Different Impact of Heart Rate Variability in the Deep Cerebral and Central Hemodynamics at Rest: An in silico Investigation

TL;DR

This in silico study investigates how variations in heart rate variability affect deep cerebral and central hemodynamics at rest, revealing that increased HRV can be more detrimental to cerebral pressure but decreases cardiac efficiency.

Contribution

The paper introduces a computational model to analyze the impact of HRV alterations on cerebral and central hemodynamics, highlighting the optimal HRV condition at baseline.

Findings

Increased HRV leads to higher probability of extreme pressure and flow events in cerebral circulation.

Decreased HRV increases cardiac effort without improving heart performance.

Baseline HRV appears optimal for maintaining balanced cerebral and cardiac hemodynamics.

Abstract

Heart rate variability (HRV), defined as the variability between consecutive heartbeats, is a surrogate measure of cardiac vagal tone. It is widely accepted that a decreased HRV is associated to several risk factors and cardiovascular diseases. However, a possible association between HRV and altered cerebral hemodynamics is still debated, suffering from HRV short-term measures and the paucity of high-resolution deep cerebral data. We propose a computational approach to evaluate the deep cerebral and central hemodynamics subject to physiological alterations of HRV in an ideal young healthy patient at rest. The cardiovascular-cerebral model was validated and recently exploited to understand the hemodynamic mechanisms between cardiac arrythmia and cognitive deficit. Three configurations (baseline, increased HRV, and decreased HRV) are built based on the standard deviation (SDNN) of RR beats. In the cerebral circulation, our results show that HRV has overall a stronger impact on pressure than flow rate mean values but similarly alters pressure and flow rate in terms of extreme events. By comparing reduced and increased HRV, this latter induces a higher probability of altered mean and extreme values, and is therefore more detrimental at distal cerebral level. On the contrary, at central level a decreased HRV induces a higher cardiac effort without improving the mechano-contractile performance, thus overall reducing the heart efficiency. Present results suggest that: (i) the increase of HRV per se does not seem to be sufficient to trigger a better cerebral hemodynamic response; (ii) by accounting for both central and cerebral circulations, the optimal HRV configuration is found at baseline. Given the relation inversely linking HRV and HR, the presence of this optimal condition can contribute to explain why the mean HR of the general population settles around the baseline value (70 bpm).