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Ann Thorac Surg 2002;73:209-219
© 2002 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri, USA
b Division of Pulmonary Medicine, Washington University School of Medicine, St. Louis, Missouri, USA
c Division of Cardiology, Department of Pediatrics, St. Louis, Missouri, USA
d Division of Pulmonary Medicine, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, USA
* Address reprint requests to Dr Mendeloff, St. Louis Children’s Hospital, One Children’s Place, Suite 5S50, St. Louis, MO 63110, USA
e-mail: mendeloffe{at}msnotes.wustl.edu
Presented at the Thirty-seventh Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 29–31, 2001.
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Abstract |
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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.
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Material and methods |
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Patients evaluated for lung transplantation are not turned down on the basis of poor right ventricular function. The general indications for HLT are single ventricle anatomy with associated PHT or other complex congenital heart diseases with associated depressed or restrictive left ventricular physiology. The details of this patient group are delineated in Table 3. The patients in our population had no other irreversible end-organ damage and otherwise satisfied the usual criteria for lung or heart-lung transplantation.
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The surgical aspects of SLTs, BLTs, and HLTs have been previously described in detail [9, 10, 11]. A thoracotomy, bilateral thoracosternotomy or midline sternotomy was used, and cardiopulmonary bypass with mild hypothermia was used in 96 patients. The 4 patients in the series who did not undergo cardiopulmonary bypass were all adults with PPH; 3 of these patients underwent SLT and 1 patient underwent BLT. Closure of all intracardiac shunts and establishment of unobstructed continuity from the right ventricle to the lungs was achieved in all patients with PHT secondary to unrepaired cardiac defects. Fibrillating arrest was used for small atrial septal defects and aortic cross clamping was used with administration of cardioplegia for larger intracardiac defects. Careful removal of air and flushing of preservation solution from the pulmonary vascular bed were undertaken just before establishing reperfusion when SLT or BLT was performed. After HLT or intracardiac repair in association with lung transplantation, air was removed carefully from the heart before weaning from bypass. Invasive hemodynamic monitoring and transesophageal echocardiography were routinely used while weaning from bypass.
Postoperative management
Perioperative and postoperative management and immunosuppressive protocols are similar to those in our prior description of transplantation in the cystic fibrosis population [12]. In the absence of systemic hypotension, a continuous infusion of Prostaglandin E1 was used at the time of reperfusion and was tapered off over the first 48 hours after the transplant. In recent years, routine administration of inhaled nitric oxide was used in the adult population to help avoid the occurrence of reperfusion injury. Routine invasive hemodynamic monitoring was used and low dose inotropic support was administered as necessary. In addition, neuromuscular blockade and sedation was used in all patients. Single lung transplants were maintained in a rotated position with transplanted side up in order to avoid pooling of secretions and to maintain excellent function of the allograft. Similarly, we also usually used 5 to 10 cm H2O of positive end-expiratory pressure as part of the mechanical ventilatory support for the first 24 to 48 hours postoperatively.
An immunosuppressive protocol based on cyclosporine, azathioprine, and prednisone was used. Azathioprine was given immediately before going to the operating room in a dose of 2.5 to 3.0 mg/kg intravenously and was continued at the same level as a single daily dose postoperatively. Cyclosporine was started as a continuous intravenous infusion immediately after the operation with the pediatric patients, whereas in adults it was started enterally on postoperative day 1 or 2. Azathioprine, steroids, and cyclosporine were converted to oral doses for the pediatric patients after tolerance of enteral feeds. Target trough cyclosporine levels were 300 to 350 ng/mL in the early postoperative interval until approximately 6 months after transplant, and then levels dropped to 250 to 300 ng/mL from 6 months to 1 year after the transplant at which time levels of 200 to 250 ng/mL were acceptable. Systemic corticosteroids were started in the immediate postoperative period with methylprednisolone (0.5 mg/kg per day). Once conversion to oral dosing was achieved, the dose was left at 0.5 mg/kg per day for the first 3 to 6 months after transplantation and was then gradually tapered to 0.1 to 0.2 mg/kg per day by 12 months postoperatively. Acute rejection episodes as documented by transbronchial biopsy were treated with a 3-day pulse of intravenous methylprednisolone at 10 mg/kg per day in the pediatric population and 0.5 to 1 gm per day in the adult population. Patients experiencing recurrent acute rejection were converted to a combination of tacrolimus and mycophenolate mofetil in lieu of cyclosporine and azathioprine. In addition, Atgam (Upjohn), methotrexate and OKT3 have been occasionally used as second and third line forms of therapy for refractory rejection.
Routine perioperative antibiotics were administered. Three to 6 weeks of cytomegalovirus prophylaxis with intravenous ganciclovir were also given to all patients who were cytomegalovirus IgG negative that received organs from a cytomegalovirus IgG positive donor. In addition, in the pediatric population, if the recipient was cytomegalovirus IgG positive, irrespective of the donor, then 6 weeks of cytomegalovirus prophylaxis was also administered. Prophylaxis against Pneumocystis carinii consisted of trimethoprim sulfamethoxazole, which was given once daily until discharge at which time the regimen was changed to 3 times per week. All heart-lung transplants and all adult lung transplants received yearly hemodynamic evaluations by cardiac catheterization. Surveillance bronchoscopy for rejection (assessed by transbronchial biopsy) and lower respiratory infection (assessed by bronchoalveolar lavage) were performed routinely at 1 to 2 weeks, 1 month, 2 months, 3 months, and every 6 months to yearly postoperatively and also when clinically indicated by chest roentgenogram, fever, increasing oxygen requirements, or decrease in pulmonary function. In addition, graft function was measured by pulmonary function testing, and overall functional status of the patients was routinely assessed. When discharged from the hospital, each patient was provided with a home spirometer (Puritan Bennet model PB110, Wilmington, MA) and was asked to perform spirometry twice daily. A drop in forced expiratory volume in 1 second of greater than 10% from base line was considered an indication for contacting out transplant service. An unexplained decline in forced expiratory volume in 1 second was thoroughly evaluated and, without other defined etiology, signaled the development of obliterative bronchiolitis syndrome (BOS) as determined by the International Society of Heart and Lung Transplantation classification [13].
Statistical analysis
The data from the patients’ evaluations, hospital stay, and posttransplantation follow-up examinations were compiled and analyzed. Follow-up was completed on 100% of the patients. For comparative analyses, we divided the patients into three groups based on operation performed: (1) single lung transplants, (2) bilateral lung transplants, or (3) heart-lung transplants. Normally distributed continuous data are expressed as mean ± standard deviation throughout. Medians with ranges are used when continuous data is not normally distributed. Categorical data are expressed as counts and proportions. Unrelated two-group comparisons were done with unpaired, two-tailed t tests for means if the data were normally distributed or with Wilcoxon’s rank-sum tests if the data were not normally distributed. One-way analysis of variance was performed on continuous data to determine the difference in the means of the three groups. Fisher’s least significant difference (LSD) was performed for pairwise comparison probabilities. Chi-squared or Fisher’s exact tests were used to analyze the categorical data. Cox multivariate proportional hazards regression methods were used to identify risk factors for death after transplantation. Time to death after transplantation was selected as the primary outcome. The likelihood ratio method was used to determine hazard ratios, and the hazard ratio was used to approximate the relative risk. Kaplan-Meier graphs were used to demonstrate survival over time and freedom from obliterative bronchiolitis. Survival and BOS-free survival comparison between groups of patients were completed using the Mantel-Haenszel log rank test. All data analysis was performed using Systat (Systat 10.0 for Windows, SPSS Inc, Chicago, IL). All p values less than 0.05 were considered to be statistically significant.
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Results |
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Postoperative results
Hospital mortality was 17% for the entire population, 10.4% in those transplanted for PPH and 23.1% in those transplanted for secondary PHT (p = 0.011). There was no significant difference in early mortality between groups stratified by type of operation performed (SLTs, 12.8%; BLTs, 17.6%; and HLTs, 30%). The major causes of death in both the postoperative interval and the first year posttransplant were primary graft failure and sepsis (Table 4). A single patient in the series underwent early redo transplantation for primary graft failure, and this patient died before hospital discharge. Median length of time on mechanical ventilation was 8 days (range, 1 to 140 days) and intensive care unit stay was 6 days (range, 2 to 140 days). Breaking down the population either by indication for transplant or by type of allograft received, there was no significant difference in intensive care unit stay or length of mechanical ventilation between groups. Median length of stay in the hospital was 21 days (range, 10 to 65 days) with no difference stratified by indication for transplant or by type of transplant performed.
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Hemodynamic results and ventricular function
Pretransplant and posttransplant hemodynamics and ventricular ejection fractions of the SLT and BLT groups are depicted in Figure 1.
There are significant and sustained decreases in pulmonary vascular resistance (15.8 ± 8.0 woods units pretransplant and 2.1 ± 0.9 woods units posttransplant; p < 0.001) and mean PAPs (65.9 ± 13.1 mm Hg pretransplant and 21.9 ± 5.9 mm Hg posttransplant; p < 0.001). Correspondingly, in these same 2 groups there is significant improvement in the right ventricular ejection fraction from a mean of 26.8% ± 12.6% pretransplant to 56.6% ± 8.8% posttransplant (p < 0.001).
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Bronchiolitis obliterans syndrome
Over the course of this study, 4 patients who underwent their primary transplant for PHT were retransplanted for BOS and all of these have died. Freedom from BOS for the entire group at 5 years after transplant is 45% (Fig 2A)
with no difference between groups when stratified by indication for transplant. When stratified by type of transplant performed and omitting the HLT subgroup, there was decreased freedom from BOS 5 years after transplant in patients who underwent SLT as opposed to BLT (27.3% vs 61.9%; p = 0.043) (Fig 2B). As with all other lung transplant populations, bronchiolitis obliterans continues to be the major cause of late mortality, and survival for the overall population at 5 years is 57% (Fig 3).
Once again, there were no significant survival differences between the groups stratified by indication for transplant (PPH or secondary PHT) or type of transplant (SLT, BLT, or HLT).
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Comment |
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Lung transplantation has been established as an effective therapy for advanced pulmonary vascular disease. Primary pulmonary hypertension remains the second most common indication for lung transplantation in the pediatric population and the fourth most common in adults. Primary pulmonary hypertension is also the second most common indication for HLT [21]. This long-term follow-up study documents that hemodynamics after SLT or BLT are characterized by a rapid and sustained drop in PAPs and substantial improvement in right ventricular function. The Toronto group reported the first lung transplant for PHT associated with a congenital heart defect patent ductus arteriosus [22]. Subsequently, lung transplantation for secondary PHT has been embraced to varying degrees [23, 24]. Because of the scarcity of heart-lung blocks, combining repair of a coexistent congenital heart defect with SLT or BLT should be considered if the heart defect lends itself to this option. Specifically, whenever the cardiac anatomy, ventricular and valvar function are such that after repair the patient is likely to have adequate cardiac function and not need a further corrective operation, then this approach should be considered. Preserving the recipient’s heart avoids the risks of cardiac rejection and graft vasculopathy and also maximizes the use of donor organs. However, patients with PHT in association with single ventricle physiology or significantly impaired left ventricular function will require HLT.
As is evidenced by the significant perioperative morbidity reported in the current study, it is not surprising that patients with pulmonary vascular disease, as an indication for transplantation, have been reported to have higher operative mortality than patients with other indications for lung transplantation [7, 25, 26]. A history of multiple prior thoracic procedures in patients with secondary PHT contributes to increased difficulty of the operation. Patients with previously palliated or repaired cyanotic congenital heart disease who have extensive chest wall collaterals related to scarring from previous surgical intervention or from aortopulmonary collaterals may have a tedious dissection with prohibitive amounts of bleeding. Two patients in the pediatric population in this study died of uncontrollable intraoperative hemorrhage, and this in part explains why the group of patients with secondary PHT in this study had a higher hospital mortality than those transplanted for PPH. The coexistence of PHT, cyanosis, and multiple bilateral thoracotomies now serves as a general contraindication to lung transplant or HLT in our program. Such patients who have had prior thoracotomies confined to only one chest may be best served by SLT or heart-SLT to avoid entrance into the previously operated pleural space.
Especially in the group with secondary PHT, relief of severe and long-standing PHT in patients with right ventricular dysfunction may unmask right ventricular muscle bundles (or supravalvular pulmonic stenosis, such as that in a patient who has undergone previous arterial switch procedure). Mild to moderate dynamic obstruction from right ventricular muscle bundles can be expected to resolve spontaneously over the course of several months. Nonetheless, one should try to avoid use of high dose inotropic agents in the early postoperative interval to prevent making these potential sites of obstruction more severe. Postoperative fluid management in the group with secondary PHT may pose a dilemma. Whereas we generally try to administer minimal intravenous fluids to lung transplant recipients, this may not be the best approach in a newly repaired heart that has just sustained an ischemic interval and may require higher filling pressures. Maintaining appropriate fluid balance to achieve ideal hemodynamics but not subject the pulmonary vasculature to high hydrostatic forces requires careful monitoring. As previously documented by our group, patients who have undergone SLT for PHT have an obligate ventilation-perfusion mismatch with 80% to 90% of their cardiac output being directed to the allograft [6]. Occurrence of rejection or infection in the transplanted lung may result in a relatively acute elevation in pulmonary vascular resistance and recurrence of overt right heart failure. We believe that this phenomenon contributes to the tenuous nature and propensity of significant hemodynamic fluxes in the early postoperative period.
Bronchiolitis obliterans continues to be the major cause of late death after SLT, BLT, and HLT. Experience from our adult population suggests that although BOS occurs with similar frequency in patients undergoing SLT as those patients undergoing BLT, this entity is likely more poorly tolerated in the former group [27]. Extending this concept to patients who undergo SLT for PHT, because the entire cardiac output is delivered to the transplanted lung, the onset and effects of BOS are likely to be more profound than if a BLT with a significantly larger pulmonary vascular bed had been performed. Specifically, when the transplanted lung that is receiving the majority of the perfusion and only approximately 50% of the ventilation is subjected to a process that destroys its ventilatory capacity, intuitively the functional debilitation associated with BOS will be realized earlier. Thus, whereas BO likely occurs with equal frequency in both SLT and BLT recipients, clinical recognition of BOS is made earlier in SLT. The importance of this phenomenon may be reflected in the most recent 8-year actuarial survival data from the International Society of Heart and Lung Transplantation for all lung transplants, pediatric and adult. This data reveals that survival curves appear to diverge after 3 years posttransplantation, with BLT having a survival advantage over SLT [21]. It is for this reason that in the later part of our experience reported herein that we have performed BLT preferentially (Table 5). Previous analysis by our group of patients transplanted for PHT comparing operative survivors with and without BOS revealed that there were no significant differences in PAPs, pulmonary vascular resistance, and right ventricular ejection fraction between these 2 groups [6]. In a group of 58 primary lung transplant recipients for PHT, investigators at the University of Pittsburgh found no early functional or late survival benefit to BLT over SLT for PHT with a mean follow-up of 4 years [5]. A remarkably low incidence of BOS in the HLT group reported by Whyte and colleagues [6] at Stanford is not observed in our experience or in other large reported experiences, such as the 186 patients from Harefield Hospital, England, in which the probability of BOS at 5 years after HLT was 71%. This possibly may be due to a smaller patient cohort, differing lengths of follow-up, differing statistical methods or the routine use of induction cytolytic therapy by the Stanford group. Despite this difference in the incidence of BOS, our actuarial survival at 5 years was 57% as compared with 42% reported by Stanford.
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Discussion |
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Briefly, this study included 100 patients, 55 adults, and 45 pediatric patients. The mean pulmonary artery pressure preoperative was 65 with very little variation, so they tended to represent a very high pulmonary artery pressure group, and the hospital mortality was 17%, and 1-year and 5-year actuarial survival, 75% and 57%, very excellent results for this difficult group. The survivors had excellent functional improvement and return of pulmonary artery (PA) pressures toward normal, with a mean of 22, and, return of right ventricular function toward normal. They evaluated outcomes for single versus bilateral versus heart-lung transplants and found no difference in survival, but a trend toward some increase in bronchiolitis obliterans with single lung transplantation.
I think one of the most difficult problems in the pulmonary hypertension group, and this is something we have struggled with, is the mixture of patients. You have in this study a mixture of pediatric and adult patients, primary pulmonary hypertension and secondary pulmonary hypertension. In the latter group all were secondary to congenital heart disease, some of which had corrected lesions and some did not. As the authors nicely note in the discussion in their article, there is a difference in behavior on how these patients behave when they still have a shunt present versus one that has been closed, the latter group being at higher risk. I think the challenge is how do you analyze data in such diverse groups?
One of our former residents, Scott Heurd, analyzed another group of secondary pulmonary hypertension patients, the group that is secondary to parenchymal disease as opposed to congenital heart disease. They tend to have mild to moderate pulmonary hypertension, which we defined as a mean PA pressure of greater than 30. This group can be managed somewhat differently, usually with a single lung transplant and without cardiopulmonary bypass in most instances. With a single lung transplant in our series, there was a return to normal PA pressures, and in terms of freedom from bronchiolitis obliterans and survival, at four years we saw no difference between the groups.
I hate to complicate things by adding a further group, but have you looked at the other causes of secondary pulmonary hypertension? Have you tried to separately analyze your primary pulmonary hypertension group, looking at the single and double transplants and even historically some heart-lung transplants in that group? Have you tried to separate out further your congenital group in terms of examining the various procedures and the results?
I wonder if, indeed in the single lung transplant group, there is an increased incidence of bronchiolitis obliterans or whether, as you suggest in your discussion, that bronchiolitis obliterans is tolerated less well in the single lung transplant group because of less pulmonary reserve, and therefore it becomes clinically apparent sooner than it does in the bilateral or the heart-lung group.
Again, I enjoyed your paper very much and look forward to your discussion. Thank you.
DR JOSHUA R. SONETT (Baltimore, MD): I enjoyed your presentation and appreciate the data coming out of St. Louis. It is always excellent and enlightening. I agree with Dr Grover’s assessment: I would like to see a split-up between the adult and primary and secondary pulmonary hypertension because they may act differently.
In regard to the adult population and the primary pulmonary hypertension, virtually all our patients now present on Prostin, and for our hard part, and I question what your group is doing; is it grappling with how long to keep them on Prostin and defer transplant? Given that the 5-year survival of lung transplantation is still around the 50% range, we can extend the patients to transplant 5, 6, 7 years on prostacyclin now with PA pressures as high as 100 and suprasystemic. But when they precipitously fall off the curve, it is really hard to gauge. I was wondering if your group has any insight on when to actually perform the transplant on the patients that are on chronic Prostin? For those patients that are on chronic Prostin for more than 2 years, do you find the morbidity and mortality of the procedure higher as they have had more right heart failure and more complications secondary to their pulmonary hypertension? Thank you.
DR ASGHAR KHAGANI (London, UK): I congratulate the group for their good results. I have two small questions. One is related to the degree of the pulmonary hypertension: Do you have a cut point for doing single lung transplantation in severe pulmonary hypertensive patients? If you don’t, how do you manage the complications related to the procedure? And the second question is the exercise capacity: Is there any difference between the single and double lung group?
DR THOMAS WOZNIAK (Carmel, IN): What percentage of your patients required bypass and did you have predictors preoperatively that were helpful in deciding which patients would and would not require bypass? Do you use anything intraoperatively, such as nitric oxide or anything else to avoid the use of bypass? Thank you.
DR MARK D. IANNETTONI (Ann Arbor, MI): Eric, I enjoyed your presentation. I noticed that your right atrial pressures were a mean of nine, with a very narrow standard deviation. Do you have any recommendations on when you decide to do a single lung versus a heart-lung, say, over 15 mm Hg for right atrial pressure, or do you not use right atrial pressure as an indicator? We find that most of our patients are being referred quite late with right atrial pressures in the twenties. What is your experience with that and your thoughts on elevated right atrial pressure?
DR MENDELOFF: I want to thank Dr Grover for his comments and review of the article. Obviously the group at Denver has contributed significantly to the understanding of this complex group of patients.
One of the obvious problems with analyzing a group of patients like this is that it does not really lend itself to a prospective randomized trial. We have performed various types of transplants (single lung, bilateral lung, or heart-lung transplant), and coming to an understanding of this group of patients has been an evolution over time. It has been our clinical sense that the patients generally do better with a bilateral lung transplant. We have done bilateral lung transplants in the pediatric age group just for the sake of making sure that there was adequate pulmonary reserve, not knowing whether or not these lungs would grow with time. We did analyze various subgroups, and in our multivariate risk analysis, we included age and indication for transplant, meaning primary pulmonary hypertension versus secondary pulmonary hypertension. Whereas the mortality was higher in the secondary pulmonary hypertension group, it did not come out as an independent risk factor for mortality.
Again, the whole issue of bilateral lung transplant versus single lung transplant is a difficult issue because obviously foremost in all of our minds is getting the patients through the transplant. Right behind that is optimal use of donor organs. So, as I said, there is a subjective sense that patients who undergo bilateral lung transplant have a smoother postoperative course, although our data do not prove either by length of mechanical ventilation, length of intensive care unit stay, or by length of hospitalization, that in fact a bilateral lung transplant is better than a single lung transplant. I think this relates to the fact that this is such a heterogeneous and complex group of patients.
Another thing that has pushed us toward doing bilateral lung transplants in this group of patients is that our data at 5 years of follow-up shows an increased trend toward bronchiolitis obliterans syndrome in the single lung transplant recipients. I would agree with you entirely, in that I don’t think bronchiolitis obliterans is any more common in single lung transplant recipients than in bilateral lung transplant recipients. Rather, I think the reality is that there is more pulmonary reserve in the bilateral lung transplant group there when it does happen. In addition, data from our emphysema population that is not published yet is showing that the emphysema patients that have undergone bilateral lung transplant are having a better long-term survival. Again, I don’t think that has anything to do with it, other than the fact that there is more pulmonary reserve. Finally, I think you have to look to the International Society of Heart and Lung Transplantation (ISHLT) as our sort of governing group in transplantation. Their most recent report suggests that bilateral lung transplant does confer an improved survival. This improvement is not drastic, but it has become significant now at 8 years of follow-up.
The question from the Baltimore group as far as length of time on Prostin and when to list is difficult to answer in a single, straightforward fashion. Again, these are really heterogeneous groups of patients, and, as Mark Iannetonni pointed out, they can present when they are nearly in extremis. In that case, we list them immediately and actually now are considering, at least in the pediatric population, bilateral living donor lobar transplantation. On the other hand, others present in a clinically stable condition and should be tried on Flolan. As far as when to list these patients, I can not give you an exact answer other than that the patients need to be followed very, very closely both hemodynamically and symptomatically. Prostin is certainly the way to go first off if the patient can tolerate it, and many patients do. But an important subset of patients don’t respond to Prostin. I would recommend that if you think someone is far along in their disease based on symptoms, severity, and right ventricular hypertrophy and dysfunction, you have nothing to lose by listing them. You can always deactivate them if you find that with Flolan they are getting along clinically well. If you can put off their lung transplant 5, 10 years, then I think you should do so.
Mark Iannetonni asked about the right atrial pressure as an indicator, and we did not look at that separately. Do I know if the people with the higher right atrial pressures do worse? There is no indication for this. Others have implicated that people with suprasystemic pulmonary pressures will do worse with a transplant, and we also did not find this in our analysis. People with the suprasystemic pulmonary artery pressures usually have the highest right atrial pressures. We had 9 patients with suprasystemic pulmonary artery pressures, and all survived the transplant.
As to what percentage of patients required cardiopulmonary bypass, 96% required cardiopulmonary bypass. There were only 4 patients that did not require it, and all were patients with primary pulmonary hypertension and all were adults.
I would be glad to entertain anything else, but I think that this covers most of what everyone asked. Thank you very much.
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