12 August 2026

People with narrowing of the coronary arteries have low-grade, uncontrolled inflammation in the body, even if they are symptom-free and receiving optimal treatment. The findings suggest that immune cells known as neutrophils drive a silent inflammation that may increase the risk of further heart attacks but is not detected by routine clinical tests. The study was conducted by researchers at Linköping University. 

A woman in a yellow lab coat and blue gloves. Photographer: Thor Balkhed
Maike Schneider, PhD student, is extracting white blood cells from whole blood.

Coronary artery disease, which is caused by plaque build-up in the arteries that supply blood to the heart, can appear stable for long periods without causing any symptoms. But the disease can become unstable at any time and cause a heart attack. Following a heart attack, low-grade inflammation can persist in the body for several months or even years. A large body of research suggests that this prolonged inflammation increases the risk of another heart attack. More than 20,000 people in Sweden suffer a heart attack every year.

A woman in a white shirt standing in front of a paintin. Thor Balkhed
Lena Jonasson, professor of cardiology at Linköping University and consultant at Linköping University Hospital.
“Treatment following a heart attack has developed tremendously, with medicines and balloon angioplasty, but we still don’t understand well enough the inflammation that persists in these patients,” says Lena Jonasson, professor of cardiology at Linköping University and consultant at Linköping University Hospital, who led the study published in the journal Arteriosclerosis, Thrombosis and Vascular Biology.

Neutrophils respond quickly

The Linköping researchers were particularly interested in a type of white blood cell known as neutrophils. They are the body’s most abundant immune cells and need to respond quickly to kill bacteria and damaged cells.

“In previous studies, however, we showed that neutrophils in patients with stable coronary artery disease are too easily activated. When exposed to stress, they respond more strongly than neutrophils from healthy individuals. They are also present in greater numbers in patients,” says Lena Jonasson.

Although neutrophils are abundant, they circulate in the bloodstream for only 24 hours. They are then programmed to die. This tight regulation of neutrophils is considered crucial for ensuring that an inflammatory reaction subsides once it is no longer needed. The LiU researchers suspected that something might be wrong with the way neutrophils behave in coronary artery disease.

T-cells help suppress inflammation

A woman standing in front of a building with her arms crossed. Thor Balkhed
Maike Schneider, PhD student at the Department of Health, Medicine and Caring Sciences (HMV) at LiU.
To investigate this, they isolated neutrophils from the blood of 20 patients who had experienced a heart attack and 19 healthy individuals of the same sex and age. The patients’ coronary artery disease was optimally treated in accordance with current guidelines, and they had no symptoms of their disease. Nor did any of them show signs of inflammation according to the routine C-reactive protein (CRP) test.

In a series of experiments, the researchers measured how neutrophils from patients and healthy individuals responded. They also investigated what happened when the neutrophils were mixed with another type of immune cell from the same person, known as regulatory T cells. As their name suggests, these cells regulate the activity of other immune cells and suppress inflammation. One way they do this is by helping neutrophils to die – if everything is functioning as it should.

“We showed that neutrophils in patients with stable coronary artery disease do not die as they should. They persist and remain highly active. We also found that regulatory T cells did not kill the patients’ neutrophils, unlike those from healthy individuals,” says Maike Schneider, doctoral student at Linköping University and first author of the paper.

Key role

The findings show that dysregulated neutrophils may play a key role in the persistent low-grade inflammation seen in chronic coronary syndrome.

“At present, only CRP is recommended for measuring inflammation in coronary artery disease, but a low CRP level tells us very little. We need to become better at diagnosing low-grade inflammation in patients and understanding the biological mechanisms, so that we can provide the right treatment and develop new medicines,” says Maike Schneider.

The study was supported by the Swedish Heart-Lung Foundation and the Swedish Research Council.

The article: Neutrophils Exhibit Delayed Spontaneous Apoptosis and Resistance to Regulatory T-Cell–Induced Apopstosis in Patients With Chronic Coronary Syndrome: Brief Report. Maike Schneider, Camilla Skoglund, Rosanna W.S. Chung and Lena Jonasson, (2026) Arterioscler Thromb Vasc Biol. 2026;0:e324652, published online 25 June 2026, DOI: 10.1161/ATVBAHA.126.324652

A woman in a lab coat standing next to a rack of blood. Thor Balkhed
The findings suggest that immune cells known as neutrophils drive a silent inflammation that may increase the risk of further heart attacks but is not detected by routine clinical tests.

Facts

Coronary artery disease 

The coronary arteries are the blood vessels that supply the heart muscle with oxygen- and nutrient-rich blood.  

When plaque builds up in the coronary arteries, they become narrowed, reducing the blood supply to the heart. These narrowings develop as a result of atherosclerosis, also known as hardening of the arteries. During physical exertion, the heart may not receive enough oxygen, causing pressure or pain in the chest known as angina. 

When coronary artery disease is stable, that is, when it causes no symptoms or symptoms only during physical exertion, it is now referred to as chronic coronary syndrome. The condition was previously known as stable coronary artery disease.  

Approximately 8–10 per cent of people over the age of 65 live with chronic coronary syndrome.  

Coronary artery disease can remain stable for long periods but may – often unpredictably – become unstable and lead to an acute heart attack.  

A heart attack is an acute event in which a blood clot forms at a plaque in a coronary artery, partially or completely blocking blood flow to the heart. The resulting lack of oxygen damages the heart muscle. 

Around 20,000 heart attacks occur in Sweden each year. Approximately one in five is fatal.  

The word coronary comes from the Latin corona, meaning “crown”. In relation to the heart, it refers to the coronary arteries, which encircle the outside of the heart like a crown. 

Neutrophils – the immune system’s hidden players 

Neutrophils are the most abundant type of white blood cell in the immune system. They account for up to 70 per cent of all white blood cells and are also known as neutrophil granulocytes.  

Neutrophils have a very short lifespan. They circulate in the bloodstream for around 24 hours. Under normal circumstances, they then return to the bone marrow, where they die through programmed cell death, a form of cellular suicide known as apoptosis.  

The current study suggests that neutrophils are overactivated in patients with coronary artery disease. It also indicates that the patients’ neutrophils are dysregulated and do not die when anti-inflammatory immune cells known as regulatory T-cells attempt to trigger the process of cellular suicide. 

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