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Cardiac diseases in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Saravanan Kuppuswamy, Sudarshan Balla
Echocardiography remains the key diagnostic test in pulmonary hypertension, and a right heart catheterization may be needed to confirm the diagnosis of pulmonary arterial hypertension and, if needed, for the assessment of response to therapy. Right heart catheterization can be done without exposure to any radiation.
Applied Physiology and Biochemistry
Published in Elizabeth Combeer, The Final FRCA Short Answer Questions, 2019
Pulmonary arterial hypertension: Idiopathic (may be familial, abnormal genes have been identified).Associated with systemic disease such as connective tissue diseases, HIV, chronic haemolytic anaemia.Drug and toxin associated.Persistent pulmonary hypertension of the newborn.
Multiple choice questions (MCQs)
Published in Tristan Barrett, Nadeem Shaida, Ashley Shaw, Adrian K. Dixon, Radiology for Undergraduate Finals and Foundation Years, 2018
Tristan Barrett, Nadeem Shaida, Ashley Shaw, Adrian K. Dixon
A 48-year-old presents with lethargy and non-specific symptoms of feeling unwell. CXR shows bilateral hilar enlargement. Which of the following should be considered in the differential? Sarcoidosis.Pulmonary arterial hypertension.Lymphoma.Histoplasmosis.Thymoma.
Xinmai 'an extract enhances the efficacy of sildenafil in the treatment of pulmonary arterial hypertension via inhibiting MAPK signalling pathway
Published in Pharmaceutical Biology, 2021
Yaolu Zhu, Yabin Sun, Shichang Zhang, Chuyuan Li, Yiwei Zhao, Boxin Zhao, Guofeng Li
Pulmonary hypertension refers to a hemodynamic and pathophysiological state in which the increase of pulmonary artery pressure exceeds a certain threshold, which can lead to right heart failure. It is a common and frequently-occurring disease with a high disability rate and fatality rate, which should arouse people’s great attention (Voelkel et al. 2012; Zangiabadi et al. 2014). The primary treatments for pulmonary arterial hypertension (PAH) include epoprostenol and derivatives, endothelin receptor antagonists, calcium channel blockers, and recently researchers have focussed on phosphodiesterase type 5 enzyme (PDE-5) inhibitors such as sildenafil (SIL), which mainly focus on expanding blood vessels selectively, weakening anti-proliferation ability of PASMCs (Montani et al. 2014). These drugs can improve the quality of life of patients with pulmonary hypertension to a certain extent. However, none of the aforementioned drugs, including SIL, can completely reverse the development of the disease, and there are many adverse reactions (Hao et al. 2020). Therefore, there is an urgent need for more new methods to treat PAH.
Caveolae, caveolin-1 and lung diseases of aging
Published in Expert Review of Respiratory Medicine, 2019
Sarah A. Wicher, Y.S. Prakash, Christina M. Pabelick
Pulmonary hypertension is defined as pulmonary pressures >25 mmHg at rest or 30 mm Hg with exercise. Pulmonary hypertension is likely multifactorial in origin and can be idiopathic in nature. Although rare compared to other lung or vascular diseases, its occurrence (often in young women) and limited medical therapy make it a devastating disease. Pulmonary arterial hypertension is a disease of the blood vessels of the lungs that results in elevated arterial pressures. In pulmonary hypertension per se, elevation of pressures is caused by another disease extrinsic to the pulmonary vasculature which are themselves not diseased [111]. The World Health Organization (WHO) categorizes pulmonary hypertension in the following five groups: 1. Pulmonary Arterial Hypertension, 2. Pulmonary Hypertension due to left heart disease, 3. Pulmonary Hypertension due to lung disease, 4. Pulmonary Hypertension due to blood clots in the lungs, and 5. Blood and other rare disorders that lead to Pulmonary Hypertension [112].
Emerging alternatives to tyrosine kinase inhibitors for treating chronic myeloid leukemia
Published in Expert Opinion on Emerging Drugs, 2018
Simon Kavanagh, Aisling Nee, Jeffrey H. Lipton
A subsequent phase 3 study, randomizing 519 newly diagnosed CML-CP patients to dasatinib 100 mg daily or imatinib 400 mg daily, demonstrated higher rates of CCyR at 12 months (77% vs. 66%) with dasatinib than imatinib [32]. The rate of MMR was higher with dasatinib than imatinib (46% vs. 28%) and responses were achieved faster with dasatinib. Five-year follow-up demonstrated higher rates of MMR and deep molecular response with dasatinib [33]. Unlike other TKIs, pleural effusion is a common side effect with dasatinib therapy and was seen in 28% of cases in this follow-up study. This complication could be managed with dose interruption and/or dose reduction, diuretics, corticosteroids, and thoracocentesis. Pulmonary arterial hypertension was also seen in small numbers of patients; the risk of cardiovascular events did not appear increased.