Corrigendum to: 'Guidelines for the diagnosis and treatment of pulmonary hypertension' [European Heart Journal (2009) 30, 2493-2537]. The Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT)

Galie, N; Hoeper, MM; Humbert, Marc; Torbicki, Adam; Vachiéry, JL; Barberà, Joan Albert; Beghetti, Maurice; Corris, Paul; Gaine, Seán; Gibbs, J. S. R.; Gómez-Sánchez, Miguel Ángel; Jondeau, Guillaume; Klepetko, Walter; Opitz, Ch.; Peacock, A.; Rubin, Leona J.; Zellweger, M.; Simonneau, G.

doi:10.1093/eurheartj/ehr046

Cited by 625 publications

(1,246 citation statements)

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“…1,2,25,26 Thus, the benefits of these treatments have not been demonstrated in PVOD; the only recommended treatment is lung transplantation for eligible PVOD patients. 1,2,27 MMC-induced PVOD in rats represents a specific model for pulmonary venous involvement associated with reduced GCN2 expression; this suggests that it could represent a general model for idiopathic, heritable, or drug-induced PVOD. Indeed, this model constituted a unique opportunity to learn more about the pathophysiology of PVOD and to test an innovative therapy.…”

Section: Discussionmentioning

confidence: 99%

Mitomycin-Induced Pulmonary Veno-Occlusive Disease

et al. 2015

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P ulmonary veno-occlusive disease (PVOD) is a rare and devastating cause of pulmonary hypertension (PH). PVOD is characterized by widespread fibrous intimal proliferation of septal veins and preseptal venules, and is frequently associated with pulmonary capillary dilatation and proliferation. 1Although the pathology firmly confirms PVOD, a noninvasive diagnostic approach is usually favored in these fragile patients in whom a lung biopsy carries a high risk of lifethreatening complications. Decreased diffusing capacity of the lung for carbon monoxide, severe hypoxemia, radiological abnormalities on high-resolution computed tomography (CT) scans of the chest, and the occurrence of pulmonary edema after starting pulmonary vasodilator therapy strongly argue for PVOD.1,2 PVOD is a difficult form of PH to diagnose; it is frequently misclassified as idiopathic pulmonary arterial hypertension (PAH). Thus, the true incidence of PVOD is not known precisely, but is considered to represent 10% of cases of PAH Background-Pulmonary veno-occlusive disease (PVOD) is an uncommon form of pulmonary hypertension characterized by the obstruction of small pulmonary veins and a dismal prognosis. PVOD may be sporadic or heritable because of biallelic mutations of the EIF2AK4 gene coding for GCN2. Isolated case reports suggest that chemotherapy may be a risk factor for PVOD. Methods and Results-We reported on the clinical, functional, and hemodynamic characteristics and outcomes of 7 cases of PVOD induced by mitomycin-C (MMC) therapy from the French Pulmonary Hypertension Registry. All patients displayed squamous anal cancer and were treated with MMC alone or MMC plus 5-fluoruracil. The estimated annual incidence of PVOD in the French population that have anal cancer is 3.9 of 1000 patients, which is much higher than the incidence of PVOD in the general population (0.5/million per year). In rats, intraperitoneal administration of MMC induced PVOD, as demonstrated by pulmonary hypertension at right-heart catheterization at days 21 to 35 and major remodeling of small pulmonary veins associated with foci of intense microvascular endothelial-cell proliferation of the capillary bed. In rats, MMC administration was associated with dose-dependent depletion of pulmonary GCN2 content and decreased smad1/5/8 signaling. Amifostine prevented the development of MMC-induced PVOD in rats. Key Words: alkylating agents ◼ antineoplastic agents ◼ complications ◼ drug-related side effects and adverse reactions ◼ GCN2 ◼ hypertension, pulmonary ◼ pulmonary veno-occlusive disease Conclusions-MMC

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Section: Discussionmentioning

confidence: 99%

Mitomycin-Induced Pulmonary Veno-Occlusive Disease

et al. 2015

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“…Non‐inclusion criteria were a chronic complaint of activity‐related dyspnoea (modified Medical Research Council (mMRC) score ≥1 during the last 6 months), any respiratory disease such as asthma, COPD, interstitial pneumonia, chronic post‐embolic pulmonary hypertension, pre‐capillary pulmonary hypertension on right heart catheterization and at least one perfusion segmental defect on V/Q scan, any cardiac disease with a significant impact on systolic function such as an ejection fraction of <50%, uncontrolled systemic hypertension, chronic arrhythmia, circulatory collapse or an indication fibrinolysis. A missing value of the mMRC score was an exclusion criterion.…”

Section: Methodsmentioning

confidence: 99%

Pathophysiology of dyspnoea in acute pulmonary embolism: A cross‐sectional evaluation

et al. 2016

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“…Background: PH is defined as an increase in the resting mean pulmonary arterial pressure to at least 25 mm Hg on right heart catheterization . Many patients with PH experience breathlessness on exertion; however, a range of other important symptoms may be present, including fatigue, dizziness, chest discomfort, chest pain, palpitations, cough, pre‐syncope, syncope, lower limb oedema and abdominal distension.…”

Section: Pico Questionsmentioning

confidence: 99%