Key result
Oral antioxidant administration for 30 days improved flow-mediated dilatation in patients with HFrEF from 2.63% to 4.90%, restoring macrovascular function to levels similar to healthy controls.
Why the study?
HFrEF is characterized by macrovascular dysfunction and elevated oxidative stress, but whether these may be mitigated by 30 days of oral antioxidant administration remained to be examined.
Does oral antioxidant administration improve macrovascular function in patients with heart failure with reduced ejection fraction?
Does oral antioxidant administration improve macrovascular function in patients with heart failure with reduced ejection fraction?
Absolute Event Rate: 4.9% vs 2.63%
A 30-day oral antioxidant regimen significantly improved macrovascular function and reduced oxidative stress in patients with HFrEF, though effects reversed upon cessation.
Antioxidants improved macrovascular function in HFrEF; hypothesis-generating and requires randomized confirmation before practice change.
NEW FINDINGS: What is the central question of this study? We aimed to examine oxidative stress, antioxidant capacity and macro- and microvascular function in response to 30 days of oral antioxidant administration in patients with heart failure with reduced ejection fraction. What is the main finding and its importance? We observed an approximately twofold improvement in macrovascular function, assessed via brachial artery flow-mediated dilatation, and a reduction in oxidative stress after antioxidant administration in patients with heart failure with reduced ejection fraction. The improvement in macrovascular function was reversed 1 week after treatment cessation. These findings have identified the potential of oral antioxidant administration to optimize macrovascular health in this patient group. ABSTRACT: Heart failure with reduced ejection fraction (HFrEF) is characterized by macrovascular dysfunction and elevated oxidative stress that may be mitigated by antioxidant (AOx) administration. In this prospective study, we assessed flow-mediated dilatation (FMD) and reactive hyperaemia responses in 14 healthy, older control participants and 14 patients with HFrEF, followed by 30 days of oral AOx administration (1 g vitamin C, 600 I.U. vitamin E and 0.6 g α-lipoic acid) in the patient group. Blood biomarkers of oxidative stress (malondialdehyde) and AOx capacity (ferric reducing ability of plasma) were also assessed. Patients with HFrEF had a lower %FMD (2.63 ± 1.57%) than control participants (5.62 ± 2.60%), and AOx administration improved %FMD in patients with HFrEF (30 days, 4.90 ± 2.38%), effectively restoring macrovascular function to that of control participants. In a subset of patients, we observed a progressive improvement in %FMD across the treatment period (2.62 ± 1.62, 4.23 ± 2.69, 4.33 ± 2.24 and 4.97 ± 2.56% at days 0, 10, 20 and 30, respectively, n = 12) that was abolished 7 days after treatment cessation (2.99 ± 1.78%, n = 9). No difference in reactive hyperaemia was evident between groups or as a consequence of the AOx treatment. Ferric reducing ability of plasma levels increased (from 6.08 ± 2.80 to 6.70 ± 1.59 mm, day 0 versus 30) and malondialdehyde levels decreased (from 6.81 ± 2.80 to 6.22 ± 2.84 μm, day 0 versus 30) after treatment. These findings demonstrate the efficacy of chronic AOx administration in attenuating oxidative stress, improving AOx capacity and restoring macrovascular function in patients with HFrEF.
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Bunsawat et al. (2020) studied Heart failure with reduced ejection fraction (HFrEF) (n=28). Oral antioxidants (vitamin C, vitamin E, α-lipoic acid) vs. Baseline / Healthy controls was evaluated on Flow-mediated dilatation (%FMD). Oral antioxidant administration for 30 days improved flow-mediated dilatation in patients with HFrEF from 2.63% to 4.90%, restoring macrovascular function to levels similar to healthy controls.
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