After a heart attack, the body triggers a powerful stress response that helps mobilize the immune system but can also intensify damage to the heart. A new study by American scientists has shown that blocking certain “stress signals” can significantly reduce dangerous inflammation after a heart attack and improve the recovery of cardiac tissue. The work was published in the journal Nature Communications.

The study was conducted by researchers from the University of Oklahoma. Scientists examined neutrophils — immune cells that are the first to arrive at the damaged heart after a heart attack. Normally, they help clear tissues and initiate repair; however, an excessive influx of these cells leads to increased inflammation and worsens damage to the myocardium.

The key discovery was that the first neutrophils do not come from the bone marrow, as previously thought, but from a kind of “reserve” located along the walls of blood vessels. After a heart attack, the body releases stress hormones — primarily norepinephrine — which trigger the “fight or flight” response.

Under the influence of these signals, neutrophils quickly detach from the vessel walls and move toward the heart. Once they reach the heart muscle, they release special protein “alarm signals” known as alarmins.

These substances prompt the bone marrow to produce even more neutrophils, amplifying the inflammatory chain reaction. The study’s lead author, Prabha Nagarajeddy, compared this process to searching for a “Goldilocks zone”: a small number of immune cells is beneficial, but an excess becomes destructive.

To test whether this response could be reduced, the researchers used a β2-blocker in mice — a drug that suppresses stress signaling. As a result, fewer neutrophils entered the heart, and tissue recovery improved. Cardiac function in animals after a heart attack was also significantly better preserved.

However, the scientists emphasize that the blockade was temporary, since completely suppressing the immune response is also dangerous.

Of particular interest is the fact that similar drugs are already used in cardiology. After a heart attack, patients are often prescribed β1-blockers, which reduce strain on the heart. However, this study focuses on β2 receptors, which are specifically linked to immune and stress responses. Some existing drugs, such as propranolol and carvedilol, act on both types of receptors, potentially opening the door to new treatment strategies.