Impaired coronary blood flow at higher heart rates during atrial fibrillation: Investigation via multiscale modelling.


Journal

Computer methods and programs in biomedicine
ISSN: 1872-7565
Titre abrégé: Comput Methods Programs Biomed
Pays: Ireland
ID NLM: 8506513

Informations de publication

Date de publication:
Jul 2019
Historique:
received: 09 10 2018
revised: 27 02 2019
accepted: 08 04 2019
entrez: 21 5 2019
pubmed: 21 5 2019
medline: 18 12 2019
Statut: ppublish

Résumé

Different mechanisms have been proposed to relate atrial fibrillation (AF) and coronary flow impairment, even in absence of relevant coronary artery disease (CAD). However, the underlying hemodynamics remains unclear. Aim of the present work is to computationally explore whether and to what extent ventricular rate during AF affects the coronary perfusion. AF is simulated at different ventricular rates (50, 70, 90, 110, 130 bpm) through a 0D-1D multiscale validated model, which combines the left heart-arterial tree together with the coronary circulation. Artificially-built RR stochastic extraction mimics the in vivo beating features. All the hemodynamic parameters computed are based on the left anterior descending (LAD) artery and account for the waveform, amplitude and perfusion of the coronary blood flow. Alterations of the coronary hemodynamics are found to be associated either to the heart rate increase, which strongly modifies waveform and amplitude of the LAD flow rate, and to the beat-to-beat variability. The latter is overall amplified in the coronary circulation as HR grows, even though the input RR variability is kept constant at all HRs. Higher ventricular rate during AF exerts an overall coronary blood flow impairment and imbalance of the myocardial oxygen supply-demand ratio. The combined increase of heart rate and higher AF-induced hemodynamic variability lead to a coronary perfusion impairment exceeding 90-110 bpm in AF. Moreover, it is found that coronary perfusion pressure (CPP) is no longer a good measure of the myocardial perfusion for HR higher than 90 bpm.

Sections du résumé

BACKGROUND BACKGROUND
Different mechanisms have been proposed to relate atrial fibrillation (AF) and coronary flow impairment, even in absence of relevant coronary artery disease (CAD). However, the underlying hemodynamics remains unclear. Aim of the present work is to computationally explore whether and to what extent ventricular rate during AF affects the coronary perfusion.
METHODS METHODS
AF is simulated at different ventricular rates (50, 70, 90, 110, 130 bpm) through a 0D-1D multiscale validated model, which combines the left heart-arterial tree together with the coronary circulation. Artificially-built RR stochastic extraction mimics the in vivo beating features. All the hemodynamic parameters computed are based on the left anterior descending (LAD) artery and account for the waveform, amplitude and perfusion of the coronary blood flow.
RESULTS RESULTS
Alterations of the coronary hemodynamics are found to be associated either to the heart rate increase, which strongly modifies waveform and amplitude of the LAD flow rate, and to the beat-to-beat variability. The latter is overall amplified in the coronary circulation as HR grows, even though the input RR variability is kept constant at all HRs.
CONCLUSIONS CONCLUSIONS
Higher ventricular rate during AF exerts an overall coronary blood flow impairment and imbalance of the myocardial oxygen supply-demand ratio. The combined increase of heart rate and higher AF-induced hemodynamic variability lead to a coronary perfusion impairment exceeding 90-110 bpm in AF. Moreover, it is found that coronary perfusion pressure (CPP) is no longer a good measure of the myocardial perfusion for HR higher than 90 bpm.

Identifiants

pubmed: 31104719
pii: S0169-2607(18)31468-8
doi: 10.1016/j.cmpb.2019.04.009
pii:
doi:

Substances chimiques

Oxygen S88TT14065

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

95-102

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

S Scarsoglio (S)

Department of Mechanical and Aerospace Engineering, Politecnico di Torino, Torino, Italy. Electronic address: stefania.scarsoglio@polito.it.

C Gallo (C)

Department of Mechanical and Aerospace Engineering, Politecnico di Torino, Torino, Italy.

A Saglietto (A)

Division of Cardiology, Cittá della Salute e della Scienza di Torino Hospital, Department of Medical Sciences, University of Turin, Torino, Italy.

L Ridolfi (L)

Department of Environment, Land and Infrastructure Engineering, Politecnico di Torino, Torino, Italy.

M Anselmino (M)

Division of Cardiology, Cittá della Salute e della Scienza di Torino Hospital, Department of Medical Sciences, University of Turin, Torino, Italy.

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Classifications MeSH