In patients with pulmonary hypertension caused by chronic lung disease, iron deficiency is linked to more severe pulmonary vascular disease.

Group 3 Pulmonary Hypertension (PH) is the second most frequent type of Pulmonary Hypertension (PH), although it has the greatest mortality rate of all PH illnesses. Group 3 PH patients have few therapy options; while inhaled treprostinil improves exercise capacity, patients nevertheless have a high morbidity and mortality rate. As a result, more research into the pathophysiologic findings of group 3 PH is needed, in the hopes of identifying possible treatment targets to battle the high symptom burden and poor outcomes experienced by these individuals. Parenteral iron treatment has been proven to enhance exercise capacity, New York Heart Association functional class, and patient wellbeing in chronic left heart failure, where iron deficiency is frequent and deleterious.The significance of iron in the natural history of Pulmonary Arterial Hypertension is gaining popularity (PAH). The availability of iron influences the pulmonary vasoconstrictor response to hypoxia, and growing evidence suggests that iron deficiency is common in both idiopathic and heritable forms of PAH, with iron status being linked to exercise capacity, symptoms, and a poorer prognosis in patients with Idiopathic PAH (IPAH). Inhibition of dietary iron intake by the master iron regulator hepcidin is one possible cause for iron shortage in IPAH. Chronic illness anemia is caused by high hepcidin levels. In preclinical models, iron deficiency promotes pulmonary vascular remodeling and is linked to worse outcomes in pulmonary arterial hypertension. The effects of iron deficiency in patients with pulmonary hypertension caused by chronic lung illness (Group 3 PH) are yet to be studied. Because of its prognostic and therapeutic potential, iron's importance in cardiopulmonary disease is gaining traction. At least one-third of PH patients have Iron Deficiency (ID). ID causes a higher symptom load, higher Mean Pulmonary Artery Pressure (mPAP), lower cardiac index, and a higher mortality rate in Pulmonary Arterial Hypertension (PAH), regardless of anemia. IV iron repletion improved body iron stores, exercise endurance time, aerobic capacity, and quality of life in 15 PAH patients in a single-arm study. However, a more recent randomized, double-blind, placebo-controlled crossover experiment in patients with ID PAH found that IV iron had no effect on cardiopulmonary exercise capacity or Pulmonary Vascular Resistance (PVR).