Drug-associated pulmonary arterial hypertension

McGee, Michael; Whitehead, N.; Martin, Jennifer; Collins, Nicholas

doi:10.1080/15563650.2018.1447119

Cited by 49 publications

(37 citation statements)

References 83 publications

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“…Besides that, the study of EYRIES et al [3] carries important implications for respiratory research at several levels. First, it puts a weighty argument in the ongoing debate on the role of VEGF/VEGFR signalling in pulmonary hypertension, which has evolved around the paradoxical findings that VEGF-A and VEGF receptors were reported to be upregulated in plexiform lesions in PAH on the one side [15,16], and that blockade of VEGF-A [17] or VEGFR2 [18,19] results in PAH. EYRIES et al [3] provide evidence for the latter by showing that VEGFR2 haplo-insuffiency contributes to PAH, indicating that upregulation of VEGF-A and receptors are secondary events, either by negative feedback or from local receptor rearrangement.…”

Section: @Erspublicationsmentioning

confidence: 99%

Vanishing vessels aboding pulmonary disease: a role for VEGFR2

Botros¹,

Vonk‐Noordegraaf²,

Aman³

2020

Eur Respir J

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Section: @Erspublicationsmentioning

confidence: 99%

Vanishing vessels aboding pulmonary disease: a role for VEGFR2

Botros¹,

Vonk‐Noordegraaf²,

Aman³

2020

Eur Respir J

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“…Pulmonary hypertension (PH) in patients with cancer can develop due to pulmonary arterial hypertension, pulmonary vascular disease, pulmonary embolism, toxicity from chemotherapeutics or RT, infectious or neoplastic pulmonary etiologies or LV disease with dismal prognosis. Patients under therapy with certain chemotherapeutics (Table 7), such as dasatinib, 11 paclitaxel, 36 interferon alpha, 37,38 tretinoin, 39 cyclophosphamide and other alkylating agents, 11 monoclonal antibodies, 38 as well as patients after stem cell bone marrow transplantation or RT, are at increased risk of developing PH 29 . Dasatinib is the most studied medication.…”

Section: Focused Echo In Cardio‐oncology In Patients At Risk Of Pulmomentioning

confidence: 99%

Focused echocardiography in cardio‐oncology

et al. 2020

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Transthoracic echocardiography (TTE) is the cornerstone of imaging in patients with a malignancy in all stages of their treatment—before, during, and after the completion of it—to identify most of the cardiotoxic complications. However, the restricted time and resources of cardio‐oncology services and the high volume of oncological patients and survivors on the other hand limit the access of this population to this modality. Focused Echo in Cardio‐Oncology (FECO) in proportion to other focused cardiac protocols is proposed as a valuable tool after the initial standard complete TTE to: (a) identify the potential toxicity expected by the specific cancer therapy applied; (b) assess sequentially the pre‐existing abnormality, if any, in relation to therapy; (c) assess the effect of any cardio‐protective intervention; (d) identify any cardiac origin of patient complaints during or after therapy; (e) assess cardiac function in asymptomatic patients who develop significant changes in cardiac biomarkers during cancer therapy. Four different protocols of FECO are proposed according to the type of cardiotoxicity anticipated: FECOm (in patients on chemotherapeutics that cause myocardial dysfunction), FECOv (in patients at risk of valvular heart disease), FECOpd (in patients at risk of pericardial disease), and FECOph (in patients at risk of pulmonary hypertension). The application of FECO protocols is aimed to ensure accuracy, reliability, and effectiveness in the early identification of cardiovascular complications, improving quality of life, and being at the same time cost‐effective.

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“…1 Over the ensuing years, the number of drugs associated with PAH has increased and recent reviews highlight the drugs and toxins associated with PAH. 2,3 A partial set of medications associated with PAH include anorexic agents aminorex, fenfluramine, and benfluorex; tyrosine kinase inhibitor dasatinib; chemotherapy mitomycin, and interferon. Moreover, drugs implicated with the development of PAH account for 10.5% of subjects enrolled in the REVEAL Registry.…”

Section: Assessmentmentioning

confidence: 99%

PH Grand Rounds: Interferon-Associated Pulmonary Arterial Hypertension

Levine¹,

Shah

Duarte

2018

Advances in Pulmonary Hypertension

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Presentation: A woman aged 54 years with multiple sclerosis (MS), chronic obstructive pulmonary disease (COPD), and hypertension presented with progressive exertional dyspnea and fatigue noted over 8 months. Multiple sclerosis was diagnosed 15 years earlier and treated with subcutaneous interferon-β for 10 years with subjective and clinical benefits. She described gradual fatigue and breathlessness with walking, climbing stairs, and performing activities of daily living but denied exertional chest pain, syncope, or lower extremity edema. She attributed her symptoms to worsening MS, however, her treating neurologist did not identify clinical or magnetic resonance imaging (MRI) indicative of worsening progressive MS. Because she was a daily smoker, her exertional dyspnea was attributed to COPD, and pulmonary function testing confirmed a diagnosis of airflow limitation with a decreased diffusion capacity; results were FEV1: 2.22 L (85% predicted), FVC: 3.44 L, FEV1/FVC: 0.65, DLCO: 9.0 mL/min/ mm Hg. In addition, an arterial blood gas (FiO 2 : 0.21) revealed 7.41/39/80. Yet, despite use of nebulized albuterol every 6 hours, her exertional dyspnea was not relieved, and she was referred for further assessment of exertional dyspnea.

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Drug-associated pulmonary arterial hypertension

Cited by 49 publications

References 83 publications

Vanishing vessels aboding pulmonary disease: a role for VEGFR2

Vanishing vessels aboding pulmonary disease: a role for VEGFR2

Focused echocardiography in cardio‐oncology

PH Grand Rounds: Interferon-Associated Pulmonary Arterial Hypertension

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