The first mechanism I could think of would be via inflammatory response. Here's an article from 2009 in the Lancet which performs a meta-analysis. http://cite

The first mechanism I could think of would be via inflammatory response. Here's an article from 2009 in the Lancet which performs a meta-analysis. http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.490.1869&rep=rep1&type=pdf http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.490... In their discussion they say: Influenza might act as an acute inflammatory and procoagulant stimulus transiently altering endothelial function. 58,59 Recent experimental studies in mice have explored the links between influenza infection and coronary artery remodelling. In one study, 60 inoculation of influenza A virus into a mouse atherosclerosis model of mice deficient in apolipoprotein E resulted in heavy infiltration of atherosclerotic plaques by inflammatory cells, as well as platelet aggregation and thrombosis— only the plaques and not normal sections of coronary arteries were disrupted. Evidence of influenza virus RNA has been found in human atherosclerotic plaques, although it is not known if this is clinically important. 61 Another study 62 revealed that infectious burden (measured by the presence of antibodies to influenza, hepatitis A virus, Chlamydophila pneumoniae , Helicobacter pylori, and cytomegalovirus in serum) was independently associated with angiographically-proven atherosclerosis.