Carotid atherosclerosis has a relevant impact on cerebral blood flow regulation. There is accruing evidence that hemodynamic impairment related to the presence of a significant carotid lumen narrowing may predispose to the development of cerebral dysfunctions, including a reduction in cognitive abilities. In the last years an increasing number of findings showed that carotid stenosis did contribute to cognitive impairment not only in relation to the occurrence of cerebral ischemic lesions, but also as an independent risk factor. The principal mechanisms involved are chronic hypoperfusion, microembolization and cerebrovascular reactivity impairment. Moreover, more recent studies showed alterations of regional functional connectivity. In this narrative review, we analyzed the relationships between carotid stenosis, cerebral hemodynamic derangement and cognitive impairment onset and progression, and underlined that cognitive impairment is the final result of the complex interaction between different elements, including also collateral circulation, cerebral hemodynamic status, brain connectivity and pro-inflammatory state. Further, therapeutic approaches, with a specific focus on vascular risk factors correction and on the effectiveness of surgical or endovascular interventions were discussed. We particularly focused our attention on the concept of "asymptomatic carotid stenosis", and how could a cognitive impairment improve after an intervention, and how this could change the indications to surgical approach. Larger studies and randomized controlled trials are urgently required to better define time, characteristics and effectiveness of both medical and surgical/ endovascular approaches.
Impact of carotid stenosis on cerebral hemodynamic failure and cognitive impairment progression: a narrative review / Viticchi, Giovanna; Falsetti, Lorenzo; Potente, Eleonora; Bartolini, Marco; Silvestrini, Mauro. - In: ANNALS OF TRANSLATIONAL MEDICINE. - ISSN 2305-5839. - ELETTRONICO. - 9:14(2021), pp. 1209-1209. [10.21037/atm-20-7226]
Impact of carotid stenosis on cerebral hemodynamic failure and cognitive impairment progression: a narrative review
Viticchi, Giovanna;Falsetti, Lorenzo;Potente, Eleonora;Bartolini, Marco;Silvestrini, Mauro
2021-01-01
Abstract
Carotid atherosclerosis has a relevant impact on cerebral blood flow regulation. There is accruing evidence that hemodynamic impairment related to the presence of a significant carotid lumen narrowing may predispose to the development of cerebral dysfunctions, including a reduction in cognitive abilities. In the last years an increasing number of findings showed that carotid stenosis did contribute to cognitive impairment not only in relation to the occurrence of cerebral ischemic lesions, but also as an independent risk factor. The principal mechanisms involved are chronic hypoperfusion, microembolization and cerebrovascular reactivity impairment. Moreover, more recent studies showed alterations of regional functional connectivity. In this narrative review, we analyzed the relationships between carotid stenosis, cerebral hemodynamic derangement and cognitive impairment onset and progression, and underlined that cognitive impairment is the final result of the complex interaction between different elements, including also collateral circulation, cerebral hemodynamic status, brain connectivity and pro-inflammatory state. Further, therapeutic approaches, with a specific focus on vascular risk factors correction and on the effectiveness of surgical or endovascular interventions were discussed. We particularly focused our attention on the concept of "asymptomatic carotid stenosis", and how could a cognitive impairment improve after an intervention, and how this could change the indications to surgical approach. Larger studies and randomized controlled trials are urgently required to better define time, characteristics and effectiveness of both medical and surgical/ endovascular approaches.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.