Hemodynamics-driven mathematical model of third heart sound generation.
cardiac vibration
heart sound (HS)
mathematical modelling (medical)
pathological heart sound
third heart sound
Journal
Frontiers in physiology
ISSN: 1664-042X
Titre abrégé: Front Physiol
Pays: Switzerland
ID NLM: 101549006
Informations de publication
Date de publication:
2022
2022
Historique:
received:
01
01
2022
accepted:
25
07
2022
entrez:
28
10
2022
pubmed:
29
10
2022
medline:
29
10
2022
Statut:
epublish
Résumé
The proto-diastolic third heart sound (S3) is observed in various hemodynamic conditions in both normal and diseased hearts. We propose a novel, one-degree of freedom mathematical model of mechanical vibrations of heart and blood that generates the third heart sound, implemented in a real-time model of the cardiovascular system (CircAdapt). To examine model functionality, S3 simulations were performed for conditions mimicking the normal heart as well as heart failure with preserved ejection fraction (HFpEF), atrioventricular valve regurgitation (AVR), atrioventricular valve stenosis (AVS) and septal shunts (SS). Simulated S3 showed both qualitative and quantitative agreements with measured S3 in terms of morphology, frequency, and timing. It was shown that ventricular mass, ventricular viscoelastic properties as well as inflow momentum play a key role in the generation of S3. The model indicated that irrespective of cardiac conditions, S3 vibrations are always generated, in both the left and right sides of the heart, albeit at different levels of audibility. S3 intensities increased in HFpEF, AVR and SS, but the changes of acoustic S3 features in AVS were not significant, as compared with the reference simulation. S3 loudness in all simulated conditions was proportional to the level of cardiac output and severity of cardiac conditions. In conclusion, our hemodynamics-driven mathematical model provides a fast and realistic simulation of S3 under various conditions which may be helpful to find new indicators for diagnosis and prognosis of cardiac diseases.
Identifiants
pubmed: 36304577
doi: 10.3389/fphys.2022.847164
pii: 847164
pmc: PMC9595280
doi:
Types de publication
Journal Article
Langues
eng
Pagination
847164Informations de copyright
Copyright © 2022 Shahmohammadi, Huberts, Luo, Westphal, Cornelussen, Prinzen and Delhaas.
Déclaration de conflit d'intérêts
Author RC was employed by the company Medtronic, BV. Author PW received research grants from Medtronic, Abbott, Biotronik and Microport CRM. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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