People who have survived a heart attack can remain at risk even when their treatment is working and they feel well.
New research from Linköping University in Sweden suggests that unusually persistent immune cells may help explain why hidden inflammation can continue after heart disease appears stable.
Coronary artery disease develops when fatty material and other substances build up inside the arteries that carry blood to the heart. These deposits, known as plaques, can gradually narrow the arteries and reduce blood flow.
For years, the disease may cause few or no symptoms. But a plaque can suddenly become unstable and help trigger a blood clot, which may block an artery and cause a heart attack.
Modern treatment has greatly improved survival after heart attacks. Medicines can lower cholesterol, reduce blood clotting and control blood pressure, while procedures such as angioplasty can reopen blocked arteries and restore blood flow.
Even so, treatment does not remove every future risk. After a heart attack, low-level inflammation may continue for months or years, and research has linked this ongoing immune activity with a greater chance of another cardiovascular event.
Researchers at Linköping University wanted to understand what might keep this inflammation active. Their attention turned to neutrophils, the most common type of white blood cell in the bloodstream.
Neutrophils are part of the body’s rapid defense system. They respond quickly to infection and damaged tissue, but because their actions can also harm healthy tissue, the body normally keeps their activity under tight control.
These cells usually live for only about a day in the bloodstream before undergoing a carefully controlled form of cell death. Removing them at the right time is one way the body switches off inflammation after a threat has passed.
Previous work from the Linköping team had shown that neutrophils from people with stable coronary artery disease appeared unusually easy to activate. The patients also tended to have more of these cells circulating in their blood.
In the new study, researchers collected neutrophils from 20 people who had previously experienced a heart attack and from 19 healthy people of similar age and sex. The heart patients were receiving recommended treatment and had no current symptoms of their coronary disease.
Importantly, routine testing did not suggest obvious inflammation in the patients. Their levels of C-reactive protein, commonly called CRP, were not elevated even though the researchers suspected that more subtle immune changes might still be present.
The scientists studied how the neutrophils behaved in laboratory experiments. They also mixed the cells with regulatory T cells, another type of immune cell that helps prevent the immune system from remaining active for too long.
In healthy people, regulatory T cells can help encourage neutrophils to die when their job is finished. This process helps the body end an inflammatory response and return to a more normal state.
But the researchers found a different pattern in the heart patients. Their neutrophils survived longer than expected and remained highly active, while their regulatory T cells were less able to trigger the normal death of these neutrophils.
This failure to switch off could provide one explanation for persistent low-grade inflammation in people with chronic coronary artery disease. Even when a patient feels well and standard tests look reassuring, overactive immune cells may continue to create a harmful inflammatory environment.
The study was led by Professor Lena Jonasson, with doctoral researcher Maike Schneider as first author. It was published in the American Heart Association journal Arteriosclerosis, Thrombosis, and Vascular Biology.
The findings may also raise questions about how doctors measure inflammation after a heart attack. CRP is widely used as an inflammation marker, but the study suggests that a normal CRP result may not reveal every important immune problem occurring in coronary disease.
There are important limitations. The study involved only 39 people and examined their cells mainly in laboratory conditions, so larger studies are needed to confirm whether the same neutrophil behavior predicts future heart attacks or other complications.
Still, the work identifies a possible biological mechanism behind inflammation that refuses to disappear. If future studies confirm the findings, tests that examine immune-cell behavior could potentially help identify patients who remain at higher risk despite receiving standard heart treatment.
The research may eventually point toward new medicines as well. Rather than broadly suppressing the immune system, future treatments might aim to restore the normal process that tells overactive neutrophils when their work is finished.
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Source: Linköping University.
