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Sympathetic activation: a potential link between comorbidities and COVID-19
Andrea Porzionato1, Aron Emmi1, Silvia Barbon1
1Section of Anatomy, Department of Neuroscience, University of Padova, Italy.
Insights
Sympathetic nervous system overactivation may worsen outcomes in coronavirus disease 2019 (COVID-19) patients with existing health conditions. This heightened sympathetic activity could create a detrimental cycle, impacting multiple organ systems and increasing disease severity.
Area of Science:
- Cardiovascular Science
- Neuroscience
- Infectious Diseases
Background:
- Coronavirus disease 2019 (COVID-19) severity is linked to age, male gender, and comorbidities like hypertension and diabetes.
- These comorbidities often involve heightened sympathetic nervous system (SNS) activity.
- The SNS role in COVID-19 pathophysiology remains under-explored.
Purpose of the Study:
- To investigate the potential role of sympathetic overactivation in the pathophysiology of COVID-19.
- To explore how SNS activity might exacerbate COVID-19 in patients with comorbidities.
Main Methods:
- This study is based on a review and conceptual analysis of existing literature.
- It synthesizes information on COVID-19, comorbidities, and the sympathetic nervous system.
Main Results:
- Increased sympathetic discharge is a common feature of COVID-19 comorbidities.
- COVID-19 itself may trigger SNS overactivation through various mechanisms.
- SNS overactivation can negatively impact the lungs, heart, kidneys, and immune system.
Conclusions:
- Sympathetic overactivation is a potential, overlooked factor in COVID-19.
- It may contribute to a vicious cycle between COVID-19 and pre-existing conditions.
- Further research into the SNS role is crucial for understanding COVID-19 severity.
Abstract:
In coronavirus disease 2019 (COVID-19), higher morbidity and mortality are associated with age, male gender, and comorbidities, such as chronic lung diseases, cardiovascular pathologies, hypertension, kidney diseases, diabetes mellitus, and obesity. All of the above conditions are characterized by increased sympathetic discharge, which may exert significant detrimental effects on COVID-19 patients, through actions on the lungs, heart, blood vessels, kidneys, metabolism, and/or immune system. Furthermore, COVID-19 may also increase sympathetic discharge, through changes in blood gases (chronic intermittent hypoxia, hyperpnea), angiotensin-converting enzyme (ACE)1/ACE2 imbalance, immune/inflammatory factors, or emotional distress. Nevertheless, the potential role of the sympathetic nervous system has not yet been considered in the pathophysiology of COVID-19. In our opinion, sympathetic overactivation could represent a so-far undervalued mechanism for a vicious circle between COVID-19 and comorbidities.
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