105 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
Rate Control Management of Atrial Fibrillation: May a Mathematical Model Suggest an Ideal Heart Rate?
Background. Despite the routine prescription of rate control therapy for
atrial fibrillation (AF), clinical evidence demonstrating a heart rate target
is lacking. Aim of the present study was to run a mathematical model simulating
AF episodes with a different heart rate (HR) to predict hemodynamic parameters
for each situation.
Methods. The lumped model, representing the pumping heart together with
systemic and pulmonary circuits, was run to simulate AF with HR of 50, 70, 90,
110 and 130 bpm, respectively.
Results. Left ventricular pressure increased by 56.7%, from 33.92+-37.56 mmHg
to 53.15+-47.56 mmHg, and mean systemic arterial pressure increased by 27.4%,
from 82.66+-14.04 mmHg to 105.29+-7.63 mmHg, at the 50 and 130 bpm simulations,
respectively. Stroke volume (from 77.45+-8.5 to 39.09+-8.08 mL), ejection
fraction (from 61.1+-4.4 to 39.32+-5.42%) and stroke work (SW, from 0.88+-0.04
to 0.58+-0.09 J) decreased by 49.5, 35.6 and 34.2%, at the 50 and 130 bpm
simulations, respectively. In addition, oxygen consumption indexes (rate
pressure product, RPP, tension time index per minute, TTI/min, and pressure
volume area per minute, PVA/min) increased from the 50 to the 130 bpm
simulation, respectively, by 185.7% (from 5598+-1939 to 15995+-3219 mmHg/min),
55.5% (from 2094+-265 to 3257+-301 mmHg s/min) and 102.4% (from 57.99+-17.9 to
117.37+-25.96 J/min). In fact, left ventricular efficiency (SW/PVA) decreased
from 80.91+-2.91% at 50 bpm to 66.43+-3.72% at the 130 bpm HR simulation.
Conclusion. Awaiting compulsory direct clinical evidences, the present
mathematical model suggests that lower HRs during permanent AF relates to
improved hemodynamic parameters, cardiac efficiency, and lower oxygen
consumption.Comment: 9 page
Higher ventricular rate during atrial fibrillation relates to increased cerebral hypoperfusions and hypertensive events
Atrial fibrillation (AF) is associated with cognitive impairment/dementia,
independently of clinical cerebrovascular events (stroke/TIA). One of the
plausible mechanisms is the occurrence of AF-induced transient critical
hemodynamic events; however, it is presently unknown, if ventricular response
rate during AF may impact on cerebral hemodynamics. AF was simulated at
different ventricular rates (50, 70, 90, 110, 130 bpm) by two coupled lumped
parameter validated models (systemic and cerebral circulation), and compared to
corresponding control normal sinus rhythm simulations (NSR). Hemodynamic
outcomes and occurrence of critical events (hypoperfusions and hypertensive
events) were assessed along the internal carotid artery-middle cerebral artery
pathway up to the capillary-venous bed. At the distal cerebral circle level
(downstream middle cerebral artery), increasing ventricular rates lead to a
reduced heart rate-related dampening of hemodynamic signals compared to NSR
(p=0.003 and 0.002 for flow rate and pressure, respectively). This response
causes a significant progressive increase in critical events in the distal
cerebral circle (p<0.001) as ventricular rate increases during AF. On the other
side, at the lowest ventricular response rates (HR 50 bpm), at the
systemic-proximal cerebral circle level (up to middle cerebral artery)
hypoperfusions (p<0.001) occur more commonly, compared to faster AF
simulations. This computational study suggests that higher ventricular rates
relate to a progressive increase in critical cerebral hemodynamic events
(hypoperfusions and hypertensive events) at the distal cerebral circle. Thus, a
rate control strategy aiming to around 60 bpm could be beneficial in terms on
cognitive outcomes in patients with permanent AF.Comment: 9 pages, 4 figures, 2 table
Hemodynamic impact of valve diseases during persistent atrial fibrillation: a computational approach
Higher resting heart rate relates to greater rise in pulmonary vein pressure under exercise during permanent atrial fibrillation: a computational study
BACKGROUND. Clinical data indicating a heart rate (HR) target during rate control therapy for permanent atrial fibrillation (AF) and regarding its eventual relationship with reduced exercise tolerance are lacking.
OBJECTIVE. The present study aims at investigating the impact of resting HR on cardiovascular response to exercise in permanent AF patients by a computational cardiovascular model.
METHODS. The AF lumped-parameter model was run to simulate resting (1 Metabolic Equivalent of Task-MET) and various exercise conditions (4 METs: brisk walking; 6 METs: skiing; 8 METs: running) starting from different resting HR (70 bpm for the slower resting HR-SHR-simulations, and 100 bpm for the higher resting HR-HHR-simulations). To allow comparison of relative variations of cardiovascular variables upon exertion, the variation comparative index (VCI)-the absolute variation between the exercise and the resting values in SHR simulations referred to the absolute variation in HHR simulations-was calculated at each exercise grade (VCI 4 , VCI 6 and VCI 8).
RESULTS. Pulmonary vein pressure (VCI 4 = 0.71, VCI 6 = 0.73 and VCI 8 = 0.77) underwent a greater increase, while systemic arterial pressure variations (VCI 4 = 1.15, VCI 6 = 1.36, VCI 8 = 1.56) experienced a less sustained increase than expected in HHR compared to SHR simulations.
CONCLUSIONS. In terms of exercise tolerance, a slower resting HR could be preferable in permanent AF patients, since pulmonary vein pressure undergoes a slighter increase and systemic blood pressure a more appropriate increase with respect to a higher resting HR
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