TY - JOUR

T1 - Influenza and cardiovascular disease pathophysiology

T2 - strings attached

AU - Skaarup, Kristoffer Grundtvig

AU - Modin, Daniel

AU - Nielsen, Lene

AU - Jensen, Jens Ulrik Staehr

AU - Biering-Sorensen, Tor

PY - 2023

Y1 - 2023

N2 - 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.

AB - 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.

KW - Cardiovascular Disease

KW - Pathophysiology

KW - Influenza Infection

KW - Heart Failure

KW - Acute Myocardial Infarction

KW - MYOCARDIAL-INFARCTION

KW - VIRUS-INFECTION

KW - CHLAMYDIA-PNEUMONIAE

KW - EXCESS MORTALITY

KW - STREPTOCOCCUS-PNEUMONIAE

KW - ATHEROSCLEROTIC PLAQUES

KW - INFLAMMATORY CYTOKINES

KW - ENDOTHELIAL-CELLS

KW - ACTIVATION

KW - EXPRESSION

U2 - 10.1093/eurheartjsupp/suac117

DO - 10.1093/eurheartjsupp/suac117

M3 - Journal article

C2 - 36937370

VL - 25

SP - A5-A11

JO - European Heart Journal Supplements

JF - European Heart Journal Supplements

SN - 1554-2815

ER -