According to researchers at Linköping University, patients with stable coronary artery disease suffer from silent, low-grade inflammation driven by dysregulated immune cells known as neutrophils, which fail to die off as expected even when optimally treated. Over 20,000 people in Sweden experience a heart attack every year, and while modern treatments like balloon angioplasty and medications have advanced significantly, the persistent underlying inflammation that triggers subsequent heart attacks remains poorly understood, according to Lena Jonasson, professor of cardiology at Linköping University and consultant at Linköping University Hospital.
Silent Inflammation in Asymptomatic Patients
Coronary artery disease develops from plaque build-up inside the arteries supplying blood to the heart. The condition can stay stable for long stretches without causing symptoms, but it can turn unstable abruptly and trigger a heart attack. Following a heart attack, low-grade inflammation often lingers in the body for months or years. According to a large body of research cited by the Linköping team, this prolonged immune activity raises the risk of recurrent cardiac events. Despite optimal treatment under current guidelines, patients frequently show no outward symptoms and pass routine C-reactive protein (CRP) blood tests without raising any red flags.
Why Neutrophils Refuse to Die
Neutrophils represent the most abundant white blood cells in the human body, serving as frontline responders designed to act quickly against bacteria and damaged tissue. Normally, these cells circulate through the bloodstream for just 24 hours before undergoing programmed cell death. This precise biological regulation ensures that acute inflammatory reactions subside once their job is done. However, according to previous studies led by Professor Jonasson, neutrophils in patients with stable coronary artery disease react much too strongly to stress and appear in elevated numbers compared to healthy individuals.
Did you know? Neutrophils make up the vast majority of your body’s white blood cells, but they have a very short lifespan of only 24 hours in the bloodstream before they are programmed to die and clear out.
T-Cell Dysregulation and Delayed Apoptosis
To pinpoint why neutrophil regulation fails in cardiac patients, researchers isolated neutrophils from the blood of 20 heart attack survivors and 19 healthy individuals matched by age and sex. As part of a series of laboratory experiments detailed in the journal Arteriosclerosis, Thrombosis and Vascular Biology, doctoral student and first author Maike Schneider tested how patient neutrophils responded when mixed with regulatory T cells from the same person. Regulatory T cells normally suppress inflammation and help trigger neutrophil cell death.
“We showed that neutrophils in patients with stable coronary artery disease do not die as they should,” Maike Schneider said, according to the study. “They persist and remain highly active. We also found that regulatory T cells did not kill the patients’ neutrophils, unlike those from healthy individuals.” These findings demonstrate that dysregulated neutrophils play a vital role in maintaining the chronic, low-grade inflammation typical of chronic coronary syndrome.
Limitations of Routine Clinical Testing
Current clinical protocols rely heavily on the CRP test to measure inflammation in coronary artery disease patients. The research team emphasizes a pressing need to improve how clinicians diagnose low-grade inflammation so that providers can tailor treatments more effectively and design new medications. The study received funding support from the Swedish Heart-Lung Foundation and the Swedish Research Council.
Frequently Asked Questions
What is chronic coronary syndrome?
Why do routine CRP tests miss this inflammation?
What are neutrophils?
Neutrophils are the most common type of white blood cell in the human body, acting as rapid responders to fight infections and clear damaged cells.
Who conducted this research?
The study was led by researchers at Linköping University, including Professor Lena Jonasson and doctoral student Maike Schneider, and was published in Arteriosclerosis, Thrombosis and Vascular Biology.
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