University of Ottawa study links heart attacks with brain damage

A new study led by a team from the University of Ottawa takes a major step forward in understanding how a heart attack can dramatically reshape brain function and trigger neurological effects, from depression and anxiety to different types of cognitive decline.

This 'heart-brain axis' concept suggests that neurological conditions following a heart attack could be driven in part by molecular changes set in motion by damage to the heart. While there are many factors and signaling pathways involved in heart-brain interactions, this newly published research suggests that a toxic byproduct produced by the body plays a major role in the brain following a heart attack.

Brain inflammation after cardiac events

At the center of the discovery is methylglyoxal (MG), a highly reactive molecule, which surges in the bloodstream and accumulates in the brain following a heart attack. Following a heart attack, the body enters a state of stress-oxygen drops, inflammation rises, metabolism shifts-causing MG levels to surge in the bloodstream and then accumulate in the brain in specific brain regions linked to mood and cognition.

The occurrence of depression and anxiety in heart attack patients is up to three times higher than the general population, with patients who suffer depression or anxiety may be up to 2.7 times more likely to experience another heart attack or death.

Charting new territory in brain-heart connection

Published in the journal Advanced Sciences, this finding could potentially transform recovery and long-term outcomes for millions as it reshapes how scientists understand long-term risks after myocardial infarction and explain why emotional and cognitive disorders are so common after cardiac events.

Methylglyoxal has been widely studied for its role in metabolic diseases, including diabetes, but much less is known about its function in other diseases. In a previous study, we discovered that methylglyoxal was produced by dying heart tissue after a heart attack (…) based on this evidence, we predicted that methylglyoxal in the blood would target other organs and tissues, including the brain-and this is what we did indeed observe."

Dr. Erik Suuronen, senior author, Full Professor in the Faculty of Medicine's Department of Surgery, a scientist in the Division of Cardiac Surgery and director of its BEaTs Research Program at the University of Ottawa Heart Institute

Moving from discovery toward therapy

The team's discoveries raise important questions about neurodegenerative disease as chronic inflammation and cellular damage in the brain are key drivers of cognitive conditions like dementia. By identifying methylglyoxal as a trigger, this research suggests a new pathway through which heart attacks could increase long-term neurological risk. Having identified methylglyoxal as a potential target for treating neurological disorders after a heart attack, the next step is to explore how MG-driven inflammation leads to neuron death and mental health conditions.

Importantly, the research team has already developed a peptide therapeutic that can trap methylglyoxal and prevent it from damaging cells. "This therapy will soon be tested to see if it can protect the brain from damage after a heart attack," says Dr. Suuronen, who believes if successful, such treatments could do more than protect brain function; they could potentially reduce the risk of future cardiac events.

"Given the increased risk of subsequent heart attacks or death in heart attack patients who experience depression or anxiety, being able to alleviate these conditions could reduce subsequent major cardiac events and improve the lives of countless patients, filling an urgent unmet clinical need," Dr. Suuronen adds.