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Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses
Published on: January 20, 2017
Influenza and cardiovascular disease pathophysiology: strings attached
Kristoffer Grundtvig Skaarup1,2, Daniel Modin1,2, Lene Nielsen3
1Cardiovascular Non-Invasive Imaging Research Laboratory, Department of Cardiology, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark.
Insights
Influenza infection elevates the risk of cardiovascular events, including death, heart attack, and heart failure. Mechanisms involve direct cardiac effects and systemic responses like inflammation and hypercoagulability.
Area of Science:
- Cardiology
- Infectious Diseases
- Pathophysiology
Background:
- A century of evidence links influenza infection to cardiovascular morbidity.
- Influenza's impact on cardiovascular health remains a significant concern.
Purpose of the Study:
- To review cardiovascular complications associated with influenza.
- To explore potential mechanisms underlying the influenza-cardiovascular link.
Main Methods:
- This study is a narrative review.
- It synthesizes existing literature on influenza and cardiovascular outcomes.
Main Results:
- Common complications include cardiovascular death, myocardial infarction, and heart failure hospitalization.
- Proposed mechanisms include direct cardiac infection, endothelial dysfunction, hypoxemia, and systemic inflammation.
- The relative contribution of each mechanism is not yet clear.
Conclusions:
- Influenza infection significantly increases the risk of acute cardiovascular morbidity and mortality.
- Pathophysiological mechanisms support this association, with systemic responses potentially playing a key role.
Abstract:
A link between influenza infection and cardiovascular morbidity has been known for almost a century. This narrative review examined the cardiovascular complications associated with influenza and the potential mechanisms behind this relationship. The most common reported cardiovascular complications are cardiovascular death, myocardial infarction, and heart failure hospitalization. There are multiple proposed mechanisms driving the increased risk of cardiovascular complications. These mechanics involve influenza-specific effects such as direct cardiac infection and endothelial dysfunction leading to plaque destabilization and rupture, but also hypoxaemia and systemic inflammatory responses including increased metabolic demand, biomechanical stress, and hypercoagulability. The significance of the individual effects is unclear, and thus whether influenza directly or indirectly causes cardiovascular events is unknown. In conclusion, the risk of acute cardiovascular morbidity and mortality is elevated during influenza infection. The proposed underlying pathophysiological mechanisms support this association, but systemic responses to infection may drive this relationship.
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