Key result
Metabolic impairment in HF affects myocardial and peripheral tissues to promote cachexia and disease progression.
Why the study?
Recent research has highlighted the complexity of metabolic impairments in heart failure affecting myocardial and peripheral tissues, but a comprehensive review of these metabolic aspects and therapeutic targets is needed.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“With our study, we want to examine whether the efficiency of the heart in patients with heart failure can be increased with an improved energy metabolism”
Review uncovers widespread myocardial and systemic energy starvation in heart failure, highlighting how metabolic breakdown and cachexia drive disease progression.
Although bioenergetic starvation is not a new concept in heart failure (HF), recent research has led to a growing appreciation of the complexity of metabolic aspects of HF pathophysiology. All steps of energy extraction, transfer, and utilization are affected, and structural metabolism is impaired, leading to compromised functional integrity of tissues. Not only the myocardium, but also peripheral tissues and organs are affected by metabolic failure, resulting in a global imbalance between catabolic and anabolic signals, leading to tissue wasting and, ultimately, to cachexia. Metabolic feedback signals from muscle and fat actively contribute to further myocardial strain, promoting disease progression. The prolonged survival of patients with stable, compensated HF will increasingly bring chronic metabolic complications of HF to the fore and gradually shift its clinical presentation. This paper reviews recent evidence on myocardial and systemic metabolic impairment in HF and summarizes current and emerging therapeutic concepts with specific metabolic targets.
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Doehner et al. (2014) conducted a review in Heart failure. Metabolic impairment in heart failure affects both myocardial and peripheral tissues, leading to a global imbalance that promotes tissue wasting, cachexia, and disease progression.
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