ArticlePulmonary circulation2016
Hemodynamic response to treatment of iron deficiency anemia in pulmonary arterial hypertension: longitudinal insights from an implantable hemodynamic monitor.
Article in Pulmonary circulation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Review
- Integrated use of cardiac MRI and the CardioMEMS™ HF system in PAH: the utility of coincident pressure and volume in RV failure-the NHLBI-VITA trial.Cardiovascular diagnosis and therapy · 2019Article
- Iron Deficiency as a Therapeutic Target in Cardiovascular Disease.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Intracellular iron deficiency in pulmonary arterial smooth muscle cells induces pulmonary arterial hypertension in mice.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite new therapeutic options, pulmonary arterial hypertension (PAH) remains a progressive disease associated with substantial morbidity and mortality. As such, additional strategies for monitoring and adjunctive management of this disease are important. A 59-year-old woman with scleroderma-associated PAH received an implantable hemodynamic monitor (IHM) as part of a research protocol at our institution. Pulmonary artery pressures, heart rate, and cardiac output (sensor-based algorithm) were measured on a daily basis, and parameters of right ventricular (RV) performance and afterload were calculated. At the time of IHM implant, the patient had functional class III symptoms, was receiving triple-drug therapy, and had normal hemoglobin levels. Four months after implant, and with further optimization of prostacyclin therapy, she had improvement in her symptoms. However, shortly thereafter, while the patient was receiving stable drug therapy, her case regressed with worsening symptoms, and the patient received a new diagnosis of iron deficiency anemia. Oral iron supplementation resulted in normalization of hemoglobin levels and improvement in the patient's iron profile. A gradual and sustained reduction in pulmonary pressures was noted after initiation of oral iron accompanied by increased RV performance and favorable reduction in RV afterload. The patient had significant symptomatic improvement. Iron deficiency is an underappreciated yet easily treatable risk factor in PAH. Use of IHM in this case longitudinally illustrates the optimization of pulmonary hemodynamics and RV afterload in tandem with clinical improvement achieved by a simple therapy.
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