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Leukocyte labile iron pool in patients with systolic heart failure
Panagiotis Korantzopoulos1, Chara Vlachou, Anna Kotsia
1Department of Cardiology, University of Ioannina Medical School, Ioannina, Greece. p.korantzopoulos@yahoo.gr
Insights
Labile iron pool (LIP) in granulocytes is linked to worsening heart failure. This finding suggests intracellular iron may drive oxidative stress in leukocytes, contributing to heart dysfunction.
Area of Science:
- Cardiology
- Biochemistry
- Immunology
Background:
- Oxidative stress sources in heart failure (HF) are not well understood.
- Leukocytes contribute to myocardial oxidative damage in HF.
- Intracellular labile iron pool (LIP) generates reactive oxygen species.
Purpose of the Study:
- To investigate LIP status in leukocyte populations in HF patients.
- To explore associations between LIP and clinical/laboratory parameters in HF.
Main Methods:
- Studied 60 patients with chronic systolic HF (LVEF ≤ 45%).
- Assessed LIP in granulocytes and monocytes.
- Correlated LIP with left ventricular ejection fraction (LVEF) and inflammatory markers.
Main Results:
- LIP in granulocytes and right ventricular systolic pressure (RVSP) independently predicted severe LV systolic dysfunction (LVEF ≤ 30%).
- LVEF inversely correlated with LIP in granulocytes and monocytes, and RVSP.
- No significant correlation found between LVEF and inflammatory indexes.
Conclusions:
- LIP in granulocytes is independently associated with reduced LVEF in systolic HF.
- Intracellular redox-active iron in leukocytes may be a source of oxidative stress in HF.
Introduction:
Data regarding sources of oxidative stress in the failing myocardium are sparse. Leukocytes actively participate in the oxidative damage observed in human heart failure (HF). The intracellular labile iron pool (LIP) represents a source of toxic reactive oxygen species.
Methods:
We studied patients with chronic systolic HF who had a left ventricular ejection fraction (LVEF) 45%. We examined the LIP status in different populations of leukocytes in HF patients and we investigated its association with clinical and laboratory parameters, including conventional inflammatory markers.
Results:
Sixty patients were finally included in the analysis (mean age: 67 ± 11 years, 54 men, 42 with ischemic cardiomyopathy). The multivariate logistic regression analysis showed that only LIP in granulocytes (OR: 0.73; 95% CI: 0.55-0.98; p=0.039) and right ventricular systolic pressure (RVSP) (OR: 0.95; 95% CI: 0.92-0.99; p=0.027) were independently associated with severe LV systolic dysfunction (LVEF30%). The correlation analysis revealed that LVEF was inversely associated with LIP in granulocytes (Spearman's rho: -0.39, p=0.002), LIP in monocytes (Spearman's rho: -0.35, p=0.007), and RVSP (Spearman's rho: -0.43, p=0.003). No significant correlation between LVEF and inflammatory indexes was noted.
Conclusions:
LIP in granulocytes is independently associated with the severity of LV dysfunction in patients with systolic HF. Intracellular redox active iron may represent a source of leukocyte reactive oxygen species in this setting.
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