The research deals with interdisciplinary fluid dynamics aspects of the cardiovascular system, by combining an integrated clinical-computational framework to investigate the human hemodynamic response to different physiological, pathological and extreme conditions (e.g., microgravity).
- Ground-based analogs and countermeasures against cardiovascular deconditioning in long-term human spaceflights (ESA Discovery Programme 2023 co-funded project)
Long-term human spaceflight induces a number of cardiovascular alterations, from blood volume reduction to cardiac atrophy, leading to cardiovascular deconditioning, that is the adaptation of the cardiovascular system to a less demanding environment. The main driver of these changes is the fluid shift from lower to upper body, which is as well believed to be the underlying cause of the Spaceflight Associated Neuro-ocular Syndrome (SANS), classified today among the major risks of the human space exploration.
For none of the countermeasures - currently adopted or investigated to mitigate cardiovascular deconditioning in view of future Moon/Mars missions - definitive findings on the optimal functioning are known. In particular, though artificial gravity is one of the most promising countermeasures, the current knowledge mainly relies on ground-based analogs. Moreover, being the association between cerebral hemodynamics and SANS a recent frontier for which the underlying mechanisms are barely understood, no ad hoc strategies to contrast cerebral hemodynamic alterations have been so far implemented.
The project aims to develop a computational approach, based on our validated multiscale cardiovascular model, able to accurately reproduce the hemodynamic response to short- and long-term microgravity exposure. The model will be validated by means of ground-based analogs cardiovascular measures - such as short-term head up tilt, short- and mid-term head down tilt bed rest, and parabolic flight - exploiting clinical data from volunteer subjects campaigns already carried out, in progress or planned, measured in collaboration with our academic partners (Cardiology Division, “Città della Salute e della Scienza” Hospital, Torino, Italy; Internal Medicine Division, “Città della Salute e della Scienza” Hospital, Torino, Italy; Space, Attention and Action Lab, Department of Psychology, University of Turin, Italy).
The project objectives are to: (i) investigate the altered cerebral hemodynamics at broad and then its role on the onset of SANS; and (ii) individuate the optimal countermeasure configuration, among the currently implementable, against cardiovascular deconditioning and neurovestibular dysfunctions induced by hemodynamic alterations (e.g., SANS) for the next manned missions. Results will shed light on the underlying mechanisms altering cerebral hemodynamics and contribute to the design of the most effective cardiovascular countermeasures for long-term missions (including short-term adaptations to each spaceflight phase) to Moon/Mars.
- Cerebral fluid dynamics: investigating the link between atrial fibrillation and dementia (PRIN 2022 funded project)
Atrial fibrillation (AF), characterized by an irregular heart rhythm, is the most common cardiac arrhythmia, counting nearly 60 million prevalent cases worldwide in 2019 and with epidemiological projections foreseeing a further rise during the next decades. Dementia is a progressive neurological degeneration leading to decline in memory, reasoning, communication, and capacity to carry out daily activities, which currently affects more than 50 million people worldwide and with 150 million cases estimated in 2050. Both diseases share several common risk factors, many of which are
modifiable, except for age and genetic factors. Through a constellation of potential underlying hemodynamic mechanisms - such as silent microembolic cerebral infarctions, altered cerebral blood flow, hypoperfusion and microbleeds - there is growing evidence that AF is independently associated with an increased risk of dementia and cognitive impairment, even in the absence of clinical strokes. However, causality mechanisms have not been established yet, and the impact of AF treatments on dementia development is far from being clear. Among the possible contributors, the hypothesis of an altered cerebral blood flow due to the AF irregular beating is the most intriguing and the least investigated. The complex interplay between pressure-flow wave propagation in a network of tapered viscoelastic vessels with different size and the irregular pulsatile flow makes AF effects on the brain microcirculation presently unknown. In fact, currently adopted clinical techniques to assess cerebral hemodynamics in vivo, such as transcranial Doppler and magnetic resonance imaging, lack the resolving power to provide insights on the deep cerebral regions.
The project is a joint and interdisciplinary collaboration between Politecnico di Torino (Prof. S. Scarsoglio, DIMEAS, Polito BioMedLab) and the University of Turin (Prof. M. Anselmino, Cardiology Unit of the “Città della Salute e della Scienza di Torino” Hospital). The main goal is to understand and computationally quantify mechanistic AF-induced effects on the cerebral microcirculation underlying the association between AF and cognitive decline. Thus, the research proposal aims to contribute at filling the gaps in the pathophysiological knowledge of the cerebral hemodynamics during AF and providing scientific evidence to improve clinical AF management in order to reduce the impact on cerebral circulation. In this respect, a delay of the onset of dementia by just few years would have huge socio-economic implications, in terms of the patient’s quality of life and burden of health care costs. The present topic has an important medical relevance due to the AF increasing prevalence in the population and, at the same time, its accurate modeling is extremely challenging both from the fluid dynamics and mathematical viewpoints.