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• W2037473973 abstract "Severe portopulmonary hypertension (POPH) is an absolute contraindication to orthotopic liver transplantation (OLT). Vasodilators have been used, but the safety of subsequent transplantation and the reversibility of pulmonary hypertension after transplantation are uncertain. This study examined the feasibility and post-transplant effects of liver transplantation following medical control of POPH. Eight consecutive patients (three females and five males, ages 39–51) with POPH as their only contraindication to transplantation were treated with continuous intravenous epoprostenol. Liver transplantation was considered if the mean pulmonary artery pressure (PAM) was lowered to <35 mmHg. Epoprostenol 2–8 ng/kg/min successfully improved hemodynamics in seven of eight patients, usually within 6.5 months of initiating therapy. PAM declined from an average of 43–33 mmHg (p = 0.03); mean pulmonary vascular resistance declined from 410 to 192 dyn s cm–5 (p = 0.01) and cardiac output increased from 6.6 to 10 L/min (p = 0.02). Six of the seven responders were actively listed for liver transplantation. Two died on the waiting list; the remaining four were transplanted and remain alive and well 9–18 months post—OLT–two without vasodilators, and two on oral medication. We conclude that pulmonary vasodilators permit safe liver transplantation in some cases, and that POPH may be reversible after transplantation. Severe portopulmonary hypertension (POPH) is an absolute contraindication to orthotopic liver transplantation (OLT). Vasodilators have been used, but the safety of subsequent transplantation and the reversibility of pulmonary hypertension after transplantation are uncertain. This study examined the feasibility and post-transplant effects of liver transplantation following medical control of POPH. Eight consecutive patients (three females and five males, ages 39–51) with POPH as their only contraindication to transplantation were treated with continuous intravenous epoprostenol. Liver transplantation was considered if the mean pulmonary artery pressure (PAM) was lowered to <35 mmHg. Epoprostenol 2–8 ng/kg/min successfully improved hemodynamics in seven of eight patients, usually within 6.5 months of initiating therapy. PAM declined from an average of 43–33 mmHg (p = 0.03); mean pulmonary vascular resistance declined from 410 to 192 dyn s cm–5 (p = 0.01) and cardiac output increased from 6.6 to 10 L/min (p = 0.02). Six of the seven responders were actively listed for liver transplantation. Two died on the waiting list; the remaining four were transplanted and remain alive and well 9–18 months post—OLT–two without vasodilators, and two on oral medication. We conclude that pulmonary vasodilators permit safe liver transplantation in some cases, and that POPH may be reversible after transplantation. Portopulmonary hypertension (POPH) was first described in 1951 (1Mantz Jr, FA Craige E Portal axis thrombosis with spontaneous portacaval shunt and resultant cor pulmonale..AMA Arch Pathol. 1951; 52: 91-97PubMed Google Scholar), and is now recognized as a fairly common complication of end-stage liver disease. Accurate figures are not established, but the condition has been reported in 2–12.5% of cirrhotic patients, and in up to 16% of patients with refractory ascites (2Benjaminov FS Prentice M Sniderman KW Siu S Liu P Wong F Portopulmonary hypertension in decompensated cirrhosis with refractory ascites..Gut. 2003; 52: 1355-1362Crossref PubMed Scopus (144) Google Scholar). Survival in the absence of transplantation has recently been reported as 38% at 3 years (3Kawut SM Taichman DB Ahya VN et al.Hemodynamics and survival of patients with portopulmonary hypertension..Liver Transpl. 2005; 11: 1107-1111Crossref PubMed Scopus (136) Google Scholar) and 28% at 5 years (4Krowka MJ Portopulmonary hypertension and the issue of survival..Liver Transpl. 2005; 11: 1026-1027Crossref PubMed Scopus (30) Google Scholar), and prognosis is worse than for idiopathic pulmonary hypertension (3Kawut SM Taichman DB Ahya VN et al.Hemodynamics and survival of patients with portopulmonary hypertension..Liver Transpl. 2005; 11: 1107-1111Crossref PubMed Scopus (136) Google Scholar). POPH is also a serious problem in the context of liver transplantation. Mild disease (PAM <35 mmHg) poses little perioperative risk (5Krowka MJ Editorial: Pulmonary hypertension, (high) risk of orthotopic liver transplantation, and some lessons from “primary” pulmonary hypertension..Liver Transpl. 2002; 8: 389-390Crossref PubMed Scopus (18) Google Scholar,6Starkel P Vera A Gunson B Mutimer D Outcome of liver transplantation for patients with pulmonary hypertension..Liver Transpl. 2002; 8: 382-388Crossref PubMed Scopus (72) Google Scholar), but moderate disease (PAM 35–45 mmHg, pulmonary vascular resistance (PVR) <250 dyn s cm–5) has been associated with a perioperative mortality of 50–80% (7Krowka MJ Plevak DJ Findlay JY Rosen CB Wiesner RH Krom RA Pulmonary hemodynamics and perioperative cardiopulmonary-related mortality in patients with portopulmonary hypertension undergoing liver transplantation..Liver Transpl. 2000; 6: 443-450Crossref PubMed Scopus (460) Google Scholar,8De Wolf AM Scott V Bjerke R et al.Hemodynamic effects of inhaled nitric oxide in four patients with severe liver disease and pulmonary hypertension..Liver Transpl Surg. 1997; 3: 594-597Crossref PubMed Scopus (24) Google Scholar), and a PAM >50 mmHg is universally fatal (5Krowka MJ Editorial: Pulmonary hypertension, (high) risk of orthotopic liver transplantation, and some lessons from “primary” pulmonary hypertension..Liver Transpl. 2002; 8: 389-390Crossref PubMed Scopus (18) Google Scholar,7Krowka MJ Plevak DJ Findlay JY Rosen CB Wiesner RH Krom RA Pulmonary hemodynamics and perioperative cardiopulmonary-related mortality in patients with portopulmonary hypertension undergoing liver transplantation..Liver Transpl. 2000; 6: 443-450Crossref PubMed Scopus (460) Google Scholar,9Ramsay MA Simpson BR Nguyen AT Ramsay KJ East C Klintmalm GB Severe pulmonary hypertension in liver transplant candidates..Liver Transpl Surg. 1997; 3: 494-500Crossref PubMed Scopus (244) Google Scholar). For this reason, liver transplant candidates are routinely screened for POPH, and many centers withhold transplantation if moderate to severe pulmonary hypertension is diagnosed. Long-term vasodilator therapy is becoming routine for patients with idiopathic pulmonary hypertension, and several reports have documented a similar salutary response in POPH (10McLaughlin VV Genthner DE Panella MM Hess DM Rich S Compassionate use of continuous prostacyclin in the management of secondary pulmonary hypertension: A case series..Ann Intern Med. 1999; 130: 740-743Crossref PubMed Scopus (202) Google Scholar, 11Krowka MJ Frantz RP McGoon MD Severson C Plevak DJ Wiesner RH Improvement in pulmonary hemodynamics during intravenous epoprostenol (prostacyclin): A study of 15 patients with moderate to severe portopulmonary hypertension..Hepatology. 1999; 30: 641-648Crossref PubMed Scopus (258) Google Scholar, 12Kuntzen C Gulberg V Gerbes AL Use of a mixed endothelin receptor antagonist in portopulmonary hypertension: A safe and effective therapy?.Gastroenterology. 2005; 128: 164-168Abstract Full Text Full Text PDF PubMed Scopus (65) Google Scholar). The literature also shows that POPH may resolve following liver transplantation, presumably by removing the root cause of the problem (13Levy MT Torzillo P Bookallil M Sheil AG McCaughan GW Case report: Delayed resolution of severe pulmonary hypertension after isolated liver transplantation in a patient with cirrhosis..J Gastroenterol Hepatol. 1996; 11: 734-737Crossref PubMed Scopus (29) Google Scholar, 14Schott R Chaouat A Launoy A Pottecher T Weitzenblum E Improvement of pulmonary hypertension after liver transplantation..Chest. 1999; 115: 1748-1749Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar, 15Losay J Piot D Bougaran J et al.Early liver transplantation is crucial in children with liver disease and pulmonary artery hypertension..J Hepatol. 1998; 28: 337-342Abstract Full Text PDF PubMed Scopus (42) Google Scholar). These facts present a potential therapeutic opportunity; POPH might initially be controlled by vasodilator therapy and subsequently cured by liver transplantation. This approach is still controversial, as pointed out in recent reviews (4Krowka MJ Portopulmonary hypertension and the issue of survival..Liver Transpl. 2005; 11: 1026-1027Crossref PubMed Scopus (30) Google Scholar,16Mandell MS Hepatopulmonary syndrome and portopulmonary hypertension in the model for end-stage liver disease (MELD) era..Liver Transpl. 2004; 10: S54-S58Crossref PubMed Scopus (42) Google Scholar) although several case reports have been published (17Chua R Keogh A Miyashita M Novel use of sildenafil in the treatment of portopulmonary hypertension..J Heart Lung Transplant. 2005; 24: 498-500Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar, 18Clift PF Townend JN Bramhall S Isaac JL Successful treatment of severe portopulmonary hypertension after liver transplantation by bosentan..Transplantation. 2004; 77: 1774-1775Crossref PubMed Scopus (23) Google Scholar, 19Laving A Khanna A Rubin L Ing F Dohil R Lavine JE Successful liver transplantation in a child with severe portopulmonary hypertension treated with epoprostenol..J Pediatr Gastroenterol Nutr. 2005; 41: 466-468Crossref PubMed Scopus (31) Google Scholar, 20Minder S Fischler M Muellhaupt B et al.Intravenous iloprost bridging to orthotopic liver transplantation in portopulmonary hypertension..Eur Respir J. 2004; 24: 703-707Crossref PubMed Scopus (57) Google Scholar, 21Plotkin JS Kuo PC Rubin LJ et al.Successful use of chronic epoprostenol as a bridge to liver transplantation in severe portopulmonary hypertension..Transplantation. 1998; 65: 457-459Crossref PubMed Scopus (116) Google Scholar, 22Tan HP Markowitz JS Montgomery RA et al.Liver transplantation in patients with severe portopulmonary hypertension treated with preoperative chronic intravenous epoprostenol..Liver Transpl. 2001; 7: 745-749Crossref PubMed Scopus (68) Google Scholar). We have undertaken this study to examine the feasibility of sequential vasodilator therapy and orthotopic liver transplantation as a therapeutic option in a group of patients with POPH. Evaluation for orthotopic liver transplantation (OLT) at our center includes a screening 2D echocardiogram. An estimated PA systolic >45 mmHg is routinely followed up with right heart catheterization. The population for this study consisted of eight consecutive patients with moderate to severe POPH who were otherwise deemed suitable liver transplant candidates. All but one of the patients had experienced clinical evidence of decompensation (see Table 1). Seven were found to have PAM >35 mmHg during evaluation, and one (#7) was identified at the time of pre-transplant anesthesia despite a previously acceptable estimated pulmonary artery pressure. The demographic features including peak model for end-stage liver disease (MELD) scores and actual MELD scores at the time of transplant are shown in Table 1.Table 1Demographic and perioperative information for the eight patients treated with epoprostenolPatient No.AgeGenderEtiology of cirrhosisTreatment time (months)Complications of cirrhosisHighest MELDMELD at OLT1All patients had 25 MELD points based on an epoprostenol therapy exception. The number in this column reflects the calculated MELD at the time of transplantation.OLT139FCryptogenic4Ascites, peripheral edema1414Yes243FCryptogenic5Ascites, peripheral edema106Yes351MAlcohol6.5Ascites, encephalopathy, variceal bleeds16N/ANo446MAlcohol15None11N/ANo548MAlcohol14Ascites, edema, encephalopathy17N/ANo649MHepatitis C2Ascites, SBP, encephalopathy, variceal bleeds1811Yes742FAlcohol2Ascites, anasarca, encephalopathy, jaundice2921Yes848MHepatitis C and alcohol4Ascites, variceal bleeds, hydrothorax, jaundice24N/ANo1 All patients had 25 MELD points based on an epoprostenol therapy exception. The number in this column reflects the calculated MELD at the time of transplantation. Open table in a new tab Criteria for vasodilator therapy were mean pulmonary artery pressure (PAM) ≥35 mmHg with pulmonary capillary wedge pressure (PCWP) ≤15 mmHg. This report covers the period between August 2003 and April 2005. All patients were treated with epoprostenol by continuous infusion at a rate of 2–8 ng/kg/min. Pulmonary artery pressure was assessed every 4–8 weeks by echocardiogram. Seven of the eight patients achieved an on-treatment PAM <35 mmHg, and six were actively listed for liver transplantation. Four of these were transplanted; two died prior to transplant. Epoprostenol was continued throughout surgery and into the post-transplant period. Epoprostenol was tapered in increments of 2 ng/kg/min as tolerated, taking into account signs and symptoms of heart failure and echocardiographic estimates of pulmonary pressure. After discontinuing epoprostenol, two patients had persistent moderate pulmonary hypertension requiring oral bosentan (23Molnar C Alber H Colleselli D Vogel W Kahler CM uccessful switch from inhalative iloprost to oral bosentan in portopulmonary hypertension associated with liver cirrhosis..Wien Klin Wochenschr. 2004; 116: 627-630Crossref PubMed Scopus (21) Google Scholar,24Suleman N Frost AE Transition from epoprostenol and treprostinil to the oral endothelin receptor antagonist bosentan in patients with pulmonary hypertension..Chest. 2004; 126: 808-815Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar). One patient was subsequently switched to oral sildenafil. Statistical analysis was performed with SAS 9.1 (SAS Institute Inc., Cary, NC, USA). All results are expressed as mean (SEM) and median. Due to the small sample size, the normality assumption is of concern, so the differences between PAM, pulmonary artery systolic pressure (PAS), cardiac output (CO), PVR and PCWP before and after the therapy were compared using the Wilcoxon signed ranks test, a nonparametric alternative to the paired t-test. A p-value of <0.05 was considered statistically significant. A significant result with the Wilcoxon signed ranks test demonstrated that the observed changes are not the result of random chance. As shown in Figure 1, six patients responded within 6.5 months (‘early responders’), and one responded after 14 months (‘late responder’). Once on epoprostenol, patients were screened every 4 weeks. Successful control of pulmonary artery resistance was demonstrated by echocardiography and confirmed by right heart catheterization. Right heart catheterization was repeated at the time of anesthesia for all patients who underwent transplantation. All early responders were activated for liver transplantation; two of these died before surgery could be performed. The other four were transplanted, and remain alive and well at 9–18 months. All transplanted patients were weaned off epoprostenol within 8 months of transplantation, but two developed recurrent pulmonary hypertension, easily controlled on oral medication. Current doses in these two patients are bosentan 62.5 mg b.i.d. and sildenafil 20 mg t.i.d., respectively. Pre-epoprostenol, pre-transplant and post-transplant pulmonary artery pressures are shown in Table 2.Table 2Pulmonary artery pressures before epoprostenol, at surgery and post-transplantPatient No. Current medication1 Bosentan2 Sildenafil3 None4 NonePAS (PAM)COPAS (PAM)COPAS (PAM)COPAS (PAM)COPre-epoprostenol52/33 (39)4.570/30 (43)7.352/38 (43)8.963/25 (38)7.6Pre-transplant45/22 (30)10.845/22 (30)13.638/25 (29)9.742/22 (29)13Post-transplant0–3 MonthsNANA785.2677416.54–6 Months60/22 (34)4.51066.5715.2ITR4.77–9 MonthsNA1Reading taken while on an oral agent.NA1Reading taken while on an oral agent.551Reading taken while on an oral agent.3.91Reading taken while on an oral agent.607.4ITR5.510–12 Months621Reading taken while on an oral agent.5.21Reading taken while on an oral agent.731Reading taken while on an oral agent.4.41Reading taken while on an oral agent.454.7NANAEach patient is shown in a vertical column.Shaded areas represent pressure readings while on epoprostenol.PAS = pulmonary artery systolic pressure estimated by 2D echocardiogram.When catheter results are available, pressures are expressed as systolic/diastolic (mean).CO = cardiac output; NA = not available.Patient 1: missed echocardiogram appointments.Patient 4: 12-month follow-up is scheduled.ITR = insufficient tricuspid regurgitation to assess PA pressure.1 Reading taken while on an oral agent. Open table in a new tab Each patient is shown in a vertical column. Shaded areas represent pressure readings while on epoprostenol. PAS = pulmonary artery systolic pressure estimated by 2D echocardiogram. When catheter results are available, pressures are expressed as systolic/diastolic (mean). CO = cardiac output; NA = not available. Patient 1: missed echocardiogram appointments. Patient 4: 12-month follow-up is scheduled. ITR = insufficient tricuspid regurgitation to assess PA pressure. Figure 2 shows the individual responses to vasodilator therapy. The changes for PAM, PAS, CO and PVR are all statistically significant. Individual changes were seen in PWCP, but results were not statistically significant. Treatment lasted 2–15 (mean 6.5) months, and seven of the eight patients achieved a satisfactory pressure, as noted above. Patient 4 failed to reach a satisfactory PAM despite a significant decline in PVR. Disease severity for liver transplant patients is routinely assessed by MELD score (25Wiesner R Edwards E Freeman R et al.Model for end-stage liver disease (MELD) and allocation of donor livers..Gastroenterology. 2003; 124: 91-96Abstract Full Text Full Text PDF PubMed Scopus (1979) Google Scholar). All patients received 25 MELD exception points by virtue of vasodilator therapy. The calculated MELD scores were widely variable in both survivors and nonsurvivors (see Table 1), and did not correlate with mortality in this series. Waiting times for transplantation after attaining a satisfactory PAM were 173, 35, 24 and 12 days. Adverse events on epoprostenol included facial flushing, nausea, anorexia and diarrhea. Diarrhea, when it occurred, was usually similar to that caused by lactulose, and necessitated the discontinuation of lactulose in most patients. Of the four patients who died, one failed to meet transplant criteria (#4; PAM = 53 mmHg after 15 months of therapy), and one became too ill for transplantation despite eventually achieving a satisfactory pressure. The other two died after activation on the transplant waiting list, one following an unexplained hypotensive episode 2 days after activation, and the other of sepsis related to empyema 17 days after activation. POPH, defined as PAM ≥25 mmHg with PCWP ≤15 mmHg, is a relatively common condition in patients undergoing transplant evaluation. Moderate to severe disease (PAM ≥35 mmHg) is uncommon, but carries a significant risk of death whether left untreated, or treated by liver transplant. Potent vasodilatory agents have been used in all forms of pulmonary hypertension, and have demonstrated efficacy in POPH (10McLaughlin VV Genthner DE Panella MM Hess DM Rich S Compassionate use of continuous prostacyclin in the management of secondary pulmonary hypertension: A case series..Ann Intern Med. 1999; 130: 740-743Crossref PubMed Scopus (202) Google Scholar,26Hoeper MM Halank M Marx C et al.Bosentan therapy for portopulmonary hypertension..Eur Respir J. 2005; 25: 502-508Crossref PubMed Scopus (185) Google Scholar,27Kahler CM Graziadei I Wiedermann CJ Kneussl MP Vogel W Successful use of continuous intravenous prostacyclin in a patient with severe portopulmonary hypertension..Wien Klin Wochenschr. 2000; 112: 637-640PubMed Google Scholar). As with other forms of secondary pulmonary hypertension, POPH is potentially reversible if the primary disease is cured, in this case by liver transplantation. While this approach has been discussed in the past, only individual cases have been reported to date (17Chua R Keogh A Miyashita M Novel use of sildenafil in the treatment of portopulmonary hypertension..J Heart Lung Transplant. 2005; 24: 498-500Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar, 18Clift PF Townend JN Bramhall S Isaac JL Successful treatment of severe portopulmonary hypertension after liver transplantation by bosentan..Transplantation. 2004; 77: 1774-1775Crossref PubMed Scopus (23) Google Scholar, 19Laving A Khanna A Rubin L Ing F Dohil R Lavine JE Successful liver transplantation in a child with severe portopulmonary hypertension treated with epoprostenol..J Pediatr Gastroenterol Nutr. 2005; 41: 466-468Crossref PubMed Scopus (31) Google Scholar, 20Minder S Fischler M Muellhaupt B et al.Intravenous iloprost bridging to orthotopic liver transplantation in portopulmonary hypertension..Eur Respir J. 2004; 24: 703-707Crossref PubMed Scopus (57) Google Scholar, 21Plotkin JS Kuo PC Rubin LJ et al.Successful use of chronic epoprostenol as a bridge to liver transplantation in severe portopulmonary hypertension..Transplantation. 1998; 65: 457-459Crossref PubMed Scopus (116) Google Scholar, 22Tan HP Markowitz JS Montgomery RA et al.Liver transplantation in patients with severe portopulmonary hypertension treated with preoperative chronic intravenous epoprostenol..Liver Transpl. 2001; 7: 745-749Crossref PubMed Scopus (68) Google Scholar). Here we report on eight consecutive patients treated with sequential vasodilator therapy followed by OLT. Our results challenge the prevailing opinion that moderate to severe POPH is an absolute contraindication to liver transplantation. Furthermore, transplantation appears to have reversed the course of POPH; two patients have been weaned off all vasodilators, and two are asymptomatic on oral agents. No obvious features including gender, etiology, severity of disease or signs of decompensation predicted response to therapy or the need for oral agents after transplantation. Pulmonary hypertension, albeit easier to control, persists in two patients after transplantation. We theorize that lesions may become ‘fixed’ after some time, and may be irreversible or slowly reversible with continued normal portal pressure and vasodilators. Long-term follow-up will be necessary to determine whether pulmonary arteriolar remodeling occurs in these patients. An alternative explanation, the coexistence of two diseases, cannot be excluded with our current state of knowledge. As reported by others, our patients exhibited a combination of elevated CO and portal hypertension (3Kawut SM Taichman DB Ahya VN et al.Hemodynamics and survival of patients with portopulmonary hypertension..Liver Transpl. 2005; 11: 1107-1111Crossref PubMed Scopus (136) Google Scholar,28Kuo PC Plotkin JS Johnson LB et al.Distinctive clinical features of portopulmonary hypertension..Chest. 1997; 112: 980-986Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar). Also as previously reported, the elevated pulmonary artery pressure is not simply a reflection of elevated CO. In fact, CO increased further in most patients as the pulmonary artery pressure declined. So far all transplanted patients have survived, and two of the four have been weaned from all vasodilator therapy. We are encouraged by the rapid response to epoprostenol; most patients achieved a satisfactory pressure within about 6 months (median time 4.5 months). However, a rapid response to epoprostenol does not assure a smooth course; patients 3 and 8 died despite rapid control of POPH. All patients who were not transplanted have died. In agreement with Kawut et al. (3Kawut SM Taichman DB Ahya VN et al.Hemodynamics and survival of patients with portopulmonary hypertension..Liver Transpl. 2005; 11: 1107-1111Crossref PubMed Scopus (136) Google Scholar), we believe this reflects the serious nature of combined liver and pulmonary disease rather than epoprostenol toxicity. In fact, epoprostenol allowed patients to survive very high CO states, as shown in Figure 2. Also illustrative is patient 5, a slow responder who was severely cachectic by the time he achieved target PAM. After removal from the transplant list, withdrawal of epoprostenol caused rapid cardiac death. We are not yet able to answer the question regarding long-term survival of pre-transplant patients on vasodilator therapy. Early death in two rapid responders suggests the need for timely transplantation once POPH is controlled. Future studies should evaluate survival in the absence of transplantation and the merit of providing MELD exception points to facilitate early transplantation in these patients. Epoprostenol places several burdens on the patient and the physician. The patient is committed to carrying an infusion pump along with ice packs, and keeping a refrigerated supply of epoprostenol available. Close follow-up is needed, and the patient must commit to regular echocardiography and at least one follow-up right heart catheterization. We recommend a dedicated central line to minimize the chance of sepsis. If an MRI is required, it must be performed before the start of therapy. Despite these limitations, most patients tolerated therapy quite well. The major adverse events were flushing, nausea, anorexia and diarrhea. Two patients had postoperative bleeding, possibly related to the anticoagulant effect of epoprostenol. In conclusion, severe POPH is a rare complication of liver disease, and has previously been an absolute contraindication to OLT. In this series, we have demonstrated the feasibility of pressure reduction with epoprostenol followed by liver transplantation. We cannot determine whether epoprostenol increases the risk of early death while also providing a window to cure the disease. We have also not yet analyzed the incremental cost of vasodilator therapy in this population. Our results suggest the need for a larger, multicenter study to expand our knowledge of the safety, efficacy, costs and optimal timing of liver transplantation in patients with moderate to severe POPH. The authors wish to thank Ms. Karla Sussman for her expert editorial assistance." @default.
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• W2037473973 title "Successful Liver Transplantation Following Medical Management of Portopulmonary Hypertension: A Single-Center Series" @default.
• W2037473973 cites W1968173552 @default.
• W2037473973 cites W1974468329 @default.
• W2037473973 cites W1999637800 @default.
• W2037473973 cites W2001942702 @default.
• W2037473973 cites W2028467903 @default.
• W2037473973 cites W2035407388 @default.
• W2037473973 cites W2041075197 @default.
• W2037473973 cites W2050548675 @default.
• W2037473973 cites W2053184228 @default.
• W2037473973 cites W2053640864 @default.
• W2037473973 cites W2069555927 @default.
• W2037473973 cites W2072313297 @default.
• W2037473973 cites W2073843207 @default.
• W2037473973 cites W2085829920 @default.
• W2037473973 cites W2091708768 @default.
• W2037473973 cites W2094867915 @default.
• W2037473973 cites W2099410981 @default.
• W2037473973 cites W2103967320 @default.
• W2037473973 cites W2117814576 @default.
• W2037473973 cites W2137700312 @default.
• W2037473973 cites W2140396673 @default.
• W2037473973 cites W2141898868 @default.
• W2037473973 cites W2143183313 @default.
• W2037473973 cites W2150922388 @default.
• W2037473973 cites W2153796667 @default.
• W2037473973 cites W2159502471 @default.
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