GLP-1 drugs may prevent deadly heart complications after heart attack

A popular class of weight-loss drugs may prevent life-threatening cardiac complications by opening microscopic blood vessels that often remain blocked after a heart attack, according to a study published this week in Nature Communications.

The research, led by the University of Bristol and University College London, identified a biological brain-gut-heart signaling pathway. 

This discovery appears to explain how GLP-1 drugs — which mimic glucagon-like peptide-1, a hormone that helps regulate blood sugar and appetite — protect heart tissue from a condition known as “no-reflow.”

“In nearly half of all heart attack patients, tiny blood vessels within the heart muscle remain narrowed, even after the main artery is cleared during emergency medical treatment,” Dr. Svetlana Mastitskaya, the study’s lead author and a senior lecturer at Bristol Medical School, said in a press release.

“This results in a complication known as ‘no-reflow,’ where blood is unable to reach certain parts of the heart tissue.”

This lack of blood flow increases the risk of heart failure and death within a year. GLP-1 medications could prevent this, according to the researchers.

How it works

When the GLP-1 hormone is released in the gut or administered as a drug, it sends a signal to the brain, which then sends a signal to the heart that switches on special potassium channels in tiny cells called pericytes.

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When these channels open, the pericytes relax, which allows the small blood vessels (capillaries) to widen and improve blood flow to the heart muscle, the researchers noted.

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The new study used animal models and cellular imaging to track how GLP-1 interacts with heart tissue. When the researchers removed the potassium channels, the drugs no longer protected the heart — confirming they play a key role.

The findings suggest that existing GLP-1 medications, already used for type 2 diabetes and obesity, could be repurposed as emergency treatments during or immediately after a heart attack to reduce tissue damage.

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The researchers noted several limitations, including that the study relied on animal models.

Clinical trials are necessary to determine whether the brain-gut-heart pathway operates with the same timing and efficacy in humans.

Additionally, while the study highlights the drug’s immediate benefits during a heart attack, it does not establish whether long-term use of the medication provides a pre-existing level of protection.

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The research was primarily funded by the British Heart Foundation.

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