Infarction isn't just about the heart: scientists have linked it to the brain and immune system

Researchers at the University of California, San Diego have offered a new perspective on myocardial infarction: according to their findings, it is not a "localised" heart problem, but an event that involves the brain, nervous system and immune response. The work is published in the journal Cell.

The authors describe the mechanism as an interconnected "loop": during a heart attack, damage to heart tissue is detected by sensory neurons, after which a signal is transmitted to the brain via nerve pathways. The brain then triggers an immune response - similar to the response to trauma. The problem is that in a heart attack, the body is dealing with tissue damage rather than infection, and an excessive or "misdirected" inflammatory response can exacerbate further damage and complicate recovery.

The experiments were conducted in mice. The researchers traced the pathway of signals from the heart to the brain and highlighted the role of the vagus nerve: after a heart attack, the activity of a certain group of sensitive neurons increased, and suppressing these signals improved heart performance and reduced signs of damage. Separately, the team also showed that reduced inflammation in the associated nerve structures was accompanied by more favourable recovery of cardiac tissue.

In essence, blocking signal exchange in the heart-brain-immunity system worked as a way to "stop the spread of damage" from the epicentre of the heart attack, the researchers describe. The authors believe that this mapping of neuroimmune connections may suggest new therapeutic approaches - for example, interventions targeting nerve signalling or inflammation as an adjunct to classical heart attack treatments.

However, the independent experts emphasise that inflammation is not "evil" in itself: in the early stages it is needed to clean up damaged tissue and trigger repair, but problems start when the response becomes excessive, prolonged or uncoordinated.