ArticlePulmonary circulation2014
Pulmonary arterial hypertension in a patient with β-thalassemia intermedia and reversal with infusion epoprostenol then transition to oral calcium channel blocker therapy: review of literature.
Article in Pulmonary circulation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Macitentan Administration for Pulmonary Hypertension Due to β-thalassemia with Multiple Organ Failure.Internal medicine (Tokyo, Japan) · 2024Article
- The improvement of pulmonary artery pressure after bosentan therapy in patients with β-thalassemia and Doppler-defined pulmonary arterial hypertension.International medical case reports journal · 2019Article
- Hemolysis-induced Lung Vascular Leakage Contributes to the Development of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2018Article
- Use of epoprostenol to treat severe pulmonary vasoconstriction induced by protamine in cardiac surgery.Medicine · 2018Observational
- Pulmonary hypertension associated with thalassemia syndromes.Annals of the New York Academy of Sciences · 2016Review
- Treatment of pulmonary hypertension in three patients with ß-thalassemia intermedia using pulmonary arterial hypertension-specific medications.Anatolian journal of cardiology · 2016Article
- The wide spectrum of β-thalassaemia intermedia-induced pulmonary hypertension: two case reports on the possible role of specific pulmonary arterial hypertension therapy.Pulmonary circulationArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) is a potentially life-threatening complication of thalassemia. A sexagenarian with β-thalassemia intermedia presented with new-onset dyspnea and syncope. Right heart catheterization confirmed severe PAH. Her functional class IV symptoms and severely elevated mean pulmonary artery pressure prompted the initiation of continuous epoprostenol therapy. Clinical follow-up documented significant improvement in functional class, 6-minute walk distance, and right ventricular size and function as well as pulmonary arterial pressure on echocardiogram. At the patient's request, epoprostenol was down-titrated and eventually discontinued. The patient was then safely transitioned to nifedipine therapy after verification of vasoresponsiveness.
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