Editorial
Pulmonary Hypertension in Interstitial Lung Disease
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"tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "687" "paginaFinal" => "688" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Jesus Isea de la Viña, Gema Ramírez-Rodríguez, Bernardino Alcázar-Navarrete" "autores" => array:3 [ 0 => array:2 [ "nombre" => "Jesus" "apellidos" => "Isea de la Viña" ] 1 => array:2 [ "nombre" => "Gema" "apellidos" => "Ramírez-Rodríguez" ] 2 => array:2 [ "nombre" => "Bernardino" "apellidos" => "Alcázar-Navarrete" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0300289622004525?idApp=UINPBA00003Z" "url" => "/03002896/0000005800000010/v2_202302271800/S0300289622004525/v2_202302271800/en/main.assets" ] "itemAnterior" => array:18 [ "pii" => "S0300289622000102" "issn" => "03002896" "doi" => "10.1016/j.arbres.2021.12.013" "estado" => "S300" "fechaPublicacion" => "2022-10-01" "aid" => "2983" "copyright" => "SEPAR" "documento" => "simple-article" "crossmark" => 1 "subdocumento" => "edi" "cita" => "Arch Bronconeumol. 2022;58:681-4" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "en" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial</span>" "titulo" => "Current Knowledge and Perspectives for Pharmacological Treatment in OSA" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "681" "paginaFinal" => "684" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1354 "Ancho" => 2500 "Tamanyo" => 261884 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">From conventional continuous positive airway pressure therapy to emerging targeted pharmacological approaches for OSA. Abbreviations: PAP: positive airway pressure; OSA: obstructive sleep apnoea.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Sébastien Baillieul, Renaud Tamisier, Danny J. Eckert, Jean-Louis Pépin" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Sébastien" "apellidos" => "Baillieul" ] 1 => array:2 [ "nombre" => "Renaud" "apellidos" => "Tamisier" ] 2 => array:2 [ "nombre" => "Danny J." "apellidos" => "Eckert" ] 3 => array:2 [ "nombre" => "Jean-Louis" "apellidos" => "Pépin" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0300289622000102?idApp=UINPBA00003Z" "url" => "/03002896/0000005800000010/v2_202302271800/S0300289622000102/v2_202302271800/en/main.assets" ] "en" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial</span>" "titulo" => "Pulmonary Hypertension in Interstitial Lung Disease" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "685" "paginaFinal" => "686" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Bruno Guedes Baldi, Rogério Souza" "autores" => array:2 [ 0 => array:4 [ "nombre" => "Bruno Guedes" "apellidos" => "Baldi" "email" => array:1 [ 0 => "bruno.baldi@hc.fm.usp.br" ] "referencia" => array:3 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] 2 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "Rogério" "apellidos" => "Souza" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Divisão de Pneumologia, Instituto do Coração (InCor), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Hospital do Coração, São Paulo, Brazil" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Patients with diverse interstitial lung diseases (ILDs) may develop pulmonary hypertension (PH) during follow-up, most with a pre-capillary pattern at invasive hemodynamics, being classified within groups 3 and 5 in the current classification of PH.<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1,2</span></a> Precapillary PH associated with ILD (PH-ILD) is currently defined as the presence of pulmonary vascular resistance (PVR) ≥3 WU associated with mean pulmonary arterial pressure (mPAP) >20<span class="elsevierStyleHsp" style=""></span>mmHg and pulmonary artery wedge pressure ≤15<span class="elsevierStyleHsp" style=""></span>mmHg at rest as assessed by right heart catheterization (RHC).<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1,3</span></a> The majority of PH-ILD is included in the group 3 and related to the parenchymal involvement, such as observed in fibrotic idiopathic interstitial pneumonia (IIP), hypersensitivity pneumonitis and lymphangioleiomyomatosis.<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1,2,4</span></a> However, PH associated with sarcoidosis, pulmonary Langerhans cell histiocytosis and metabolic disorders, given the diversity of potential pathophysiological events that might be responsible for the development of PH, are currently classified within the group 5, with unclear and/or multifactorial mechanisms.<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1,2,5</span></a> Nevertheless, hypoxic vasoconstriction, remodeling of small pulmonary vessels, destruction and obliteration of the microvasculature, and upregulation of vascular modifying cytokines,<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a> isolated or in combination, represent some of the recognized mechanisms potentially involved in the pathogenesis of PH-ILD.</p><p id="par0010" class="elsevierStylePara elsevierViewall">PH determines significant morbidity and mortality in patients with ILD. Most data of PH associated with fibrotic IIP were obtained from studies with idiopathic pulmonary fibrosis (IPF), and demonstrate that the prevalence of PH increases with advanced disease. However, the development of PH in IPF is multifactorial so that the severity of PH is not always correlated with the impairment of the parenchymal involvement<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">2</span></a>; some patients with mild disease may present PH, which can be consistent with other groups of PH classification.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Therefore, it is reasonable to screen PH in symptomatic patients with ILD. However, the most adequate method for screening PH-ILD is still unknown. Different tools may be used to screen PH in patients with parenchymal lung diseases, including peripheral oxygen saturation (SpO<span class="elsevierStyleInf">2</span>) at rest or exercise, transthoracic doppler echocardiography, six-minute walk test, diffusing capacity for carbon monoxide (DLCO), whose reduction can be compared to the decline of lung volumes, and assessment of the main pulmonary artery and aorta diameters on CT scan. These screen methods have different sensitivities according to each ILD.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">3–5</span></a> RHC is the confirmatory diagnostic method of PH associated with ILD and should be considered mainly for those in which therapeutic interventions will be performed.<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">2,4,5</span></a> It is important to emphasize that the presence of PH in a patient with ILD does not preclude the need exclude other causes of PH, beside the parenchymal disease. In this sense, it is important to exclude the presence of left heart dysfunction and chronic thromboembolic disease. Furthermore, the main end-points to assess the response to therapeutic interventions in PH include dyspnea and quality of life scores, six-minute walking distance, decline in forced vital capacity (FVC) and in DLCO, hospitalizations, acute exacerbation, death from any cause or lung transplantation, and pulmonary hemodynamic parameters.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Several advances have been made in the approach to diseases in the area of pulmonary circulation, but consistent innovations in the treatment of PH-ILD have only occurred very recently, mostly in IIP, with a main focus in IPF.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a> Systematic reviews and randomized clinical trials with different systemic pulmonary vasoactive drugs, such as endothelin-receptor antagonists (ambrisentan and bosentan), phosphodiesterase-5 inhibitors (sildenafil) and riociguat, had conflicting results and did not demonstrate robust benefits with some of them even determining harm effects in relevant clinical, functional and pulmonary hemodynamic outcomes in patients with PH secondary to IIP. The main mechanisms speculated for the lack of positive effects of such drugs are the worsening of pulmonary ventilation/perfusion mismatch and gas exchange, and the presence of left sided heart failure.<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">7–11</span></a> For other ILDs, data are still scarce and less robust. A placebo-controlled trial demonstrated that bosentan improved pulmonary hemodynamics in patients with PH associated with sarcoidosis after 16 weeks, with no benefits on the distance walked.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">12</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">In this scenario, the use of inhaled vasodilators, such as pulse nitric oxide (NO) and treprostinil, a prostacyclin analogue, could mitigate the worsening of ventilation/perfusion mismatching through the pulmonary vasodilation of better ventilated areas.<a class="elsevierStyleCrossRefs" href="#bib0140"><span class="elsevierStyleSup">13,14</span></a> Treatment with pulse NO for eight weeks in subjects with fibrotic ILD was safe, well tolerated, and showed improvement in physical activity and in oxygen saturation.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">14</span></a> The benefit of inhaled treprostinil was demonstrated in patients with PH associated with diffuse parenchymal lung disease (INCREASE trial), with a significant improvement in the six-minute walking distance (31<span class="elsevierStyleHsp" style=""></span>m) after 16 weeks and a lower risk of clinical worsening, without increase in adverse events.<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">13</span></a> Additionally, a post-hoc analysis demonstrated potential favorable effects of inhaled treprostinil on FVC, mainly in those with IPF.<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">15</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Although the role of oxygen supplementation on PH in patients with ILD was not clearly assessed, hypoxaemia at rest, during sleep or exercise should be treated. Additionally, it is essential to optimize treatment of the parenchymal component of the underlying ILD.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">2</span></a> However, the impact of antifibrotics on PH-ILD remains unknown. Lung transplantation, preferably bilateral, remains the unique current option with impact on survival in patients with PH-ILD.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Therefore, appropriate drug treatment of PH-ILD has not been established yet. Despite the favorable perspectives with inhaled vasodilators, several questions remain unknown. It is essential to evaluate the impact of inhaled vasodilators on larger samples of patients with fibrotic ILD and on other causes of ILD, such as sarcoidosis and cystic lung diseases. Further research is warranted to address the role of inhaled vasodilators on exercise capacity, functional variables and gas exchange in the long-term, and also on mortality, need of lung transplantation and hospitalizations. The impact of combination therapy, with vasodilators and antifibrotics, in PH-ILD is unknow. It is still not determined whether inhaled vasodilators have impact not only on vascular properties, but also on parenchymal fibrosis. Furthermore, it is essential to identify the subgroups of patients, according to severity of PH and the group of ILD, that would benefit from the use of vasodilators, and to assess other treatment modalities acting on other pathways regarding the potential pathogenesis of PH-ILD, including attenuation of vascular remodeling. Due to the high complexity of the issue and to many unanswered questions, patients with PH-ILD should preferably be referred to experienced centers in PH and ILD, especially if there is a prospect of specific therapy, inclusion in clinical trials, or lung transplantation.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:15 [ 0 => array:3 [ "identificador" => "bib0080" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Haemodynamicdefinitions and updated clinical classification of pulmonary hypertension" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "G. Simonneau" 1 => "D. Montani" 2 => "D.S. Celermajer" 3 => "C.P. Denton" 4 => "M.A. Gatzoulis" 5 => "M. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 11 | 6 | 17 |
| 2024 October | 93 | 43 | 136 |
| 2024 September | 100 | 26 | 126 |
| 2024 August | 108 | 37 | 145 |
| 2024 July | 122 | 33 | 155 |
| 2024 June | 134 | 32 | 166 |
| 2024 May | 109 | 43 | 152 |
| 2024 April | 107 | 36 | 143 |
| 2024 March | 94 | 17 | 111 |
| 2024 February | 102 | 33 | 135 |
| 2024 January | 93 | 35 | 128 |
| 2023 December | 141 | 35 | 176 |
| 2023 November | 107 | 27 | 134 |
| 2023 October | 189 | 49 | 238 |
| 2023 September | 153 | 47 | 200 |
| 2023 August | 150 | 38 | 188 |
| 2023 July | 168 | 50 | 218 |
| 2023 June | 152 | 28 | 180 |
| 2023 May | 154 | 33 | 187 |
| 2023 April | 141 | 53 | 194 |
| 2023 March | 183 | 106 | 289 |
| 2023 February | 173 | 72 | 245 |
| 2023 January | 132 | 65 | 197 |
| 2022 December | 195 | 61 | 256 |
| 2022 November | 256 | 124 | 380 |
| 2022 October | 776 | 322 | 1098 |
| 2022 September | 6 | 4 | 10 |
| 2022 August | 2 | 2 | 4 |
| 2022 June | 9 | 8 | 17 |
| 2022 May | 3 | 0 | 3 |
| 2022 April | 1 | 2 | 3 |
| 2022 March | 10 | 11 | 21 |
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