Symptoms to Diagnosis

Right ventricular failure in a young man

Keerthana Sankar, MD and Yuri Matusov, MD
Cleveland Clinic Journal of Medicine February 2026, 93 (2) 106-112; DOI: https://doi.org/10.3949/ccjm.93a.25048

A 31-year-old man presented to the hospital for dyspnea that had progressively worsened over the previous 2 years. Initially, his dyspnea was present only on exertion, but during the past 2 months it had progressed to shortness of breath at rest. He also noted an intermittent dry cough. He reported no fevers, chills, chest pain, dizziness, syncopal episodes, hemoptysis, wheezing, or unintentional weight loss.

The patient’s past medical history included a reported but undetermined fungal infection 12 years earlier that had been treated with itraconazole. He had no significant surgical or family history and did not take any medications on a regular basis. He did not smoke cigarettes, drink alcohol, or use illicit drugs.

Physical examination revealed 2+ pitting edema in the bilateral lower extremities and crackles throughout bilateral lung fields. The cardiac examination was notable for a prominent second pulmonary heart sound, right ventricular heave, grade 3 of 6 holosystolic murmur most evident at the left sternal border, jugular venous distention, and hepatojugular reflux.

Initial laboratory values included elevated levels of troponin and B-type natriuretic peptide. Serum creatinine, lactate, and complete blood cell count were within normal range (Table 1). The patient’s initial chest radiograph is shown in Figure 1.

View this table:
TABLE 1

The patient’s initial laboratory results

Figure 1
Figure 1

Chest radiograph obtained at admission was notable for consolidations in the left lower and middle lung field concerning for alveolar edema (white arrows); blunting of the left costophrenic angle, likely reflecting a small left pleural effusion (blue arrow); and scattered rounded lesions in the left lung field (red arrows). The cardiac silhouette appears enlarged, with a prominent, bulging right heart border (green arrow), suggesting possible right atrial enlargement and volume overload. The right lung field appears clear.

FURTHER STUDIES: ECHOCARDIOGRAM AND RIGHT HEART CATHETERIZATION

The initial transthoracic echocardiogram demonstrated a diffusely hypokinetic left ventricle with an ejection fraction of 45%, dilated inferior vena cava of 3.3 cm (reference range 1.5–2.5) with abnormal collapse of less than 50% consistent with volume overload, and flattening of the interventricular septum. Right-sided measurements of the heart revealed a severely dilated right ventricle of 7.4 cm (2–4.1), severely depressed right ventricular function, moderately dilated right atrium of 30.3 cm2 (10–18), moderate tricuspid valve regurgitation, and elevated pulmonary artery systolic pressure of 58 mm Hg (< 30) (Figure 2).

Figure 2
Figure 2

Transthoracic echocardiography apical 4-chamber view showed severe right ventricular dilation (white arrow), dilated right atrium (blue arrow), and flattening of the intraventricular septum (red arrow) consistent with right ventricular pressure and volume overload.

Given his severe right ventricular dysfunction, the patient underwent a right heart catheterization during which the following measurements were obtained:

  • Mean right atrial pressure: 28 mm Hg (0–8)

  • Right ventricular pressure: 118/10 mm Hg (systolic 15–25, diastolic 0–10)

  • Pulmonary artery pressure: 137/31 mm Hg; mean 77 mm Hg (systolic 15–25, diastolic 4–12, mean < 25)

  • Pulmonary capillary wedge pressure: 8 mm Hg (4–14)

  • Cardiac output: 5.76 L/min using the thermodilution method (4–8)

  • Cardiac index: 2.56 L/min/m2 (2.5–4)

  • Pulmonary vascular resistance: 12 Wood units (< 2).

The findings indicated the presence of severe precapillary pulmonary hypertension. The right ventricular stroke work index ([mean pulmonary artery pressure − mean right atrial pressure] × stroke volume index), a measure of how much energy the right ventricle expends to pump blood into the pulmonary circulation, was severely elevated at 17.39 g/m/beat/m2, indicating a high ventricular workload. The pulmonary artery pulsatility index ([pulmonary artery systolic pressure − pulmonary artery diastolic pressure]/right atrial pressure), a measure of how strongly the right ventricle is pumping, was elevated at 3.78. Both calculations, derived from right heart catheterization measurements, indicate that the right ventricle was functioning under extreme pressure and volume overload, with concern for imminent right ventricle failure.

FINDING THE CAUSE OF PULMONARY HYPERTENSION

1. Which of these diagnostic tests is indicated to identify the etiology of this patient’s pulmonary hypertension?

  • Computed tomography (CT) of the chest

  • Ventilation-perfusion scan

  • Autoimmune serologies

  • All of these

Right heart catheterization is the gold standard for diagnosing pulmonary hypertension, defined as a mean pulmonary arterial pressure of 20 mm Hg or higher.1–3 Pulmonary hypertension is classified into 5 subgroups (Table 2).3 Patients are grouped based on hemodynamic measurements on right heart catheterization.

View this table:
TABLE 2

Clinical classification of pulmonary hypertension

Precapillary pulmonary hypertension (groups 1, 3, 4, and 5) is defined by mean pulmonary arterial pressure greater than 20 mm Hg, pulmonary capillary wedge pressure 15 mm Hg or less, and pulmonary vascular resistance 2 Wood units or higher.

Postcapillary pulmonary hypertension (groups 2 and 5) is defined by mean pulmonary arterial pressure greater than 20 mm Hg, pulmonary capillary wedge pressure greater than 15 mm Hg, and pulmonary vascular resistance less than 3 Wood units.

Combined pre- and postcapillary pulmonary hypertension is defined by a mean pulmonary arterial pressure greater than 20 mm Hg, pulmonary capillary wedge pressure greater than 15 mm Hg, and pulmonary vascular resistance 2 Wood units or higher.1,3,4

Further diagnostic evaluation is critical for classifying patients into the correct group and has significant implications for guiding treatment.

Patients with isolated precapillary pulmonary hypertension or combined pre- and postcapillary pulmonary hypertension require further workup with chest CT, autoimmune serologies, and ventilation-perfusion scan. This workup is especially important in patients who have left heart disease insufficient to explain the degree of pulmonary hypertension.

CT of the chest permits thorough evaluation of the lung parenchyma and pulmonary vasculature, helping clinicians determine whether a patient’s pulmonary hypertension is due to parenchymal lung disease.5 Additionally, chest CT may help identify occult systemic diseases such as scleroderma if characteristic findings (eg, esophageal dilation) are seen.6,7

Autoimmune serologies, including but not limited to antinuclear antibodies, rheumatoid factor, double-stranded DNA antibodies, and scleroderma-70 antibodies, should be requested because there is an association between various connective tissue diseases and group 1 pulmonary hypertension, particularly in women.8,9 Among all connective tissue diseases, systemic sclerosis places patients at the highest risk of developing pulmonary arterial hypertension, with an 8% to 12% lifetime risk.8 However, serologies are nondiagnostic and can only support a diagnosis of connective tissue disease in the appropriate clinical context. Careful physical examination to identify rashes, skin thickening, joint pain, and other autoimmune stigmata are critical in making the diagnosis.

Ventilation-perfusion scan, necessary to evaluate for chronic thromboembolic hypertension and group 4 pulmonary hypertension, has a diagnostic sensitivity of 97.4%.10,11 Ventilation-perfusion scan measures both airflow and blood flow through the lungs using radioactive tracers. If mismatched perfusion defects are indicative of chronic thromboembolic hypertension, patients should be evaluated for pulmonary thromboendarterectomy as definitive treatment.12 False-positive results on ventilation-perfusion scan can be seen with conditions that can lead to extrinsic compression of the pulmonary artery and reduced distal flow such as mediastinal lymphadenopathy or fibrosis.13,14

CASE CONTINUED: FURTHER EVALUATION

The patient underwent CT of the chest, which showed extensive mediastinal soft tissue infiltration (Figure 3). He also had calcified lymph nodes, severe enlargement of the pulmonary artery, and narrowing of the bilateral pulmonary arteries. The lung parenchyma appeared normal. The findings were consistent with a diagnosis of fibrosing mediastinitis.

Figure 3
Figure 3

(A) Chest computed tomography with contrast demonstrated extensive mediastinal soft tissue infiltration (white arrow). (B) Calcified lymph nodes (red arrows), severe pulmonary artery enlargement with a diameter of 39.4 mm (blue double-head arrow), and narrowing of the bilateral pulmonary arteries (white arrow shows narrowing of the right pulmonary artery) were noted.

Ventilation-perfusion scan showed 90% perfusion going to the right lung and 10% going to left lung, with severe parenchymal pulmonary disease involving the entire left lung and right upper lung.

Serology tests for antinuclear antibodies, double-stranded DNA antibodies, rheumatoid factor, and scleroderma-70 antibodies were negative. Fungal serologies were notable for the following:

  • Histoplasma antigen: negative

  • Histoplasma mycelial antibody: 1:16 (> 1:8 = antibody detected)

  • Coccidioides immunoglobulin (Ig) G: negative

  • Coccidioides IgM: negative

  • Galactomannan: negative

  • Respiratory culture and acid-fast bacilli smear: negative for bacteria.

FINDING THE CAUSE OF FIBROSING MEDIASTINITIS

2. What is the most likely etiology of this patient’s fibrosing mediastinitis?

  • Histoplasmosis

  • Sarcoidosis

  • IgG4 disease

Fibrosing mediastinitis, also known as mediastinal fibrosis or sclerosing mediastinitis, is a rare cause of group 5 pulmonary hypertension characterized by abnormal proliferation of fibrous tissue within the mediastinum.15 With continued proliferation, fibrous tissue can encase, invade, and compress mediastinal structures, resulting in obstruction of airways, cardiac vessels, and the esophagus.

Fibrosing mediastinitis affects individuals ages 13 to 65 years and has a strong predilection for affecting young women.16 Radiographic abnormalities confirm its presence. A chest radiograph most commonly shows mediastinal widening and lymphadenopathy in the subcarinal, paratracheal, and hilar regions. Calcifications of the mediastinal lymph nodes may also be present and can suggest a fungal etiology. Contrast-enhanced CT of the chest can show mediastinal enhancement, calcified lymph nodes, and complications of fibrosing mediastinitis, including pulmonary vascular stenosis, bronchial stenosis, postobstructive pneumonias, and superior vena cava compression.17

Fibrosing mediastinitis has 2 major subtypes: granulomatous and nongranulomatous. The granulomatous form is more common and typically is associated with tuberculosis and fungal infections such as blastomycosis, aspergillosis, and histoplasmosis.16

Histoplasmosis

In the United States, fibrosing mediastinitis is most commonly associated with Histoplasma capsulatum infection; the reported prevalence of H capsulatum infection–related fibrosing mediastinitis is 3 in 100,000 individuals.15

Diagnostic association of fibrosing mediastinitis with fungal infection can be made via serologic assays and fungal staining from lymph node biopsies.18 However, fungal stains have a reported sensitivity of 32% and do not help differentiate between active and prior H capsulatum infection.19 Assays that detect antibodies against the H and M antigens specific to H capsulatum demonstrate a sensitivity of 64% to 95% in acute, subacute, chronic, and prior infection.20 A negative antigen test can support a previous infection as the cause of a positive antibody test, though the sensitivity of each assay and clinical context must be considered.

Sarcoidosis, characterized by formation of granulomas in various organs, is a rare cause of granulomatous fibrosing mediastinitis. Its diagnosis is confirmed with a tissue biopsy of the organ involved, which reveals noncaseating granulomas.21

IgG4 disease, a fibroinflammatory condition in which IgG4-positive plasma cells infiltrate various organs, is a rare cause of nongranulomatous fibrosing mediastinitis. Diagnostic evaluation of IgG4 disease begins with serum protein electrophoresis and investigation of IgG subclasses to assess for elevated IgG4 levels. A biopsy is required to confirm the diagnosis; it reveals dense polyclonal, lymphoplasmacytic infiltrate with IgG4-positive plasma cells.22,23 Rare cases of nongranulomatous fibrosing mediastinitis have been reported in patients with radiation exposure and those with a diagnosis of primary sclerosing cholangitis.24

If fibrosing mediastinitis is identified on imaging, fungal serologies may help establish evidence of prior infection. In our patient, a positive histoplasmosis antibody test combined with a negative histoplasmosis antigen test suggested the diagnosis of fibrosing mediastinitis secondary to prior histoplasmosis infection. If noninvasive diagnostics are inconclusive, a bronchoscopy with bronchoalveolar lavage, lymph node biopsy, or mediastinal biopsy may be required.

CASE CONTINUED: MANAGEMENT OF PULMONARY HYPERTENSION

After the patient was diagnosed with fibrosing mediastinitis secondary to prior histoplasmosis, he was transferred to the intensive care unit for further management of his severe pulmonary hypertension and right ventricular failure. He received inotropic support with dobutamine and diuresis with furosemide and metolazone.

A cautious trial of pulmonary hypertension therapy with inhaled treprostinil was initiated to reduce right ventricular afterload, which was due in part to the marked elevation in pulmonary vascular resistance. A Swan-Ganz catheter was placed to monitor changes in cardiac output, cardiac index, pulmonary artery pressures, and central venous pressures. Despite multiple days of inotropic support, pulmonary hypertension–directed therapy, and diuresis, the patient developed worsening cardiogenic shock due to refractory ventricular failure with the following right heart catheterization measurements:

  • Mean right atrial pressure: 21 mm Hg

  • Right ventricular pressure: 109/6 mm Hg

  • Pulmonary artery pressure: 116/29 mm Hg; mean 48 mm Hg

  • Pulmonary capillary wedge pressure: not measured

  • Cardiac output: 4.32 L/min using the thermodilution method

  • Cardiac index: 1.92 L/min/m2.

TREATMENT DECISIONS

3. What is the best treatment modality for this patient?

  • Antifungal therapy

  • Mediastinal tissue resection

  • Endovascular stenting of the pulmonary arteries

  • Combined heart and bilateral lung transplantation

Antifungal and anti-inflammatory therapies are ineffective for the treatment of fibrosing mediastinitis. The most recent guidelines from the Infectious Diseases Society of America25 recommend against routine antifungal treatment as fibrosing mediastinitis is a late complication of fungal infections; further, antifungal therapy has minimal utility in the setting of irreversible, fibrotic changes.18 As for medical management of fibrosing mediastinitis–associated pulmonary hypertension, no robust data exist on the use of pulmonary hypertension–specific therapy.

Mediastinal tissue resection. Minimally invasive techniques and surgical options should be considered to alleviate the mechanical burden of disease. The type of intervention depends on which structures are affected. Mediastinal debulking surgeries are unfavorable due to the high risk of bleeding and intraoperative complications. Surgical case series have reported an operative mortality as high as 20%.15,26,27

Endovascular stenting of the pulmonary arteries has been evaluated in small case series and is associated with a lower acute mortality and improved symptom relief. However, patients often require additional procedures for stent restenosis, stent migration, hemoptysis, and other graft-related complications.15,28

Combined heart and lung transplantation provides definitive management of fibrosing mediastinitis complicated by severe pulmonary hypertension and right ventricular failure. Typically, bilateral lung transplantation alone is curative for severe pulmonary hypertension.29 However, with dense adhesions and extensive fibrous tissue within the mediastinum, a combined en bloc heart-lung transplant in which the heart and lungs are removed as one may be technically more feasible, with a lower intraoperative bleeding risk.30 There are no standardized criteria for heart-lung transplant, although common indications include right ventricular failure with extensive right ventricular fibrosis, pulmonary arterial hypertension with severe cardiomyopathy, and interstitial lung disease with associated right ventricular dysfunction.31 All surgical approaches must be considered in relation to the experience and expertise of a particular center. A multidisciplinary evaluation may help weigh the risks and benefits of each approach.

CASE CONCLUSION

Our patient’s case was reviewed in a multidisciplinary conference that included clinicians in cardiology, transplant pulmonology, lung transplant surgery, cardiac surgery, and thoracic surgery. The group considered multiple surgical approaches and the risks and benefits of each. Given our patient’s severe right ventricular failure and extensive mediastinal fibrosis, the panel made the decision to proceed with combined heart-lung transplantation, determined to be the lowest-risk surgical procedure for definitive management of right ventricular failure secondary to fibrosing mediastinitis.

The patient tolerated the surgery with minimal postoperative complications and was discharged from the hospital with outpatient transplant follow-up. He has retained excellent cardiac and pulmonary function during routine clinical follow-up.

TAKE-HOME POINTS

  • A thorough diagnostic evaluation is required for patients newly diagnosed with pulmonary hypertension; the workup should include chest CT, ventilation-perfusion scan, autoimmune serologies, human immunodeficiency virus testing, and schistosomiasis antibody testing in endemic areas.32

  • Fungal infections are the most common cause of fibrosing mediastinitis, with histoplasmosis the most common cause in the United States.16

  • Antifungal and anti-inflammatory treatments are ineffective in treating fibrosing mediastinitis due to the irreversibility of fibrotic changes.18,25

  • We recommend a multidisciplinary evaluation to determine the best surgical or catheter-directed approach for the management of fibrosing mediastinitis, with possible need for lung or heart-lung transplantation.26,28,29

DISCLOSURES

Dr. Matusov has disclosed being a research principal investigator for Aerovate, BioAegis Therapeutics, Mallinckrodt Inc., Penumbra Inc., and Tenax Therapeutics and being an advisor or review panel participant for Jupiter Endovascular. Dr. Sankar reports no relevant financial relationships which, in the context of their contributions, could be perceived as a potential conflict of interest.

REFERENCES

  1. ↵
    1. Maron BA
    . Revised definition of pulmonary hypertension and approach to management: a clinical primer. J Am Heart Assoc 2023; 12(8):e029024. doi:10.1161/JAHA.122.029024
    OpenUrlCrossRefPubMed
    1. Gonzalez-Hermosillo LM,
    2. Cueto-Robledo G,
    3. Roldan-Valadez E, et al
    . Right heart catheterization (RHC): a comprehensive review of provocation tests and hepatic hemodynamics in patients with pulmonary hypertension (PH). Curr Probl Cardiol 2022;47(12):101351. doi:10.1016/j.cpcardiol.2022.101351
    OpenUrlCrossRefPubMed
  3. ↵
    1. Kovacs G,
    2. Bartolome S,
    3. Denton CP, et al
    . Definition, classification and diagnosis of pulmonary hypertension. Eur Respir J 2024;64(4):2401324. doi:10.1183/13993003.01324-2024
    OpenUrlAbstract/FREE Full Text
  4. ↵
    1. Simonneau G,
    2. Gatzoulis MA,
    3. Adatia I, et al
    . Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol 2013; 62(25 suppl):D34–D41. doi:10.1016/j.jacc.2013.10.029
    OpenUrlFREE Full Text
  5. ↵
    1. Kreitner KF
    . Noninvasive imaging of pulmonary hypertension. Semin Respir Crit Care Med 2014; 35(1):99–111. doi:10.1055/s-0033-1363456
    OpenUrlCrossRef
  6. ↵
    1. Ascha M,
    2. Renapurkar RD,
    3. Tonelli AR
    . A review of imaging modalities in pulmonary hypertension. Ann Thorac Med 2017; 12(2):61–73. doi:10.4103/1817-1737.203742
    OpenUrlCrossRefPubMed
  7. ↵
    1. Rutka K,
    2. Garkowski A,
    3. Karaszewska K,
    4. Łebkowska U
    . Imaging in diagnosis of systemic sclerosis. J Clin Med 2021; 10(2):248. doi:10.3390/jcm10020248
    OpenUrlCrossRef
  8. ↵
    1. Vonk MC,
    2. Vandecasteele E,
    3. van Dijk AP
    . Pulmonary hypertension in connective tissue diseases, new evidence and challenges. Eur J Clin Invest 2021; 51(4):e13453. doi:10.1111/eci.13453
    OpenUrlCrossRef
  9. ↵
    1. Krzyzewska A,
    2. Kurakula K
    . Sex dimorphism in pulmonary arterial hypertension associated with autoimmune diseases. Arterioscler Thromb Vasc Biol 2024; 44(10):2169–2190. doi:10.1161/ATVBAHA.124.320886
    OpenUrlCrossRef
  10. ↵
    1. Ha S,
    2. Han S
    . The role of lung ventilation/perfusion scan in the management of chronic thromboembolic pulmonary hypertension. Nucl Med Mol Imaging 2024; 58(7):449–458. doi:10.1007/s13139-023-00830-5
    OpenUrlCrossRef
  11. ↵
    1. Tunariu N,
    2. Gibbs SJ,
    3. Win Z, et al
    . Ventilation-perfusion scintigraphy is more sensitive than multidetector CTPA in detecting chronic thromboembolic pulmonary disease as a treatable cause of pulmonary hypertension. J Nucl Med 2007; 48(5):680–684. doi:10.2967/jnumed.106.039438
    OpenUrlAbstract/FREE Full Text
  12. ↵
    1. Kim NH,
    2. Delcroix M,
    3. Jais X, et al
    . Chronic thromboembolic pulmonary hypertension. Eur Respir J 2019;53(1):1801915. doi:10.1183/13993003.01915-2018
    OpenUrlAbstract/FREE Full Text
  13. ↵
    1. Eichhorn J,
    2. Eluvathingal T
    . Non-embolic causes of perfusion defects on VQ scan (abstract 1219). J Nucl Med 2018; 59(suppl 1):1219.
    OpenUrlPubMed
  14. ↵
    1. Matusov Y,
    2. Singh I,
    3. Yu YR, et al
    . Chronic thromboembolic pulmonary hypertension: the bedside. Curr Cardiol Rep 2021;23(10):147. doi:10.1007/s11886-021-01573-5
    OpenUrlCrossRef
  15. ↵
    1. Wang A,
    2. Su H,
    3. Duan Y, et al
    . Pulmonary hypertension caused by fibrosing mediastinitis. JACC Asia 2022;2(3):218–234. doi:10.1016/j.jacasi.2021.11.016
    OpenUrlCrossRefPubMed
  16. ↵
    1. Jain N,
    2. Chauhan U,
    3. Puri SK,
    4. Agrawal S,
    5. Garg L
    . Fibrosing mediastinitis: when to suspect and how to evaluate? BJR Case Rep 2016; 2(1):20150274. doi:10.1259/bjrcr.20150274
    OpenUrlCrossRef
  17. ↵
    1. McNeeley MF,
    2. Chung JH,
    3. Bhalla S,
    4. Godwin JD
    . Imaging of granulomatous fibrosing mediastinitis. AJR Am J Roentgenol 2012; 199(2):319–327. doi:10.2214/AJR.11.7319
    OpenUrlCrossRefPubMed
  18. ↵
    1. Kuranga AO,
    2. Eubank AM,
    3. Bowling MR
    . Fibrosing mediastinitis: a review of epidemiology, diagnosis and management. Int J Respir Pulm Med 2018; 5:079. doi:10.23937/2378-3516/1410079
    OpenUrlCrossRef
  19. ↵
    1. Leitão TMJS,
    2. Oliveira Filho AMP,
    3. Sousa Filho JEP, et al
    . Accuracy of buffy coat in the diagnosis of disseminated histoplasmosis in AIDS-patients in an endemic area of Brazil. J Fungi (Basel) 2019; 5(2):47. doi:10.3390/jof5020047
    OpenUrlCrossRef
  20. ↵
    1. Barros N,
    2. Wheat JL,
    3. Hage C
    . Pulmonary histoplasmosis: a clinical update. J Fungi (Basel) 2023; 9(2):236. doi:10.3390/jof9020236
    OpenUrlCrossRef
  21. ↵
    1. Teirstein AS,
    2. Judson MA,
    3. Baughman RP, et al
    . The spectrum of biopsy sites for the diagnosis of sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis 2005; 22(2):139–146. pmid:16053030
    OpenUrlPubMed
  22. ↵
    1. Chen LYC,
    2. Mattman A,
    3. Seidman MA,
    4. Carruthers MN
    . IgG4-related disease: what a hematologist needs to know. Haematologica 2019; 104(3):444–455. doi:10.3324/haematol.2018.205526
    OpenUrlAbstract/FREE Full Text
  23. ↵
    1. Chandrashekaran S,
    2. Karnatovskaia L,
    3. Johnson M
    . Fibrosing mediastinitis from IgG4-related sclerosing disease (abstract 491A). Chest 2013; 144(4):491A. doi:10.1378/chest.1700905
    OpenUrlCrossRef
  24. ↵
    1. Parish JM,
    2. Rosenow EC 3rd.
    . Mediastinal granuloma and mediastinal fibrosis. Semin Respir Crit Care Med 2002; 23(2):135–143. doi:10.1055/s-2002-25302
    OpenUrlCrossRefPubMed
  25. ↵
    1. Wheat LJ,
    2. Freifeld AG,
    3. Kleiman MB, et al; Infectious Diseases Society of America
    . Clinical practice guidelines for the management of patients with histoplasmosis: 2007 update by the Infectious Diseases Society of America. Clin Infect Dis 2007; 45(7):807–825. doi:10.1086/521259
    OpenUrlCrossRefPubMed
  26. ↵
    1. Fender EA,
    2. Widmer RJ,
    3. Knavel Koepsel EM, et al
    . Catheter based treatments for fibrosing mediastinitis. Catheter Cardiovasc Interv 2019; 94(6):878–885. doi:10.1002/ccd.28152
    OpenUrlCrossRef
  27. ↵
    1. Loyd JE,
    2. Tillman BF,
    3. Atkinson JB,
    4. Des Prez RM
    . Mediastinal fibrosis complicating histoplasmosis. Medicine (Baltimore) 1988; 67(5): 295–310. doi:10.1097/00005792-198809000-00002
    OpenUrlCrossRefPubMed
  28. ↵
    1. Peikert T,
    2. Colby TV,
    3. Midthun DE, et al
    . Fibrosing mediastinitis: clinical presentation, therapeutic outcomes, and adaptive immune response. Medicine (Baltimore) 2011; 90(6):412–423. doi:10.1097/MD.0b013e318237c8e6
    OpenUrlCrossRefPubMed
  29. ↵
    1. Hu X,
    2. Ding N,
    3. Songchen W, et al
    . Lung transplantation for pulmonary arterial hypertension: optimized referral and listing based on an evolving disease concept. J Cardiovasc Dev Dis 2023;10(8):350. doi:10.3390/jcdd10080350
    OpenUrlCrossRef
  30. ↵
    1. Bonser RS,
    2. Jamieson SW
    . Heart-lung transplantation. Clin Chest Med 1990; 11(2):235–246. pmid:2189659
    OpenUrlPubMed
  31. ↵
    1. Gidea CG,
    2. Smith D,
    3. Reyentovich A, et al
    . Contemporary indications for heart-lung transplantation (abstract S267). J Heart Lung Transplant 2021; 40(4 suppl):S267. doi:10.1016/j.healun.2021.01.760
    OpenUrlCrossRef
  32. ↵
    1. Fukuda K,
    2. Date H,
    3. Doi S, et al
    . Guidelines for the treatment of pulmonary hypertension (JCS 2017/JPCPHS 2017). Circ J 2019; 83(4):842–945. doi:10.1253/circj.CJ-66-0158
    OpenUrlCrossRef
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