4 ms·

I can't get to the full article here, but naively, I'd expect "Illness increasing stress on the bodily systems increases likelihood of heart attack" to be the u

I can't get to the full article here, but naively, I'd expect "Illness increasing stress on the bodily systems increases likelihood of heart attack" to be the unsurprising result. Is there some other reason that we'd expect this not to be the case? Are there other infections as agressive that don't increase the risk in similar ways? Or did we just suspect this and haven't had the data to back it up before? i.e. I'm not sure why this is interesting or revelatory? The free summary doesn't seem to answer this.

rrmm 9y ago
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.

rrmm 9y ago

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.