Circulation, Ahead of Print. BACKGROUND:End-stage heart failure (HF) remains a major global health challenge, and left ventricular assist devices (LVADs) represent an important therapeutic option.
LVAD-mediated mechanical unloading improves cardiac function and promotes myocardial recovery in many patients with HF. How cardiac unloading by LVADs leads to myocardial recovery and whether impairment of these processes underlies the limited myocardial recovery benefit in obese patients remain poorly understood.METHODS:Patients with HF with LVADs were recruited for an investigation of the correlation between patients’ body mass index and their response to LVAD-mediated myocardial recovery.
Moreover, a mouse model of heterotopic cervical heart transplantation was used to simulate LVAD unloading. Single-nucleus RNA sequencing and stable-isotope tracing metabolomics were performed to explore the changes of signaling pathways and metabolic processes in unloaded hearts.
In vitro cyclic stretch assays were used to evaluate how reduced mechanical load regulates cardiomyocyte metabolic pathways. Unloaded hearts from HF mice were used to determine whether the identified metabolic process contributed to unloading-induced myocardial recovery.
Circulation published a clinical update in Cardiology on 06 Feb 2026.
The item focuses on Insulin Resistance Compromises the Pentose Phosphate Pathway and Impairs Left Ventricular Assist Device–Mediated Myocardial Recovery in Obese Patients with Heart Failure.
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