Document Type

Article

Publication Date

10-29-2025

Comments

This article is the author’s final published version in PloS one, Volume 20, Issue 10, 2025, Article number e0334086.

The published version is available at https://doi.org/10.1371/journal.pone.0334086. Copyright © 2025 Adeodu et al.

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.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.

PubMed ID

41160578

Language

English

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