Effect of Iron Deficiency on Right Ventricular Strain in Patients Diagnosed with Acute Heart Failure

TL;DR

Iron deficiency in heart failure patients is linked to subtle right ventricular dysfunction, even when standard measures appear normal.

Contribution

This study is the first to show that iron deficiency is associated with subclinical right ventricular strain in acute heart failure patients.

Findings

Patients with iron deficiency had significantly lower TAPSE and RV free wall GLS compared to those without ID.

Conventional RV systolic parameters like RVEF and FAC were not significantly affected by iron deficiency.

The findings suggest subclinical RV dysfunction in iron-deficient heart failure patients.

Abstract

Background: Iron deficiency (ID) is a prevalent comorbidity of heart failure (HF), affecting up to 59% of patients, regardless of the presence of anaemia. Although its negative impact on left ventricular (LV) function is well documented, its effect on right ventricular (RV) function remains unclear. This study assessed the effects of ID on RV global longitudinal strain (RV-GLS) in patients diagnosed with acute decompensated HF (ADHF). Methods: This study included data from 100 patients hospitalised with ADHF irrespective of LV ejection fraction (LVEF) value. ID was defined according to the European Society of Cardiology HF guidelines as serum ferritin <100 ng/mL or ferritin 100–299 ng/mL, with transferrin saturation <20%. Anaemia was defined according to World Health Organization criteria as haemoglobin level <12 g/dL in women and <13 g/dL in men. RV systolic function was assessed using parameters including RV ejection fraction (RVEF), tricuspid annular plane systolic excursion (TAPSE), RV fractional area change (FAC), peak systolic tissue Doppler velocity of the RV annulus (RV TDI S′), acceleration time of the RV outflow tract, and RV free wall GLS. Results: The mean (±SD) age of the study population (64% male) was 70 ± 10 years. The median LVEF was 35%, with 66% of patients classified with HF with reduced ejection fraction, 6% with HF with mid-range ejection fraction, and 28% with HF with preserved ejection fraction. Fifty-eight percent of patients had ID. There were no significant differences between patients with and without ID regarding demographics, LVEF, RV FAC, RV TDI S′, or systolic pulmonary artery pressure. However, TAPSE (15.6 versus [vs.] 17.2 mm; p = 0.05) and RV free wall GLS (−14.7% vs. −18.2%; p = 0.005) were significantly lower in patients with ID, indicating subclinical RV systolic dysfunction. Conclusions: ID was associated with subclinical impairment of RV systolic function in patients diagnosed with ADHF, as evidenced by reductions in TAPSE and RV-GLS, despite the preservation of conventional RV systolic function parameters. Further research validating these findings and exploring the underlying mechanisms is warranted.

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