Our brain plays a surprising role in recovering from a heart attack

After a heart attack, the brain picks up and acts on signals that come directly from sensory neurons located in the heart. The discovery suggests that there is a feedback loop that involves both the immune system and the brain that plays an important role in recovery.

“The body and the brain do not exist in isolation. There is immense crosstalk between different organ systems, the nervous system and the immune system,” he says. Vineet Augustin at the University of California, San Diego.

Augustine and his colleagues knew from previous work that the heart and brain are connected by cardiac sensory neurons that regulate blood pressure and fainting behavior.

So they set up an experiment to understand whether similar nerves are involved in the response to heart attacks. They made the mouse heart transparent by getting rid of the lipids it contains using a state-of-the-art technique called tissue cleaninginduced a heart attack by blocking blood flow and then observed which cardiac nerves were called into action the most.

They found a previously undiscovered cluster of sensory neurons that emerge from the vagus nerve and wrap tightly around the thick muscular wall of the heart chamber, particularly where the tissue has been damaged by insufficient blood flow. Before the heart attack, there were only a handful of these nerve fibers. But after a heart attack, the fibers grew severalfold, Augustine says, suggesting that the heart actually activates these neurons to grow after the injury.

When Augustine’s team genetically manipulated these nerves to shut them down and prevent them from sending signals back to the brain, the heart quickly healed. “The injured area is really, really small,” says Augustine. “The revival has been remarkable.”

After heart attacks, patients often have to undergo surgery to restore blood flow to the heart and prevent further tissue damage. A future drug that targets the newly found neurons, Augustine says, could provide patients with an alternative, especially if surgery isn’t immediately available.

The researchers also noticed that the signals produced by these nerves traveled to cells in an area of ​​the brain that is activated in response to stress, sending the mouse into a fight-or-flight response. This in turn activated the immune system and directed immune cells to travel to the heart. Immune cells form scar tissue that repairs injured heart muscle, but too much scarring can alter the function of the muscle and lead to subsequent heart failure. By blocking this immune response in time, Augustine and his colleagues showed another way mice recover after a heart attack.

Experiments in recent decades have suggested communication between the heart, brain and immune system in heart attacks. What has changed is that scientists now have the tools to identify changes at a level of detail that affect specific populations of neurons, he says Matthew Kay at George Washington University in Washington, DC, who was not involved in the study.

“This gives us really exciting opportunities to develop new therapies for patients who have heart attacks,” he says, which could potentially include gene therapies.

Doctors regularly prescribe beta blockers to help patients recover from tissue damage caused during a heart attack. These findings help clarify that beta blockers may work by targeting part of the nervous and immune system feedback loop that is activated by a heart attack.

“Maybe we’re already interfering.” [the newly discovered] journey,” he says Robin Choudhury at the University of Oxford, who was not involved in the study.

However, Choudhury adds that this pathway likely does not exist in isolation and is part of a complex picture of responses that we do not yet fully understand, involving other immune cells and signals.

Factors such as genetic and gender differences or conditions such as diabetes and hypertension could also potentially affect how the newly identified response plays out. That means there needs to be a way to know if and when it’s active in the wider population before designing new drugs that target the pathway, Choudhury says.

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