The original title is "Myocardial infarction may be an infectious disease" which appears to be clickbait, with the title posted here being much more accurate.
Immune response to bacteria in arterial plaques can cause them to break up and cause the attack (my lay-interpretation) so the bacteria is a trigger, but "infectious disease" is a bit of hyperbole.
This is a nicely-designed study. For decades, we've known that inflammation is a risk factor for heart attacks.
In this study, the researchers designed a custom antibody that binds to oral bacteria. Then they used histological staining to identify specific biofilm structures inside the atherosclerotic tissue. Bacteria released from the biofilm were observed in heart attack cases, which gives us evidence that when the body's immune system responded to these bacteria, it triggered inflammation which ruptured cholesterol-laden plaque. So now we have more insight into the mechanism behind why inflammation is associated with heart attack risk.
The "pantheon" of risk factors for heart disease are:
* hs-CRP (inflammation): the mechanism studied by this research. High inflammation roughly doubles your risk of heart disease.
* ApoB - 20% of people with normal cholesterol will have abnormal ApoB, and be at risk of heart disease (ApoB is a structural protein in lipoproteins which cause arterial plaque).
* Lp(a) - the strongest hereditary risk factor for heart disease (Lp(a) acts as a multiplier on ApoB, since it camouflages cholesterol particles from your liver)
* HbA1c - insulin resistance /diabetes is a risk factor for just about everything.
* eGFR - estimates the volume of liquid your kidneys can filter, and is an input to the latest heart disease risk models (PREVENT).
“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix…”
Phages can penetrate biofilms [1]. (They have practice.)
Anecdotally, I had a myocardial infarction at 23, and I was honestly surprised to learn that it wasn’t already well known that infectious diseases could trigger such events.
Up until that point, I’d never had any heart-related issues, nor does anyone in my family. Just two days before being admitted to the hospital with a suspected heart attack, I came down with food poisoning. It wasn’t pleasant, of course, but I thought it was nothing unusual—something a couple of days of rest and hydration would normally resolve.
Since my bloodwork at the hospital matched the expected results for a heart attack, and I underwent surgery, the doctors understandably focused on treating the immediate problem rather than identifying the underlying cause (I’m eternally grateful to the team and staff at St. Vincentius-Kliniken. I truly don’t think I’d be here without them).
That said, I’m glad to see this area receiving more attention. Hopefully, it will lead to further studies and the development of better strategies for prevention and treatment.
Titles like this are very confusing. The paper better explains it, but a disease can't be contagious or infectious. The paper describes a link between a potential bacterial infection and myocardial infarctions that may take years or decades to develop.
The disease is only the named group of symptoms. The potential cause of the disease is the bacterial infection. Those are very different concepts.
The article differs substantively from the actual conclusions of the study. This study shows a minor correlation in some bacterial DNA "signatures" in arterial plaque in about 200 people (~40% had the correlated bacteria). The study only included tissues from people who died of heart disease or had surgery related to heart disease. There does not currently appear to be a strong baseline about how widespread this bacterial signature may exist in a broad population regardless of health.
In a nutshell there is a slightly interesting idea that deserves further study. That's it.
Have always been fascinated with Paul Ewald's arguments (as laid out in his books The New Germ Theory of Disease and Evolution of Infectious Disease) that most chronic illnesses are due to pathogens.
Typical of the medical field: one of the most studied diseases in the past several decades and now there is a ground-breaking new study that questions all knowledge.
I blame the corruption from American medical experts and organizations which only object is to sell drugs.
"The most unique finding in our study was that viridans streptococci seemed to colonize the lipid core and wall of an atheroma as a biofilm and that this biofilm was not recognized by cells of the innate immune system. "
This is a pretty cool finding. Biofilms are also beyond reach of antibacterials usually. And seing a commensal become a problem due to "location, location, location" is also cool.
It's been known for many years that the flu vaccine reduces heart attack incidence. The flu either causes lasting damage to the cardiovascular system or directly causes heart attacks.
This is perfectly well known and absolutely nothing new.
This study merely expands research on the topic (focus on bacteria+biofilm instead of flu).
So "Myocardial infarction may be an infectious disease" is a weird clickbait title. We know. We knew for a long time.
We also have quite a few of anti biofilm agents in IV formulations that could have an effect inside of the cardiovascular system if used in high dosages, but the molecules are old, cheap and unsexy, so no one will try. (ambroxol and NAC come to mind)
Wild I see only one mention of COVID so far, it has been shown to attack all kinds of organ tissues, the perspectives around "with or from" somehow permanently prevents people from discussing the underlying changes from this continued global cycling of the pathogen.
Arterial plaque is a long standing, foreign body without vessels causing high flows. No surprise it can be infected by bacteria sometime. That is infection can exacerbate the MI, not cause it.
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[ 3.0 ms ] story [ 34.5 ms ] threadImmune response to bacteria in arterial plaques can cause them to break up and cause the attack (my lay-interpretation) so the bacteria is a trigger, but "infectious disease" is a bit of hyperbole.
In this study, the researchers designed a custom antibody that binds to oral bacteria. Then they used histological staining to identify specific biofilm structures inside the atherosclerotic tissue. Bacteria released from the biofilm were observed in heart attack cases, which gives us evidence that when the body's immune system responded to these bacteria, it triggered inflammation which ruptured cholesterol-laden plaque. So now we have more insight into the mechanism behind why inflammation is associated with heart attack risk.
The "pantheon" of risk factors for heart disease are:
* hs-CRP (inflammation): the mechanism studied by this research. High inflammation roughly doubles your risk of heart disease.
* ApoB - 20% of people with normal cholesterol will have abnormal ApoB, and be at risk of heart disease (ApoB is a structural protein in lipoproteins which cause arterial plaque).
* Lp(a) - the strongest hereditary risk factor for heart disease (Lp(a) acts as a multiplier on ApoB, since it camouflages cholesterol particles from your liver)
* HbA1c - insulin resistance /diabetes is a risk factor for just about everything.
* eGFR - estimates the volume of liquid your kidneys can filter, and is an input to the latest heart disease risk models (PREVENT).
All of these risk factors can be measured with a blood test + doctor review. Easy to order online: https://www.empirical.health/product/comprehensive-health-pa...
Phages can penetrate biofilms [1]. (They have practice.)
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC8875263/
- Does this suggest that courses of antibiotics might reduce heart attack risk?
- Does this suggest that regular use of, e.g., Listerine might reduce heart attack risk? (While, perhaps, slightly increasing esophageal cancer risk.)
It would be interesting to run an epidemiological study to see if current interventions move the needle in a meaningful way.
https://www.thelancet.com/journals/laninf/article/PIIS147330...
Hopefully it leads somewhere that brings us new preventative care.
Up until that point, I’d never had any heart-related issues, nor does anyone in my family. Just two days before being admitted to the hospital with a suspected heart attack, I came down with food poisoning. It wasn’t pleasant, of course, but I thought it was nothing unusual—something a couple of days of rest and hydration would normally resolve.
Since my bloodwork at the hospital matched the expected results for a heart attack, and I underwent surgery, the doctors understandably focused on treating the immediate problem rather than identifying the underlying cause (I’m eternally grateful to the team and staff at St. Vincentius-Kliniken. I truly don’t think I’d be here without them).
That said, I’m glad to see this area receiving more attention. Hopefully, it will lead to further studies and the development of better strategies for prevention and treatment.
The disease is only the named group of symptoms. The potential cause of the disease is the bacterial infection. Those are very different concepts.
https://www.nejm.org/doi/full/10.1056/NEJMoa043526
still hasn't really panned out
I think I'll go floss.
In a nutshell there is a slightly interesting idea that deserves further study. That's it.
This is a pretty cool finding. Biofilms are also beyond reach of antibacterials usually. And seing a commensal become a problem due to "location, location, location" is also cool.
Nice article. Cool leads
This is perfectly well known and absolutely nothing new.
This study merely expands research on the topic (focus on bacteria+biofilm instead of flu).
So "Myocardial infarction may be an infectious disease" is a weird clickbait title. We know. We knew for a long time.
We also have quite a few of anti biofilm agents in IV formulations that could have an effect inside of the cardiovascular system if used in high dosages, but the molecules are old, cheap and unsexy, so no one will try. (ambroxol and NAC come to mind)