Cerebral hemodynamics during atrial fibrillation: Computational fluid dynamics analysis of lenticulostriate arteries using 7 T high-resolution magnetic resonance imaging.

Atrial fibrillation (AF) is the most common cardiac arrhythmia, inducing irregular and faster heart beating. Aside from disabling symptoms-such as palpitations, chest discomfort, and reduced exercise capacity-there is growing evidence that AF increases the risk of dementia and cognitive decline, even in the absence of clinical strokes. Among the possible mechanisms, the alteration of deep cerebral hemodynamics during AF is one of the most fascinating and least investigated hypotheses. Lenticulostriate arteries (LSAs)-small perforating arteries perpendicularly departing from the anterior and middle cerebral arteries and supplying blood flow to basal ganglia-are especially involved in silent strokes and cerebral small vessel diseases, which are considered among the main vascular drivers of dementia. We propose for the first time a computational fluid dynamics analysis to investigate the AF effects on the LSAs hemodynamics by using 7 T high-resolution magnetic resonance imaging (MRI). We explored different heart rates (HRs)-from 50 to 130 bpm-in sinus rhythm and AF, exploiting MRI data from a healthy young male and internal carotid artery data from validated 0D cardiovascular-cerebral modeling as inflow condition. Our results reveal that AF induces a marked reduction of wall shear stress and flow velocity fields. This study suggests that AF at higher HR leads to a more hazardous hemodynamic scenario by increasing the atheromatosis and thrombogenesis risks in the LSAs region.

Wall-induced anisotropy effects on turbulent mixing in channel flow: A network-based analysis.

Turbulent mixing is studied in the Lagrangian framework with an approach based on the complex network formalism. We consider the motion of passive, noninertial particles inside a turbulent channel simulated at Re_{τ}=950. The time-dependent network is built to evaluate the transfer of tracers between thin wall-parallel layers which partition the channel in the wall-normal direction. By doing so, we are able to assess the spatial and temporal complexities arising from turbulence dynamics and their influence on the mixing process. This approach highlights the effects of small-scale features of turbulent flow structures and also the larger scale effects determined by wall-induced anisotropy. Complex networks, coupled to the Lagrangian description of turbulence, are effective in providing novel insights into inhomogeneous turbulence and mixing.

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 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.

Spatial characterization of turbulent channel flow via complex networks.

A network-based analysis of a turbulent channel flow numerically solved at Re_{τ}=180 is proposed as an innovative perspective for the spatial characterization of the flow field. Two spatial networks corresponding to the streamwise and wall-normal velocity components are built, where nodes represent portions of volume of the physical domain. For each network, links are active if the correlation coefficient of the corresponding velocity component between pairs of nodes is sufficiently high, thus unveiling the strongest kinematic relations. Several network measures are studied in order to explore the interrelations between nodes and their neighbors. Specifically, long-range links are localized between near-wall regions and associated with the temporal persistence of coherent patterns, namely high and low speed streaks. Furthermore, long-range links play a crucial role as intermediary for the kinematic information flow, as emerges from the analysis of indirect connections between nodes. The proposed approach provides a framework to investigate spatial structures of the turbulent dynamics, showing the full potential of complex networks. Although the network analysis is based on the two-point correlation, it is able to advance the level of information, by exploiting the texture created by active links in all directions. Based on the observed findings, the current approach can pave the way for an enhanced spatial interpretation of the turbulence dynamics.

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 flow rate) 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.

Fluid dynamics of heart valves during atrial fibrillation: a lumped parameter-based approach.

Atrial fibrillation (AF) consequences on the heart valve dynamics are usually studied along with a valvular disfunction or disease, since in medical monitoring, the two pathologies are often concomitant. Aim of the present work is to study, through a stochastic lumped-parameter approach, the basic fluid dynamics variations of heart valves, when only paroxysmal AF is present with respect to the normal sinus rhythm in absence of any valvular pathology. Among the most common parameters interpreting the valvular function, the most useful turns out to be the regurgitant volume. During AF, both atrial valves do not seem to worsen their performance, while the ventricular efficiency is remarkably reduced.