“…2 Multiple pathophysiological mechanisms have been proposed to explain the associated increase in CV outcomes in individuals with influenza infection, such as atherosclerotic plaque rupture and an increased risk of atherothrombosis (secondary to the release of pro-inflammatory cytokines resulting in a pro-thrombotic milieu, influx of inflammatory cells, plaque destabilization, and endothelial dysfunction), increased metabolic demand due to sympathetic activation (leading to tachycardia and hypoxaemia, exacerbating supply-demand mismatch), or by direct viral effect or triggering of myocarditis. 3,4 Influenza vaccination (IV) is widely acknowledged as the most effective way to prevent seasonal influenza, reduce disease severity, and lower the incidence of complications and deaths. 1 It is, therefore, intuitive that IV might reduce the risk of CV events in at-risk patients, although until recently randomized controlled trials (RCTs) specifically addressing this hypothesis were small and varied in quality.…”