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Chronic antioxidant administration restores macrovascular function in patients with heart failure with reduced ejection fraction
Author(s) -
Bunsawat Kanokwan,
Ratchford Stephen M.,
Alpenglow Jeremy K.,
Park Soung Hun,
Jarrett Catherine L.,
Stehlik Josef,
Drakos Stavros G.,
Richardson Russell S.,
Wray D. Walter
Publication year - 2020
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep088686
Subject(s) - ejection fraction , oxidative stress , medicine , heart failure , antioxidant , vitamin c , cardiology , malondialdehyde , brachial artery , hyperaemia , blood flow , blood pressure , chemistry , biochemistry
New FindingsWhat 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 m m , day 0 versus 30) and malondialdehyde levels decreased (from 6.81 ± 2.80 to 6.22 ± 2.84 μ m , 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.