Why the study?
Heart failure frequently coexists with comorbidities including iron deficiency, but the relationship between iron deficiency and the development of heart failure remains poorly understood.
Does iron deficiency increase the risk of incident left ventricular dysfunction in patients with coronary artery disease?
Does iron deficiency increase the risk of incident left ventricular dysfunction in patients with coronary artery disease?
In patients with coronary artery disease, iron deficiency (specifically TSAT <20%) is an independent predictor of incident left ventricular dysfunction over long-term follow-up.
TSAT <20% may flag higher risk for incident LV dysfunction in CAD; hypothesis-generating and requires prospective trials before practice change.
Background: Heart failure (HF) is a complex and life-threatening condition that often coexists with comorbidities such as hypertension, type 2 diabetes mellitus, coronary artery disease (CAD), and iron deficiency (ID). However, the relationship between ID and the development of HF remains poorly understood. Aim: This study aimed to investigate the correlation between ID and the development of left ventricular dysfunction. Methods: A total of 64,661 patients diagnosed with CAD at a tertiary hospital between 2011 and 2023 were recruited. Of these, 4813 patients who underwent iron status evaluation, including serum iron (SI), total iron-binding capacity (TIBC), and ferritin within 30 days, were included in the analysis. We compared the incidence and hazard ratio (HR) of new-onset left ventricular (LV) dysfunction (LV ejection fraction <50%) between patients with and without ID, defined as SI/TIBC or transferrin saturation (TSAT) <20% or ferritin <100 ng/mL. Results: The incidence of new-onset LV dysfunction was higher in patients with ID, defined by TSAT <20% compared to those with normal TSAT (HR, 1.40; 95% confidence interval [CI], 1.14–1.72) over a 13-year follow-up. In multivariable analysis, TSAT <20% retained its predictive value for new-onset LV dysfunction (adjusted HR, 1.24; 95% CI, 1.01–1.54), while ferritin levels were not correlated with the incidence of new-onset LV dysfunction in this cohort. The all-cause mortality rate was also higher in patients with ID, defined by TSAT <20% compared to those with normal TSAT. A subgroup analysis revealed no significant difference in predicting new-onset LV dysfunction between patients with ID, with or without coexisting anemia ( P = 0.165). Conclusion: In patients with CAD, ID, particularly defined by TSAT <20%, was predictive of future LV dysfunction and associated outcomes. Further studies are needed to investigate the underlying mechanisms and causal relationship between ID and the risk of LV dysfunction.
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Chang et al. (2025) studied this question.
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