doppler echocardiographic examination was performed in all patients as part of the preoperative assessment. Systolic pulmonary artery pressure (SPAP) was calculated using Bernoulli equation; a value of >30 mm Hg was accepted as PHT.

Results

The mean age of the study population was 31.6 ± 10.2 years. The mean duration of dialysis was 40 months; 432 patients (86.4%) were on hemodialysis (HD) and 68 (13.6%) on peritoneal dialysis (PD). PHT was detected in 85 (17%) patients with a mean SPAP of 46.7 ± 8.7 mm Hg (range = 35-75 mm Hg). The mean age, sex, and laboratory variables were similar between patients with versus without PHT (P > .05 for all). The mean duration of dialysis therapy was longer in the PHT group than those subjects with normal SPAP (50.8 vs 38.5 months; P = .008). Concerning the type of dialysis, the ratio of patients having PHT was higher in the HD compared with the PD group (18.8% vs 5.9%; P = .008). The prevalence of chronic obstructive pulmonary artery disease, asthma, smoking, hypertension, and diabetes mellitus did not differ between patients with versus without PHT (P > .05 for all).

Conclusion

The findings of this study revealed that PHT was a common clinical condition among patients with ESRD evaluated for renal transplantation. The time on renal replacement therapy particularly HD as the treatment was associated with greater prevalences. Since it may be of prognostic importance in patients undergoing renal transplantation, a careful preoperative assessment including a comprehensive Doppler echocardiographic examination is needed to identify PHT.     

Right ventricle-sparing heart transplantation effective against iatrogenic pulmonary hypertension.

BACKGROUND: Right heart failure is the predominant cause of death following heart transplantation, occurring with disturbingly high frequency in patients with severe antecedent pulmonary hypertension. We have recently reported a novel technique of heart transplantation that spares the recipient right ventricle, excising only the recipient left ventricle. The resulting model has 2 right hearts and 1 left heart. The aim is to preserve the recipient's right ventricle, which is already conditioned to pulmonary hypertension. The hope is that, in this way, death due to right heart failure can be prevented in humans. Our prior report was a feasibility study in normal dogs. This study challenges this new technique by creating iatrogenic pulmonary hypertension in the recipient animals. METHODS: Iatrogenic pulmonary hypertension was created in 4 recipient canines by intravenous injection of the pulmonary toxin monocrotaline pyrrole (single bolus of 3.5 to 4.5 mg/kg intravenously [i.v.]). RESULTS: Within 6 weeks of monocrotaline administration, relative pulmonary hypertension occurred (mean pulmonary artery [PA] pressure 20 mm Hg vs 10 mm Hg for controls [p < 0.01]) (pulmonary vascular resistance [PVR] 4.2 vs 1.5 Wood units [P < 0.01]), and right ventricular (RV) hypertrophy developed (RV thickness 11 mm vs 2 mm [P < 0.04]). Histologic examination confirmed severe muscle infiltration and thickening of the media of the pulmonary arterioles. RV-sparing heart transplantation was performed successfully in all 4 animals with pulmonary hypertension. In all cases, the animals were weaned without difficulty from cardiopulmonary bypass, despite the ambient pulmonary hypertension, on low-dose epinephrine, maintaining systolic blood pressure of 104 mm Hg at right atrial pressure of 7 mm Hg. Both right hearts contracted well without dilation or strain. A single "control" traditional orthotopic transplant experiment in an animal with monocrotaline-induced pulmonary hypertension resulted in immediate death from right heart failure. CONCLUSIONS: Right ventricle-sparing heart transplantation ("one-and-one-half heart model") can handle pulmonary hypertension without difficulty. This evidence adds impetus for further pursuing of right ventricle-sparing heart transplantation to decrease the incidence of death from right heart failure in recipients with severe antecedent pulmonary hypertension.     

Haemodynamic changes in children with portal hypertension during the postoperative period

The cardiovascular changes following portosystemic shunt surgery (PSSS) in 33 children with extrahepatic portal hypertension (EPH) were studied to determine if portosystemic shunt surgery had any influence on the cardiovascular state. Haemodynamic data were obtained using two-dimensional and M-mode echocardiography, pulsed-wave Doppler and direct invasive techniques. Postoperatively all patients developed a hyperdynamic state, associated with an increase in cardiac index (CI), heart rate (HR) and a decrease in systemic vascular resistance index (SVRI). In 16 patients (group I), who preoperatively exhibited a hyperdynamic state accompanied by pulmonary hypertension, postoperative studies found an increase in acceleration time to ejection time ratio (AT/ET) in the pulmonary artery from 0.32 ± 0.05 (mean ± SEM) to 0.43±0.01; P < 0.01. Nine patients (group II) who were normodynamic preoperatively developed pulmonary hypertension and right ventricular (RV) dysfunction postoperatively: decrease in AT/ET from 0.42 ± 0.02 (mean ± SEM) to 0.32 ± 0.01; P < 0.01 and an increase in maximal peak pulmonary artery velocity to acceleration time ratio (Vmax/AT) from 702.56 ± 69.10 (mean ± SEM) to 1127 ± 105.30 cm·sec^-2; P < 0.01. In eight patients (group III) who were normodynamic preoperatively and were treated with dobutamine infusions at a rate of 5 μg·kg^-1·min^-1 postoperatively, the CI was found to increase from 5.28 ± 1.1 (mean ± SEM) to 7.97 ± 1.64 L·min^-1·m^-2; P < 0.01, left ventricular ejection fraction (LVEF) from 69.0 ± 4.1 (mean ± SEM) to 81.0 ± 2.9%; P < 0.01 and AT/ET from 0.37 ± 0.04 (mean ± SEM) to 0.44 ± 0.03; P < 0.01. Hence, dobutamine infusion at a dose of 5 μg·kg^-1·min^-1 can markedly increase cardiac performance and prevent pulmonary hypertension and RV dysfunction in children with EPH during the postoperative period.     

Inhaled nitric oxide for pulmonary hypertension after heart transplantation.

BACKGROUND: Recipient pulmonary hypertension due to chronic congestive heart failure is a major cause of right ventricular (RV) dysfunction after heart transplantation. We hypothesized that inhaled nitric oxide (NO), in the postoperative period, would a) selectively reduce pulmonary vascular resistance and improve RV hemodynamics and b) reduce the incidence of RV dysfunction compared with a matched historical group. METHODS: Sixteen consecutive adult heart transplant recipients with lowest mean pulmonary artery (PA) pressures >25 mmHg were prospectively enrolled. Inhaled NO at 20 parts per million (ppm) was initiated before termination of cardiopulmonary bypass (CPB). At 6 and 12 hours after CPB, NO was stopped for 15 minutes and systemic and pulmonary hemodynamics were measured. RV dysfunction was defined as central venous pressure >15 mmHg and consistent echocardiographic findings. The incidence of RV dysfunction and 30-day survival in this group was compared with a historical cohort of 16 patients matched for pulmonary hypertension. RESULTS: Discontinuation of NO for 15 minutes at 6 hours after transplantation resulted in a significant rise in mean PA pressure, pulmonary vascular resistance (PVR), and RV stroke work index. Systemic hemodynamics were not affected by NO therapy. One patient in the NO-treated group, compared with 6 patients in the historical cohort group, developed RV dysfunction (P< .05). The 30-day survival in the NO-treated group and the historical cohort group were 100% and 81%, respectively (P> .05). CONCLUSION: In heart transplant recipients with pulmonary hypertension, inhaled NO in the postoperative period selectively reduces PVR and enhances RV stroke work. Furthermore, NO reduces the incidence of RV dysfunction in this group of patients when compared with a historical cohort matched for pulmonary hypertension. Inhaled NO is a useful adjunct to the postoperative treatment protocol of heart transplant patients with pulmonary hypertension.     

Inhaled prostacyclin is safe, effective, and affordable in patients with pulmonary hypertension, right heart dysfunction, and refractory hypoxemia after cardiothoracic surgery

Background

The purpose of this study was to describe our institutional experience in using inhaled prostacyclin as a selective pulmonary vasodilator in patients with pulmonary hypertension, refractory hypoxemia, and right heart dysfunction after cardiothoracic surgery.

Methods

Between February 2001 and March 2003, cardiothoracic surgical patients with pulmonary hypertension (mean pulmonary artery pressure >30 mm Hg or systolic pulmonary artery pressure >40 mm Hg), hypoxemia (Pao₂/fraction of inspired oxygen <150 mm Hg), or right heart dysfunction (central venous pressure >16 mm Hg and cardiac index <2.2 L · min⁻¹ · m⁻²) were prospectively administered inhaled prostacyclin at an initial concentration of 20,000 ng/mL and then weaned per protocol. Hemodynamic variables were measured before the initiation of inhaled prostacyclin, 30 to 60 minutes after initiation, and again 4 to 6 hours later.

Results

One hundred twenty-six patients were enrolled during the study period. At both time points, inhaled prostacyclin significantly decreased the mean pulmonary artery pressure without altering the mean arterial pressure. The average length of time on inhaled prostacyclin was 45.6 hours. There were no adverse events attributable to inhaled prostacyclin. The average cost for inhaled prostacyclin was $150 per day. Compared with nitric oxide, which costs $3000 per day, the potential cost savings over this period were $681,686.

Conclusions

Inhaled prostacyclin seems to be a safe and effective pulmonary vasodilator for cardiothoracic surgical patients with pulmonary hypertension, refractory hypoxemia, or right heart dysfunction. Overall, inhaled prostacyclin significantly decreases mean pulmonary artery pressures without altering the mean arterial pressure. Compared with nitric oxide, there is no special equipment required for administration or toxicity monitoring, and the cost savings are substantial.     

Effects of respiration on the velocity of tricuspid regurgitation and estimation of systolic pulmonary artery pressure in patients with right ventricle systolic dysfunction

Objective. We investigated the effects of quiet respiration on the peak velocity of tricuspid regurgitation (TR) and estimation of systolic pulmonary artery pressure (SPAP) in patients with right ventricle (RV) systolic dysfunction using Doppler echocardiography. Methods. Continuous-wave Doppler spectra of TR were recorded in 32 patients with and 28 controls without RV systolic dysfunction. Electrocardiography and respiratory tracing were recorded simultaneously. Expiratory and inspiratory peak velocities of TR were acquired and averaged for five consecutive respiratory cycles. The SPAP during expiration and inspiration was calculated. Results. The velocity of TR and SPAP was not significantly different between expiration and inspiration in controls (2.77 ± 0.23 and 2.82 ± 0.26 m/s, P = 0.776; 35.94 ± 4.96 and 36.18 ± 5.12 mmHg, P = 0.747), whereas the velocity of TR and SPAP decreased significantly from expiration to inspiration in patients with RV systolic dysfunction (3.27 ± 0.35 and 2.59 ± 0.22 m/s, P < 0.001; 53.72 ± 7.39, 38.45 ± 5.63 mmHg, P < 0.001). Conclusions. Quiet respiration has significant effects on the velocity of TR in patients with RV systolic dysfunction. This factor should be taken into account when using Doppler echocardiography to estimate these patients’ SPAP, and the measurements should be performed in patients at the end of expiration.     

The Role of Arterio-Venous Shunt in the Pathogenesis of Pulmonary Hypertention in Patients with End-stage Renal Disease

Pulmonary hypertension (PHT) is an overlooked cardiovascular morbidity in patients with end stage renal disease. The pathogenesis of PHT in this group of patients is not explained satisfactorily. The aim of our study to evaluate the prevalence and the role of AV shunt in pathogenesis of pulmonary hypertention. Our study included 58 patients with ESRD without a known cause of PHT who were either in the predialysis period (stage 1V CKD) (14 patients) or maintained on chronic hemodialysis (stage V CKD) (44 patients) in Theodor Bilharz Research Institute (TBRI), Cairo, Egypt. In the chronic hemodialysis group, there were 27 males and 17 females with a mean age of 57.11 ± 12.31 years (range 28–65). In the predialysis group, there were 8 males and 6 females with a mean age 53.45 ± 9.41 years (range 28–66). Pulmonary arterial pressure (PAP) and cardiac output were evaluated by Doppler echocardiography in the 14 pre-dialysis patients without PHT few (4.3 ± 0.8) months after creation of AV fistula and in the 44 hemodialysis patients (33.6 ± 4.2 months) after creation of AV fistula within 1 h of completion of hemodialysis session. Arteriovenous fistula (AVF) flow was measured by Doppler sonography. PHT (systolic PAP ≥35 mm Hg) was observed in 25 (56.8%) patients receiving hemodialysis with a mean systolic PAP of 46.4 ± 13.6 mm Hg. In the predialysis group after creation of AV fistula, PHT was found in 6 (42.9%) patients with a mean systolic PAP of 42.8 ± 12.8 mm Hg. The cardiac output and AV shunt flow were found to be increased in patients with elevated systolic PAP in both groups (p < 0.05). CRF duration and AV fistula duration were positively correlated with systolic PAP in patients receiving hemodialysis (p < 0.05). After compression of AV fistula in 11 hemodialysis patients, the mean value of PHT decreased (from 43.98 ± 15.6 to 33.22 ± 11.7 mm Hg). This study demonstrates a high prevalence of PHT among patients with ESRD in predialysis period after creation of AV fistula and on chronic HD via a surgical A-V fistula. Cardiac output, AV shunt flow and duration, and ESRD duration may be involved in the pathogenesis of PHT. The development of PHT following access formation represents a failure of the pulmonary circulation to accommodate the access-mediated elevated CO. Pre-dialysis patients scheduled for access formation should be screened for the presence of sub-clinical PHT.     

Atrial Septal Defect Revealed by Repeat Echocardiography in a Brain-Dead Donor: A Case Report

BackgroundThe number of patients undergoing heart transplantation is limited because of the shortage of donor hearts. Expanding the donor pool with precise evaluation of donor heart is the most practical way to increase the number of patients undergoing heart transplantation. However, echocardiographic evaluation of especially right ventricle (RV) in brain-dead donors is challenging. Repeated echocardiography with volume overload may reveal unrecognized congenital heart disease such as atrial septal defect (ASD).Materials and MethodsA case of repeated echocardiography revealed ASD secundum in a donor with significant RV enlargement and dysfunction from previously unknown origin. An almost-discarded donor heart was used in heart transplantation after simple patch closure.ResultsThe patient was discharged after a month. One year later, he has been doing well without significant adverse events.ConclusionsRV dysfunction prior to heart transplantation increases the risk of post-transplant graft failure. Secundum-type ASD and ventricular septal defect, which are relatively common adult congenital heart diseases that cause RV enlargement and dysfunction, are not contraindications for heart transplantation. Our case showed that repeat echocardiography revealed congenital heart disease and rescued the almost-discarded heart. This simple maneuver is essential in donor heart evaluation to maximize the utility of marginal donors.