A heart attack can be treated successfully, blocked arteries can be reopened and standard blood tests can return to normal.
Yet inside the body, part of the immune system may still behave as though the danger has not ended.
A Swedish study has uncovered a possible reason for this hidden problem. Researchers at Linköping University found that certain immune cells in people with stable coronary artery disease may remain alive and active longer than they should.
Coronary artery disease is caused by a gradual buildup of plaque inside the arteries supplying the heart. Plaque contains cholesterol, fats, immune cells and other material, and its growth can narrow the space available for blood to flow.
A person can live with this condition for years without obvious symptoms. Trouble can begin suddenly if a plaque breaks open and a blood clot forms around it, cutting off blood flow to part of the heart and causing a heart attack.
Surviving the first heart attack does not mean the danger has completely disappeared. Doctors can treat blocked arteries and control major risk factors, but people who have already had a heart attack remain more likely to experience another one.
Inflammation is thought to be part of that continuing risk. Inflammation normally helps the body fight infection and repair injury, but it can become harmful when immune activity continues after it is no longer needed.
Professor Lena Jonasson and colleagues at Linköping University have been studying this problem in coronary artery disease. Their earlier research suggested that neutrophils, a common type of immune cell, behave differently in people with heart disease.
Neutrophils act like rapid-response cells. They can attack microbes and react to damaged tissue within minutes, making them extremely useful during an emergency but potentially damaging if they remain activated for too long.
The body therefore gives neutrophils a short life. Most circulate for only around 24 hours before they are programmed to die, allowing inflammation to settle once the immediate threat has passed.
The researchers wondered whether this shutdown system might be disturbed in coronary artery disease. To test the idea, they studied blood from 20 patients who had previously suffered a heart attack and compared it with blood from 19 healthy people matched for age and sex.
The patients were not obviously ill. Their coronary artery disease was being treated according to current medical guidelines, they had no active symptoms and a common blood test for inflammation called CRP did not show elevated levels.
That made the results particularly interesting. When the researchers isolated neutrophils and studied them in the laboratory, cells from the heart patients did not die as readily as neutrophils taken from healthy participants.
The team then investigated another part of the immune system. They combined the neutrophils with regulatory T cells, which normally act as immune-system brakes and help prevent inflammatory reactions from continuing unnecessarily.
In samples from healthy participants, these regulatory cells helped push neutrophils toward their normal death. In the heart patients, however, the same control system did not work properly, leaving neutrophils alive and highly active.
This suggests that chronic coronary disease may involve an immune system that has difficulty ending its own response. The continuing activity could contribute to the low-level inflammation associated with repeated heart problems.
The findings are also relevant to the way inflammation is currently assessed. CRP can be useful for detecting inflammation in the body, but these patients had normal routine CRP results despite showing clear differences in immune-cell behavior in laboratory tests.
Researchers therefore believe better ways of identifying low-level cardiovascular inflammation may be needed. A more detailed picture could eventually help doctors distinguish patients whose arteries appear stable but whose immune systems remain unusually active.
The study was led by Professor Lena Jonasson, and Maike Schneider was the first author. The research was published in Arteriosclerosis, Thrombosis, and Vascular Biology, a peer-reviewed journal of the American Heart Association.
The study offers an intriguing explanation for persistent inflammation, but it is still early-stage research. Only 20 heart patients and 19 healthy controls were included, and the experiments cannot yet show that these abnormal neutrophils directly cause another heart attack.
Future studies will need to follow larger groups of patients and determine whether these immune changes predict real-world cardiovascular events. Researchers will also need to learn whether safely changing neutrophil survival or improving the control provided by regulatory T cells can reduce risk.
The broader message is that successful heart treatment may involve more than opening an artery and lowering cholesterol. Understanding why inflammation stays active could reveal another layer of coronary disease and, eventually, offer doctors new ways to protect heart attack survivors from a second event.
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Source: Linköping University.
