Heart attacks are medical emergencies in which blood supply to the heart is blocked — usually by a blood clot. A new study from Sweden has made an intriguing discovery that may change existing guidelines about treating heart attacks.

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Do certain antibodies play a role in heart attacks?

Antibodies, or immunoglobulins (Ig), are a type of protein produced by plasma cells (a kind of blood cell). The immune system often co-opts these to fight potentially harmful foreign bodies.

Now, researchers from the Karolinska Institutet in Solna, Sweden, have discovered that certain antibodies — once associated with rheumatic diseases — are also present in high numbers inside the bodies of people who have had a heart attack.

These are the antiphospholipid antibodies (aPLs), which are abnormal antibodies that react to types of tissue produced by the body itself, such as cardiolipin (a lipoprotein) and beta-2-glycoprotein-I (a plasma protein).

Th scientists note that aPLs typically appear in the context of rheumatic diseases, such as systemic lupus erythematosus, or lupus.

The presence of these antibodies, they continue, can increase a person’s risk of blood clots. This happens in antiphospholipid syndrome (APS), an autoimmune condition in which the body overproduces aPLs.

In the recent study — the findings of which appear in the Annals of Internal Medicine — the authors note that aPL is distinctly present in the bodies of many people who have experienced heart attacks and are free of autoimmune conditions.

They also report that it has so far remained unclear just how common aPLs are in the case of such people, because scientists have conducted previous studies at too small a scale to provide the appropriate data.

For the new study, the investigators worked with 800 people admitted as patients at 17 Swedish hospitals after having experienced a heart attack for the first time.

To be able to compare data, the researchers also recruited an equal number of healthy participants to act as the control group.

The researchers analyzed blood samples from the first group at 6 and then again at 10 weeks after the heart attack. They looked for three distinct types of aPL: immunoglobulin G (IgG), M (IgM) and A (IgA).

When they looked at the data, the investigators saw that 11 percent of the participants who had experienced heart attacks had aPL that reacted to both cardiolipin and beta-2-glycoprotein-I. That was 10 times more people than in the control group.

“I’ve long been convinced that the antibodies are more common than we think and have now been able to analyze their presence in a large patient material,” says study author Prof. Elisabet Svenungsson.

“It was a surprisingly high proportion of the patients and the levels were also clearly high,” explains Prof. Svenungsson.

Specifically, the volunteers had high levels of IgG antibodies, which are most commonly associated with a heightened risk of blood clots.

However, the researchers admit that they only collected one set of blood samples, which may not accurately reflect the levels of aPL over time and may instead be a one-off reaction to the heart attack.

Still, should their aPL levels remain high over 3 months, this would mean that the participants have APS, which would predispose them to blood clots.

“In which case they should,” notes Prof. Svenungsson, “according to current recommendations, be prescribed lifelong treatment with the anticoagulant warfarin, which reduces the risk of new blood clots,” concluding:

This would change the prevailing guidelines for the investigation and treatment of heart attacks.”