Myocardial iron content and mitochondrial function in human heart failure: a direct tissue analysis
Vojtech Melenovsky1, Jiri Petrak2, Tomas Mracek3
1Department of Cardiology and Cardiac Surgery, Institute of Clinical and Experimental Medicine-IKEM, Prague, Czech Republic.
European Journal of Heart Failure
|September 21, 2016
Summary
Iron deficiency in the heart muscle (myocardial iron deficiency) is common in heart failure (HF). This deficiency impairs mitochondrial function and may worsen heart failure outcomes.
Area of Science:
- Cardiology
- Biochemistry
- Mitochondrial Biology
Background:
- Iron replacement therapy improves heart failure (HF) symptoms, but the underlying mechanisms are not fully understood.
- Iron is crucial for cellular energy production, and its role in myocardial iron deficiency (MID) and mitochondrial function in HF is unknown.
Purpose of the Study:
- To investigate the direct impact of MID on mitochondrial function in the failing human heart.
- To quantify myocardial iron content and assess mitochondrial respiration and enzyme activities in HF patients.
Main Methods:
- Left ventricular tissue samples were analyzed from 91 HF patients and 38 controls.
- Measurements included myocardial iron content, mitochondrial respiration, citric acid cycle and respiratory chain enzyme activities, and levels of reactive oxygen species (ROS)-protective enzymes.
Main Results:
- HF patients had significantly lower myocardial iron content than controls, independent of anemia.
- MID in HF was associated with reduced activity of key citric acid cycle enzymes (aconitase, citrate synthase) and decreased expression of ROS-protective enzymes.
- HF patients exhibited overall impaired mitochondrial respiration and enzyme activities compared to controls.
Conclusions:
- Advanced HF is characterized by decreased myocardial iron and impaired mitochondrial function.
- MID in HF is linked to reduced citric acid cycle enzyme activity and diminished ROS-protective enzymes.
- MID may contribute to altered substrate utilization and exacerbate mitochondrial dysfunction in heart failure.
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