Malnutrition in pulmonary arterial hypertension: a possible role for dietary intervention.

PURPOSE OF REVIEW: The last decade's progress has been made in the pharmacological treatment of pulmonary arterial hypertension (PAH). The role of nutrition in relation to quality of life in this group of patients is not investigated yet. In addition to avoiding salt and high-fluid intake based on left heart failure diet, there is no evidence-based diet recommendation for PAH. RECENT FINDINGS: It was recently demonstrated that patients with PAH suffer from malnutrition resulting in iron and vitamin D deficiency and glucose/insulin resistance. Recent experimental studies suggest that besides reduced malabsorption of important nutrients, the microbiome of the gut is also less diverse in PAH. In this review, we summarize the current knowledge on malnutrition and dietary intake in PAH. We discuss the possible underlying mechanisms and discuss novel therapeutic interventions validated in patients with left heart failure. SUMMARY: Large-scaled studies on dietary interventions are needed in PAH.

Intravenous iron therapy in patients with idiopathic pulmonary arterial hypertension and iron deficiency.

UNLABELLED: In patients with idiopathic pulmonary arterial hypertension (iPAH), iron deficiency is common and has been associated with reduced exercise capacity and worse survival. Previous studies have shown beneficial effects of intravenous iron administration. In this study, we investigated the use of intravenous iron therapy in iron-deficient iPAH patients in terms of safety and effects on exercise capacity, and we studied whether altered exercise capacity resulted from changes in right ventricular (RV) function and skeletal muscle oxygen handling. Fifteen patients with iPAH and iron deficiency were included. Patients underwent a 6-minute walk test, cardiopulmonary exercise tests, cardiac magnetic resonance imaging, and a quadriceps muscle biopsy and completed a quality-of-life questionnaire before and 12 weeks after receiving a high dose of intravenous iron. The primary end point, 6-minute walk distance, was not significantly changed after 12 weeks (409 ± 110 m before vs. 428 ± 94 m after; P = 0.07). Secondary end points showed that intravenous iron administration was well tolerated and increased body iron stores in all patients. In addition, exercise endurance time (P < 0.001) and aerobic capacity (P < 0.001) increased significantly after iron therapy. This coincided with improved oxygen handling in quadriceps muscle cells, although cardiac function at rest and maximal [Formula: see text] were unchanged. Furthermore, iron treatment was associated with improved quality of life (P < 0.05). In conclusion, intravenous iron therapy in iron-deficient iPAH patients improves exercise endurance capacity. This could not be explained by improved RV function; however, increased quadriceps muscle oxygen handling may play a role. ( TRIAL REGISTRATION: ClinicalTrials.gov identifier NCT01288651).