346 research outputs found
Impaired coronary blood flow at higher heart rates during atrial fibrillation: investigation via multiscale modelling
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. 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 \emph{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. 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. 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.Comment: 8 pages, 5 figures, 3 table
Alteration of cerebrovascular haemodynamic patterns due to atrial fibrillation: an in silico investigation
There has recently been growing evidence that atrial fibrillation (AF), the
most common cardiac arrhythmia, is independently associated with the risk of
dementia. This represents a very recent frontier with high social impact for
the number of individuals involved and for the expected increase in AF
incidence in the next 40 years. Although a number of potential haemodynamic
processes, such as microembolisms, altered cerebral blood flow, hypoperfusion
and microbleeds, arise as connecting links between the two pathologies, the
causal mechanisms are far from clear. An in silico approach is proposed that
combines in sequence two lumped-parameter schemes, for the cardiovascular
system and the cerebral circulation. The systemic arterial pressure is obtained
from the cardiovascular system and used as the input for the cerebral
circulation, with the aim of studying the role of AF on the cerebral
haemodynamics with respect to normal sinus rhythm (NSR), over a 5000 beat
recording. In particular, the alteration of the haemodynamic (pressure and
flowrate) patterns in the microcirculation during AF is analysed by means of
different statistical tools, from correlation coefficients to autocorrelation
functions, crossing times, extreme values analysis and multivariate linear
regression models. A remarkable signal alteration, such as a reduction in
signal correlation (NSR, about 3 s; AF, less than 1 s) and increased
probability (up to three to four times higher in AF than in NSR) of extreme
value events, emerges for the peripheral brain circulation. The described
scenario offers a number of plausible cause-effect mechanisms that might
explain the occurrence of critical events and the haemodynamic links relating
to AF and dementia.Comment: 13 pages, 9 Figures, 3 Table
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