Treatment of Pulmonary Artery Compression Due to Fibrous Mediastinitis With Endovascular Stent Placement

Guerrero, Alejandro; Hoffer, Eric K.; Hudson, Leonard D.; Schüler, Paul; Karmy-Jones, Riyad

doi:10.1378/chest.119.3.966

Cited by 34 publications

(23 citation statements)

References 11 publications

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“…The age of diagnosis of PH complicating fibrosing mediastinitis was 60 years in our cohort, older than the previously reported age in the largest American posthistoplasmosis cohort (median of 42 years). 9,24,34,35 This difference may be explained at least in part by the differences in the causes of fibrosing mediastinitis.…”

Section: Discussionmentioning

confidence: 99%

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Pulmonary hypertension complicating fibrosing mediastinitis

Seferian

Steriade

Jaïs

et al. 2016

4.3 Pulmonary Circulation and Pulmonary Vascular Diseases

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Fibrosing mediastinitis is caused by a proliferation of fibrous tissue in the mediastinum with encasement of mediastinal viscera and compression of mediastinal bronchovascular structures. Pulmonary hypertension (PH) is a severe complication of fibrosing mediastinitis caused by extrinsic compression of the pulmonary arteries and/or veins.We have conducted a retrospective observational study reviewing clinical, functional, hemodynamic, radiological characteristics, and outcome of 27 consecutive cases of PH associated with fibrosing mediastinitis diagnosed between 2003 and 2014 at the French Referral Centre for PH.Fourteen men and 13 women with a median age of 60 years (range 18-84) had PH confirmed on right heart catheterization. The causes of fibrosing mediastinitis were sarcoidosis (n ¼ 13), tuberculosis-infection confirmed or suspected (n ¼ 9), mediastinal irradiation (n ¼ 2), and idiopathic (n ¼ 3). Sixteen patients (59%) were in NYHA functional class III and IV. Right heart catheterization confirmed moderate to severe PH with a median mean pulmonary artery pressure of 42 mm Hg (range 27-90) and a median cardiac index of 2.8 L/min/m 2 (range 1.6-4.3). Precapillary PH was found in 22 patients, postcapillary PH in 2, and combined postcapillary and precapillary PH in 3. Severe extrinsic compression of pulmonary arteries (>60% reduction in diameter) was evidenced in 2, 8, and 12 patients at the main, lobar, or segmental levels, respectively. Fourteen patients had at least one severe pulmonary venous compression with associated pleural effusion in 6 of them. PAH therapy was initiated in 7 patients and corticosteroid therapy (0.5-1 mg/kg/day) was initiated in 3 patients with sarcoidosis, with 9 other being already on low-dose corticosteroids. At 1-year follow-up, 3 patients had died and among the 21 patients evaluated, 3 deteriorated, 14 were stable, and only 4 patients with sarcoidosis improved (4 receiving corticosteroids and 1 receiving corticosteroids and PAH therapy). Survival was 88%, 73%, and 56% at 1, 3, and 5 years, respectively.We found no clear clinical improvement with the use of specific PAH therapy. Corticosteroid therapy may be associated with clinical improvement, in some patients with fibrosing mediastinitis due to sarcoidosis. Although never performed for this indication, lung transplantation may be proposed in eligible patients with severe PH and fibrosing mediastinitis. (Medicine 94(44):e1800)Abbreviations: 6MWD = 6-minute walking distance, CO = cardiac output, CTEPH = chronic thromboembolic pulmonary hypertension, DLCO = diffusion capacity for carbon monoxide, ERA = endothelin receptor antagonist, FEV-1 = forced expiratory volume in 1 second, FVC = forced vital capacity, HRCT = highresolution computer tomography, mPAP = mean pulmonary arterial pressure, NYHA = New York Heart Association, PaCO 2 = partial pressure of arterial carbon dioxide, PAH = pulmonary arterial hypertension, PaO 2 = partial pressure of arterial oxygen, PAwP = pulmonary artery wedge pressure, PDE5-I = phosphodiester...

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Section: Discussionmentioning

confidence: 99%

“…9,24,34, 35 Peikert et al reported that balloon pulmonary artery angioplasty/stent, balloon pulmonary vein angioplasty, or bypass surgery for the superior vena cava syndrome were sometimes feasible in fibrosing mediastinitis. 9 However, hemodynamic effects and long-term efficacy of these procedures are currently unknown.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary hypertension complicating fibrosing mediastinitis

Seferian

Steriade

Jaïs

et al. 2016

4.3 Pulmonary Circulation and Pulmonary Vascular Diseases

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“…Treatment varies from medical therapy (the systemic administration of antifungal agents or corticosteroids) to surgical or endovascular treatment. 6,7 Although stenting provides an important alternative to surgery, there are potential sequelae. These include stent migration, dissection, thrombosis, intimal hyperplasia, pseudoaneurysm formation, vascular rupture, and death.…”

Section: Discussionmentioning

confidence: 99%

Endovascular Treatment of Bilateral Pulmonary Artery Stenoses and Superior Vena Cava Syndrome in a Patient with Advanced Mediastinal Fibrosis

Valentin¹,

Kuban²,

Ramanathan³

et al. 2016

Texas Heart Institute Journal

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1 In severe cases, it can progress to obstruction of the superior vena cava (SVC), pulmonary vessels, esophagus, or airways. Whereas SVC obstruction is relatively common, pulmonary artery (PA) involvement is less frequently encountered.2 Very few reports of long-term outcomes exist in the medical literature of either SVC or PA stents in this patient population. We discuss a case in which MF resulted in PA and SVC stenoses that were treated endovascularly, with early symptom improvement and 5-year survival with primary patency. Case ReportA 54-year-old man with histoplasmosis presented at our institution with worsening right-sided chest tightness and difficulty sleeping on his right side because of shortness of breath. Three years before this episode, he had developed SVC syndrome from progressive MF that we had successfully treated endovascularly with an SVC stent. Therefore, differential diagnosis for the current episode of dyspnea included restenosis of the SVC stent, pulmonary embolism, pneumonia, and pulmonary hypertension. A computed tomographic angiogram (CTA) revealed high-grade right-PA stenosis caused by continued progression of MF. In addition, imaging revealed near-complete occlusion of the truncus anterior to the right PA. Results of CTA also revealed that the SVC stent remained widely patent.Subsequently, we performed pulmonary arteriography to evaluate right-PA stenosis and PA hypertension, and to judge the possibility of intervention. Using a femoral approach, we advanced a Mott pulmonary catheter over the wire and into the right ventricle. The catheter was next advanced into the main PA, where the pressure was 35/12 mmHg, and then into the left PA-where digital subtraction arteriography revealed no abnormalities. The left main PA pressure was 36/10 mmHg. The catheter was then modified to make it more amenable to entering the stenosed right main PA. We used a 260-cm, modified stiff Glidewire ® (Terumo Medical Corporation; Somerset, NJ), advancing the wire and catheter into the right main PA. Digital subtraction arteriography revealed approximately 75% stenosis at the origin of the right main PA, extending distally 3.6 cm (Fig. 1). A pressure recording obtained distal to the obstruction was 11/5 mmHg (pressure gradient, 22 mmHg). Given the patient's symptoms, imaging findings, and pressure gradient, intervention was judged necessary.

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“…Matisen ve arkadaşları 20 vakalık serilerinde 18 hastaya rezeksiyon uygulamışlar, 4 (%20) hasta postoperatif dönemde kaybedilmiştir (14). Vena kava superior ve pulmoner artere stent konularak obstruksiyon açılmış vakalar mevcuttur (22)(23)(24).…”

Section: Tedavi̇unclassified

Mediastenin Akut Ve Kronik Enfeksiyonlari

Kılıç¹

2011

Toraks Cer Bult

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Mediastinit oldukça ölümcül seyredebilen, göğüs ve kalp cerrahisi doktorlarının dikkatle üzerine eğildiği bir hastalıktır. Mediasten dokusunun iltihabıdır. Akut ve kronik şekilde enfeksiyon ve enfeksiyon dışı etyolojiler ile karşımıza çıkabilir. Akut mediastinitlerin çoğu öze-fagus perforasyonuna veya göğüs travmasına sekonder olarak gelişebilir. Kronik form veya yavaş gelişen form ise tuberküloz, histoplasmozıs gibi bakteriel veya fungal enfeksiyonlara veya sarkoidoza ikincil gelişen durumdur.Bu bölümde mediastinitlerin tanı ve tedavi metodları literatür eşliğinde gözden geçirilmiştir. Akut MediastinitAkut mediastinit tüm tıbbi gelişmelere rağmen günümüzde halen ciddi bir klinik antite olarak kalmıştır. Mediastenin gözeli bir doku olması, kalbin ve akciğerin hareketi ile mikroorganizmaların daha hızlı yayılabilme olasılığı, ayrıca en sık etken özefagus rüptürü olduğu için özefageal içeriğin (ph=1.5) reflü ile ve tükürük içe-riğinin mediastene yayılabilmesi (kimyasal mediastinit) özefageal mukozanın mikroorganizma içeriği nedeni ile enfeksiyonun çok çabuk yayılma ve şiddetlenme eğili-mi mevcuttur. Mutlak hızlı tedavi protokolü geçerlidir.

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Treatment of Pulmonary Artery Compression Due to Fibrous Mediastinitis With Endovascular Stent Placement

Cited by 34 publications

References 11 publications

Pulmonary hypertension complicating fibrosing mediastinitis

Pulmonary hypertension complicating fibrosing mediastinitis

Endovascular Treatment of Bilateral Pulmonary Artery Stenoses and Superior Vena Cava Syndrome in a Patient with Advanced Mediastinal Fibrosis

Mediastenin Akut Ve Kronik Enfeksiyonlari

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