The Inflammatory Way Flu Can Lead To A Heart Attack

A major study just revealed that in the first week of infection, some people may experience as much as a 600 per cent increase in the risk for a cardiac arrest.

02/02/2018 10:21 EST | Updated 02/13/2018 12:58 EST

Last week, a major study revealed influenza infection can lead to an increased chance for a heart attack. The data revealed in the first week of infection, some people may experience as much as a 600 per cent increase in the risk for a cardiac arrest. Not surprisingly, the finding has led to an increased effort to reduce flu spread particularly in light of the fact this year has seen an increase in hospitalizations.

Despite the shock this report has brought, the risk for a heart attack during flu infection has been known for well over a decade. At first, researchers believed the reason was due to the increased stress put on an individual during the fight against the virus. Yet, taking a closer look at what may be the actual cause has revealed a culprit pretty much known to everyone these days. It's inflammation.

Considering how common the term inflammation is used in the world of health, the assignment of blame may not appear to be much of a surprise. This branch of the immune system has been implicated as a major factor in various chronic diseases such as diabetes, depression and cancer. Yet these are all longer term issues, usually allowing the time to find appropriate treatments and therapies. When it comes to cardiac arrest, which is a sudden event, a mechanism needs to be known as soon as possible so that options can be found quickly. In other words, researchers need to find the common link at the molecular level between the flu and the heart attack.

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The search took years before the first step was made with the discovery of large molecules involved in the inflammation process aptly named inflammasomes. These complexes were found to control many of the triggers for inflammatory conditions in the body. More importantly, they control these effects in real time. Not surprisingly, inflammasomes have proven to have a major impact on diseases both short term and chronic, including cardiovascular diseases.

Research on inflammasomes continued and eventually a handful were found to exist in the human body. Yet, when it came to a possible suspect, there was only one choice. It was NLRP3, officially known as Nucleotide binding domain Leucine-rich-repeat-containing Receptor, Pyrin domain-containing 3. This molecule was implicated both in the development of influenza symptoms as well as in the onset of a heart attack.

With a suspect in sight, researchers needed to find exactly how the connection worked at the molecular level. Something had to lead to an increase or at least sustained NLRP3 production in the lungs, where the infection took place, and in the circulatory system such that the heart could be affected. But the research of the human body continued to come up empty.

The actual lynchpin to this equation was not human in nature, but viral. When researchers examined how influenza coped with NLRP3, they found a rather clever means to neutralize the actions of inflammasomes. As infection progressed past the first few days and into that critical first week, NLRP3 would do no good in keeping the infection at bay no matter how much was produced.

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At this point, the link forms itself. Normally, the immune system has an internal trigger to slow down inflammation if the strategy appears to be lost. However, should those barriers be lost either due to age or compromised immunity, then the production of NLRP3 will not cease. The concentration will rise in the lungs and eventually the bloodstream. As this is a rapid process, the accumulation of inflammasomes could reach a threshold that impacts the heart and sends it into arrest within hours to days.

While knowing the role of NLRP3 in increasing the risk of a heart attack during flu infection is a major step forward, identifying means to prevent cardiac arrest continues to be the goal. At the moment, there are means to reduce the effect of NLRP3. Some are in clinical trials and may eventually reach the market in the next decade.

In the meantime, the best way to prevent a heart attack from the flu is simply to prevent or minimize infection. The appropriate us of hygiene, social distancing and barrier protection of the respiratory tract with a mask or a scarf are highly recommended. Then there's the vaccine, which can help to prevent most strains of the flu and minimize the effect of others.

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