Key result
Severe aortic stenosis linked to ~23% lower PBMC mitochondrial coupling that persists 30 days post-TAVR.
Why the study?
Severe aortic stenosis is characterized by pressure overload leading to cardiac mitochondrial dysfunction, and its association with PBMC mitochondrial respiration alterations is unclear.
Does TAVR alter PBMC mitochondrial respiration in patients with severe aortic stenosis?
Observational (n=34)
No
Does TAVR alter PBMC mitochondrial respiration in patients with severe aortic stenosis?
Severe aortic stenosis is associated with altered PBMC mitochondrial respiration that is not reversed by TAVR at 30 days, though increased complex IV respiration correlates with reduced mortality.
Answers are grounded in this paper and cite their sources.
Mitochondrial changes in severe AS may persist after TAVR; leaves open their prognostic value and need for targeted therapies.
Background: Circulating peripheral blood mononuclear cell (PBMC) mitochondrial respiration is impaired in heart failure and transplanted patients. Severe aortic stenosis (AS), characterized by pressure overload leading to cardiac mitochondrial dysfunction, might also be associated with PBMC mitochondrial respiration alterations, likely related to systemic inflammation and left heart hypertrophy and diastolic dysfunction. Population and Methods: We determined PBMC mitochondrial respiration by high-resolution respirometry (Oroboros Instruments) in 9 healthy subjects and 25 AS patients before and until 30 days after transcatheter aortic valve replacement (TAVR) and investigated potential correlates with the clinical, biological and echocardiographic characteristics of the patients. Results: AS patients with a transaortic valvular gradient of 45 mm Hg were older and demonstrated slightly impaired renal function, inflammation markers, increased brain natriuretic peptide, left ventricular hypertrophy, and impaired diastolic function. PBMC mitochondrial coupling was decreased in the AS patients compared to controls (2.12 ± 0.10 vs. 2.76 ± 0.17, p = 0.003) and mitochondrial complex IV respiration was increased (31.07 ± 2.84 vs. 18.69 ± 2.09, p = 0.017). TAVR did not modify the alterations. Interestingly, increased complex IV mitochondrial respiration was associated with reduced mortality (p < 0.01). Conclusions: Severe aortic stenosis is associated with bioenergetic remodeling of circulating mononuclear cells that were not significantly associated with valvular hemodynamic impairment and ventricular function, before and after the mechanical relief of afterload. Nevertheless, future studies will be useful to determine whether such systemic immuno-metabolic phenotype, particularly PBMC mitochondrial complex IV respiration stimulation, may contribute to reduce the risk following TAVR.
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Marchandot et al. (2026) conducted an observational in Severe aortic stenosis (n=34). Severe aortic stenosis vs. Healthy controls was evaluated on PBMC mitochondrial coupling (respiratory control ratio) (p=0.003). Severe aortic stenosis was associated with decreased PBMC mitochondrial coupling and increased complex IV respiration compared to healthy controls, which were not reversed 30 days after TAVR.
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