ArticleJournal of human hypertension2021
A greater burden of atrial fibrillation is associated with worse endothelial dysfunction in hypertension.
Article in Journal of human hypertension, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- One-year Aerobic Interval Training Improves Endothelial Dysfunction in Patients with Atrial Fibrillation: A Randomized Trial.Internal medicine (Tokyo, Japan) · 2023Trial
- Cyclooxygenase-dependent contribution to increased flow mediated dilatation following a week of repeated ischemic preconditioning.European journal of applied physiology · 2026Article
- Hypertension Exacerbates Endothelial Dysfunction in Patients With Atrial Fibrillation.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- The effect of hypertension on cerebrovascular carbon dioxide reactivity in atrial fibrillation patients.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Atrial Fibrillation and Early Vascular Aging: Clinical Implications, Methodology Issues and Open Questions-A Review from the VascAgeNet COST Action.Journal of clinical medicine · 2024Review
- Relationship of Warfarin and Apixaban with Vascular Function in Patients with Atrial Fibrillation.Journal of vascular research · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrillation (AF) and hypertension often co-exist and both are associated with endothelial dysfunction. We hypothesised that AF would further worsen endothelium-dependent flow-mediated dilatation (FMD) in hypertension patients compared to those without AF. In a cross-sectional comparison, we measured brachial artery diameter at rest and during reactive hyperaemia following 5 min of arterial occlusion in two patient groups: AF (and hypertension) (n = 61) and hypertension control groups (n = 33). The AF (and hypertension) subgroups: permanent AF (n = 30) and paroxysmal AF (n = 31) were also assessed. The permanent AF patients received heart rate and blood pressure (BP) control optimisation and were then followed up after eight weeks for repeat FMD testing. There was no significant difference in FMD between AF (and hypertension) group and hypertension control group (4.6%, 95% CI [2.6-5.9%] vs 2.6%, 95% CI [1.9-5.3%]; p = 0.25). There was a significant difference in FMD between permanent AF and paroxysmal AF groups (3.1%, 95% CI [2.3-4.8%] vs 5.9%, 95% CI [4.0-8.1%]; p = 0.02). Endothelium-dependent FMD response showed a non-significant improvement trend following eight weeks of heart rate and BP optimisation (3.1%, 95% CI [2.3-4.8%] (baseline) vs 5.2%, 95% CI [3.9-6.5%] (follow up), p = 0.09). Presence of AF generally does not incrementally worsen endothelial dysfunction in hypertension patients, although the duration and frequency of AF (paroxysmal AF to permanent AF) does lead to worsening endothelial function. Eight weeks of BP optimisation did not significantly improve endothelial dysfunction as measured by FMD.
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