ArticlePloS one2025
Short term hemodynamic effects of atrial fibrillation in a closed-loop human cardiac-baroreflex system.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- A Lumped-Parameter Cardiovascular Model for Investigating Hemodynamic Alterations During Atrial Fibrillation.Bioengineering (Basel, Switzerland) · 2026Article
- Closed-loop modeling of central and intrinsic cardiac nervous system circuits underlying cardiovascular control.AIChE journal. American Institute of Chemical Engineers · 2023Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Atrial fibrillation (AF) remains the leading cardiac cause of stroke and AF-related death rate in the United States has been increasing for over twenty years. While the effect of standalone AF on heart rate is well established, there is a lack of clarity on its impact on other critical hemodynamic metrics. This is ostensibly due to interaction with other common comorbidities, especially hypertension. In addition, AF has a complex relationship with the state of the baroreflex. Evidence indicates that baroreflex sensitivity (BRS), the ability of the intrinsic cardiac control system to initiate parasympathetic response, is suppressed during AF. Therefore, a proper assessment of the hemodynamic impact of AF must take the state of the baroreflex into consideration. In this paper, we present a lumped parameter model of the human cardiovascular-baroreflex system that adequately translates AF-induced electrophysiological changes to measurable hemodynamic effects. We consider the stochastic effects of the electrical disruption in the sinus node, the absence of atrial contraction and BRS suppression. Our model provides insight into the impact of standalone AF on key benchmarks: heart rate, arterial pressure and stroke volume, under varying degrees of BRS suppression. In addition, the development of a tractable mathematical model is essential for the in-silico evaluation of emerging neuromodulation therapies for AF. Our model predictions are in agreement with published clinical data and suggest that high blood pressure during standalone AF is strongly dependent on the extent of damage to the baroreflex, which may explain conflicting reports of AF-related hypertension and normotension.
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Registered trials
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