Following a heart attack, the brain processes signals directly from sensory neurons in the heart, indicating a crucial feedback loop that involves not only the brain but also the immune system—both vital for effective recovery.

According to Vineet Augustine from the University of California, San Diego, “The body and brain are interconnected; there is significant communication among organ systems, the nervous system, and the immune system.”

Building on previous research demonstrating that the heart and brain communicate through blood pressure and cardiac sensory neurons, Augustine and his team sought to explore the role of nerves in the heart attack response. They utilized a groundbreaking technique to make mouse hearts transparent, enabling them to observe nerve activity during induced heart attacks by cutting off blood flow.

The study revealed novel clusters of sensory neurons that extend from the vagus nerve and tightly encompass the ventricles, particularly in areas damaged by lack of blood flow. Interestingly, while few nerve fibers existed prior to the heart attack, their numbers surged significantly post-incident, suggesting that the heart stimulates the growth of these neurons during recovery.

In a key experiment, Augustine’s team selectively turned off these nerves, which halted signaling to the brain, resulting in significantly smaller damaged areas in the heart. “The recovery is truly remarkable,” Augustine noted.

Patients recovering from a heart attack often require surgical interventions to restore vital blood flow and minimize further tissue damage. However, the discovery of these new neurons could pave the way for future medications, particularly in scenarios where immediate surgery is impractical.

Furthermore, the signals from these neurons activated brain regions associated with the stress response, triggering the immune system to direct its cells to the heart. While these immune cells help form scar tissue necessary for repairing damaged muscle, excessive scarring can compromise heart function and lead to heart failure. Augustine and colleagues identified alternative methods to facilitate healing in mice post-heart attack by effectively blocking this immune response early on.

Recent decades have indicated that communication occurs between the heart, brain, and immune system during a heart attack. The difference now is that researchers possess advanced tools to analyze changes at the neuron level. Matthew Kay from George Washington University noted, “This presents an intriguing opportunity for developing new treatments for heart attack patients, potentially including gene therapy.”

Current medical practices frequently include beta-blockers to assist in the healing process following heart attack-induced tissue damage. These findings clarify the mechanism by which beta-blockers influence the feedback loops within nervous and immune systems activated during heart attacks.

As Robin Choudhury from the University of Oxford remarked, “We might have already intervened with the newly discovered routes.” Nevertheless, he cautioned that this pathway likely interacts with various other immune signals and cells that remain not fully understood.

Moreover, factors like genetics, gender differences, and conditions such as diabetes or hypertension could affect the evolution of this newly identified response. Hence, determining when and if a pathway is active in a wider population remains essential before crafting targeted drugs, Choudhury added.