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Assessment of neurovascular control and cerebral blood flow autoregulation during different physiological maneuvers in patients with heart failure

Grant number: 20/03375-9
Support Opportunities:Scholarships abroad - Research
Effective date (Start): November 03, 2022
Effective date (End): December 02, 2022
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Edgar Toschi Dias
Grantee:Edgar Toschi Dias
Host Investigator: Ronney Bernardes Panerai
Host Institution: Diretoria de Pós-Graduação e Pesquisa. Universidade Metodista de São Paulo (UMESP). Instituto Metodista de Ensino Superior (IMS). São Bernardo do Campo , SP, Brazil
Research place: University of Leicester, England  


Heart failure (HF) is a complex clinical syndrome, classically defined as the heart's inability to supply adequate blood supply to meet the body's metabolic needs. The systemic repercussion of this failure of cardiac function has been the focus of scientific interest, especially in the attempt to understand possible mechanisms involved in target organ damage, such as the brain. Thus, HF is considered a risk factor for ischemic stroke and is associated with the cognitive decline of patients affected by this syndrome, in part, by a reduction in cerebral blood flow (CBF). It is known that autoregulation of the CBF occurs through the interaction of three complex physiological mechanisms, myogenic, metabolic and neurogenic. In the neurogenic mechanism, the innervation of brain vessels by the sympathetic nervous system may also contribute to cerebral autoregulation. A justification for this hypothesis is that blocking the cervical sympathetic ganglion or ±-adrenergic receptors in brain vessels results in an increase in CBF for a given increase in blood pressure. Furthermore, it has been documented that in healthy individuals, by directly stimulating carotid baroreceptors through the neck suction method to increase cardiac sympathetic modulation, there is an increase in the speed of the CBF and that after the adrenergic block these effects are buffered. Thus, based on these findings, we can imagine that pathologies associated with changes in sympathetic tonus, as in the case of HF, can alter cerebral perfusion and compromise cerebral autoregulation and be associated with cognitive decline. However, what calls our attention is that even though there is scientific evidence that patients with HF in more advanced stages have a reduction in the CBF, until now, little is known about the role of the neurogenic mechanism in the autoregulation of the CBF both at rest as during physiological maneuvers in these patients. Therefore, the study of sympathetic nerve activity quantified directly and simultaneously with the evaluation of the autoregulation of the CBF, as well as its temporal evolution, can bring not only greater knowledge about brain neurovascular physiology, but also elucidate this possible pathophysiological mechanism responsible by the reduction of cerebral autoregulation in patients with HF. Besides, another important scientific contribution of the present study will be the development of a new analysis tool for brain hemodynamics considering sympathetic nervous activity as one of the variables involved in the dynamic regulation of CBF that can be used both in healthy individuals and in patients with HF in rest conditions or during different physiological maneuvers. (AU)

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