ArticleJournal of cardiovascular translational research2019
Reduced Myocardial Mitochondrial ROS Production in Mechanically Unloaded Hearts.
Article in Journal of cardiovascular translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- METAB-HTX: prospective, longitudinal cohort study evaluating cardiac and systemic metabolism after heart transplantation.ESC heart failure · 2025Article
- Myocardial inflammation is associated with impaired mitochondrial oxidative capacity in ischaemic cardiomyopathy.ESC heart failure · 2025Article
- Cellular and Molecular Mechanisms Activated by a Left Ventricular Assist Device.International journal of molecular sciences · 2023Review
- Receptor autoantibodies: Associations with cardiac markers, histology, and function in human non-ischaemic heart failure.ESC heart failure · 2023Article
- Non-invasive mapping of systemic neutrophil dynamics upon cardiovascular injury.Nature cardiovascular research · 2023Article
- Systemic and local vascular inflammation and arterial reactive oxygen species generation in patients with advanced cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Article
- Metabolic Factors Predict Changes in Endothelial Function During the Early Course of Type 1 and Type 2 Diabetes.The Journal of clinical endocrinology and metabolism · 2022Article
- Multiparametric MRI identifies subtle adaptations for demarcation of disease transition in murine aortic valve stenosis.Basic research in cardiology · 2022Article
- Human myocardial mitochondrial oxidative capacity is impaired in mild acute heart transplant rejection.ESC heart failure · 2021Article
- Reverse Remodeling With Left Ventricular Assist Devices.Circulation research · 2021Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanical ventricular unloading in advanced heart failure (HF) has been shown to induce reverse remodeling in myocardial tissues. Little is known about the impact of ventricular unloading on myocardial energy metabolism. We hypothesized that left ventricular unloading reduces myocardial mitochondrial reactive oxygen species (ROS) production and improves mitochondrial coupling efficiency in patients suffering from advanced HF. Left ventricular tissue specimens were harvested from explanted hearts at the time of transplantation. We compared myocardial metabolism in explanted hearts supported with an unloading ventricular assist device prior to transplantation (LVAD-HTX; n = 9) with tissue specimens of unsupported failing hearts (HTX; n = 6). Myocardial mitochondrial ROS production was decreased by 40% in LVAD-HTX compared to HTX patients (1.5 ± 0.3 vs. 0.9 ± 0.1 pmol/(s/mg); p < 0.05). High-resolution respirometry revealed increased mitochondrial coupling efficiency in LVAD-HTX patients (respiratory/control ratio 1.7 ± 0.2 vs. 1.2 ± 0.2; p < 0.05). In conclusion, ventricular unloading is related to decreased mitochondrial ROS production and increased coupling efficiency in myocardium of human failing hearts, suggesting a novel pathomechanism of unloading-associated cardioprotection.
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