Heart failure & cardiomyopathies
Mitochondrial dysfunction in human hypertrophic cardiomyopathy is linked to cardiomyocyte architecture disruption and corrected by improving NADH-driven mitochondrial respiration
Authors' conclusion
Mitochondrial dysfunction is explained by cardiomyocyte architecture disruption and is linked to septal hypertrophy in genotype-negative HCM. Despite severe myocardial remodelling mitochondria were responsive to treatments aimed at restoring respiratory function
Study context
- Population
- Patients with hypertrophic cardiomyopathy (HCM) undergoing septal myectomy (genotype-positive and genotype-negative)septal myectomy tissue
- Participants
- 59 patients
- Outcome
- Mitochondrial respiratory function (respirometry)
Main finding
As reported in the abstract
- Mitochondrial dysfunction most notably reflected by impaired NADH-linked respiration
- Genotype-negative (not genotype-positive): NADH-linked respiration markedly depressed with indexed septal thickness ≥10 vs <10
- Mitochondrial dysfunction not explained by reduced abundance or fragmentation of mitochondria (transmission electron microscopy)
- % disorganized mitochondria relative to myofibrils strongly associated with mitochondrial dysfunction
- Pre-incubation with elamipretide and raising mitochondrial NAD+ levels both boosted NADH-linked respiration
Original publication
Mitochondrial dysfunction in human hypertrophic cardiomyopathy is linked to cardiomyocyte architecture disruption and corrected by improving NADH-driven mitochondrial respiration. Eur Heart J. Published 3 February 2023. doi:10.
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