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Myocardial infarction may be an infectious disease

brandonb

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).

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...

lr4444lr

IANAD, but

1) Isn't ApoB measurement pretty much in tandem with LDL, VLDL, and triglycerides? I realize it's being recognized now as the necessary factor for arterial dysfunction, but it seems like a lot of hoopla is being made as if it were some "silent" overlooked factor when for the vast, vast majority of people their ApoB levels are entirely explained by the other 3 lipid panel line items carrying it, and they have been in use for decades and are strongly targeted by the medical establishment

2) Isn't Lp(a) a separate lipoprotein altogether which is an independent risk factor for MACE? I've never heard of it "disguising" other cholesterol in testing.

andy99

Understanding this is a shameless plug, it's very cool this exists.

stavros

You don't need to use this specific blood test, by the way. Any lab near you will test these biomarkers for you.

andy99

I live in Canada, despite being free this would be way more complicated to get. I don't want to be political, but just paying for this would be very appealing.

gblargg

It being an ad casts suspicion on the entire post.

giveita

What do you do next if one is high? See your Doctor?

A_D_E_P_T

Yeah. If you don't have obvious symptoms, they'd likely prescribe you a statin, metformin, or some sort of dietary intervention. But you'd want to discuss it with your doctor in any case...

brandonb

This particular panel includes a consult with a doctor (who can advise on next steps, prescribe medication, and so on). Or you can take the results to your doctor.

OutOfHere

For lipids, besides the named tests, HDL, LDL, and triglyceride tests are older but shouldn't be overlooked.

For measuring inflammation, besides hs-CRP, additional tests are relevant and overlooked: regular CRP, ESR, and homocysteine.

Additionally, a heart attack can result from parasite induced inflammation too, e.g. in chagas disease, which is becoming increasingly common in the US while being very undetected without explicit testing. It is also very difficult to treat, but the gist 4196f31d12a43a95756e792500ff516f has some info on treating it. Lyme disease too can harm the heart permanently. In both cases a pacemaker could help as applicable.

brandonb

Can you expand more on why you'd want regular CRP over hs-CRP (specifically for cardiovascular risk)?

For homocysteine, one proxy is B12 or folate (which are more cost-effective to test). To my knowledge, ESR is used in certain rheumatologic conditions, and was used more often in the past, but isn't currently used for heart disease.

OutOfHere

It is true that hs-CRP is relevant for cardiovascular risk. CRP and ESR are more for broader inflammatory risk, for acute and chronic values respectively.

hollerith

Do you happen to know how much that test costs? (Clicking a link to try to find out brought me to a page that asks for my zip code.)

brandonb

That panel is $190.

DaveZale

in the US? There was a question from Canada

DaveZale

are you a cardiologist? Excellent points, thanks

brandonb

Not a cardiologist, but adjacent to this type of research. I'm an MLE but have published research in cardiology.

mitchbob

TIL MLE = Machine Language Engineer. It wasn't listed in Google's AI overview, although I did get

Major League Eating (MLE): a professional organization focused on competitive eating contests.

Mister Leather Europe (MLE): an event within the European leather subculture.

DaveZale

thanks for your input on this

faangguyindia

Wasn't that a plot in DBZ where a virus weakens Goku's heart?

JumpCrisscross

“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.)

[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC8875263/

jimbo808

But you can't patent phages, so we'll just continue ignoring them

JumpCrisscross

> you can't patent phages, so we'll just continue ignoring them

Nope. Plenty of governments fund this sort of research. And chances are there isn’t an off-the-shelf phage that ticks the boxes, which means you need some amount of genetic engineering, in which case Monsanto has your back.

XorNot

"simple, obvious and wrong".

Phages are intensely species specific to bacterial species, so they don't work unless you identify exactly what you're targeting. Also, even if they can penetrate biofilms, that doesn't mean you can successfully deliver them to the biofilm in the human body, since they have to survive the whole blood stream and the normal human immune response to "not self" things.

tbrownaw

I assume this is a "here's another way this can happen" rather than "actually this is caused only by this and not by what we used to think"?

tialaramex

Of course it depends on fractions. You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection. So knowing that all the plans towards eliminating this disease focus on HPV.

On the other hand most people with "flu" in summer months are not infected with Influenza, so an improved influenza treatment isn't going to make a big difference for them unlike in winter. We know other reasons you might get those symptoms which are more likely in summer.

lostlogin

Surely this? The number of ‘oh, it turned out to be more more complicated’ scenarios in medicine is high.

jimbo808

This has been suspected for decades.

https://www.thelancet.com/journals/laninf/article/PIIS147330...

Hopefully it leads somewhere that brings us new preventative care.

andy99

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.

JumpCrisscross

> bacteria in arterial plaques can cause them to break up and cause the attack

“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix” whose rupture “result[s] in thrombus formation and ultimately myocardial infarction” sounds like infection more than careless bacteria kicking up muck.

A_D_E_P_T

This raises two questions.

- 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.

ygouzerh

For the Listerine part: they are referencing this study: https://pubmed.ncbi.nlm.nih.gov/16373688/ that seems to show a correlation between poor oral health and sudden cardiac death, so it might help indeed, with other good oral health practices.

DaveZale

I only use very dilute Listerine - for the fluoride. A dentist told me that undiluted, alcohol based products can cause tissue damage (which conceivably would result in a vector for oral bacteria infiltrating to the bloodstream?)

prmph

Listerine would make it worse for sure.

Don't use "antiseptic" mouthwash; it kills beneficial bacteria in the mouth, causing bad bacteria to multiply.

I have personal experience of this.

dionian

agreed, after much research the only mouth wash i use is therasol

dreamcompiler

TFA says the biofilms protect the bacteria from antibiotics. Better approach is probably engineered antibodies or even a phage (engineered virus that attacks the bacteria).

syntaxing

I probably should find sources first but I was always under the impression that the mouth biome is strongly correlated to gut biome which strongly correlated to immune system.

tim333

Yes, there are studies where they compared heart attack rates for people who'd taken a course of antibiotics with those who hadn't and there was quite a large effect in some of them.

eg. https://www.science.org/content/article/antibiotics-cut-hear...

op00to

This seems like a good explanation of how my father died. He had the flu, and died overnight from a massive heart attack.

awesome_dude

https://www.health.harvard.edu/heart-health/what-does-the-fl...

How does flu affect the heart? The virus only rarely infects the heart directly. Instead, the adverse effects of the virus on the heart are due to atherosclerosis of the arteries of the heart. Many people over age 50 have atherosclerosis — and in some people it has not yet been diagnosed. Because atherosclerosis narrows the arteries and reduces the flow of blood, less oxygen reaches the heart muscle. When the effect of the flu on the lungs lowers the amount of oxygen in the blood, this further reduces the supply of oxygen to the heart. This can lead to a heart attack or cardiac arrest (sudden death).

Is this risk more than theoretical? Many careful studies have shown there is an increased risk of heart disease following a bout of flu. In one study of 80,000 adults with influenza, nearly 12% had a serious cardiac event, such as a heart attack, during or in the weeks after getting the flu.

op00to

For sure it exacerbated an existing cardiovascular system. Once the system is weakened things cause big problems quickly.

y1n0

In the context of the article, it's inflammation rupturing the 'fibrous cap' on plaque deposits leading to a heart attack, so I presume OP is talking about the inflammatory response to having the flu.

smt88

> How does flu affect the heart?

Even temporary stress on the respiratory system can cause long-term damage to the brain, lungs, and heart. Because of Covid, we started to learn that an acute, severe infection can affect people much later.

That research led to the beginning of an understanding that repeated flu infections can contribute to premature death even many decades later.

DaveZale

sure does. chain of events. The epidemiologists should be able to validate these claims.