Abstract
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.
Highlights
During the last two decades, atrial fibrillation (AF), the most common cardiac tachyarrhythmia, has become one of the most relevant public health problems[1]
The present study aims to investigate, based on a validated computational model, if the cerebral hemodynamic alterations induced by Atrial fibrillation (AF) are modulated by mean ventricular response
The heart beating, RR [s], is defined as the temporal interval between two consecutive heart beats, while the heart rate HR [bpm] is the number of heart beats per minute. Both in normal sinus rhythm (NSR) and AF conditions, artificially-built RR intervals to span the range of average HR between 50 and 130 bpm, avoiding the patient-specific characteristics inherited by real RR beating
Summary
During the last two decades, atrial fibrillation (AF), the most common cardiac tachyarrhythmia, has become one of the most relevant public health problems[1]. Several mechanisms have been proposed to clarify this association[5,6,7], such as silent cerebral ischemia (SCI), microbleeds, altered cerebral blood flow dynamics and pro-inflammatory conditions. Among these possible contributors, the hypothesis of an altered cerebral blood flow dynamics during AF has been the least investigated, most likely due to the evident concerns related to a direct sampling in the cerebral circulatory system. Schematic representation of the cardiovascular system, together with examples of the resulting Pa time series in NSR and AF conditions (HR = 50 and 130 bpm). Schematic representation of the cerebral model evidencing the three main regions (large arteries, distal arteries, capillary-venous circulation), together with examples of the resulting Pc time series in NSR and AF conditions (HR = 50 and 130 bpm). With an altered cerebral hemodynamics, characterized by transient hypoperfusions and hypertensive events in the deep cerebral circle
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