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Whole Body Imaging May Help Researchers Understand Why Heart Attack Survivors Have Cognitive Impairment

A new imaging study in mice shows that inflammation after a heart attack could be a potential link between cardiovascular and neurodegenerative diseases.

Vijay Shankar Balakrishnan, Contributor
Tue, 02/27/2018


When doctors treat patients for heart attack, they usually do not think about the patient’s brain. However, several studies have shown some heart attack survivors can have problems with cognitive functions, such as memory and attention, more frequently than their healthy counterparts.

“This clearly requires more insightful research to understand the mechanism of interaction between cardiac and brain dysfunctions,” said Frank Bengel, a nuclear medicine specialist at the Hannover Medical School in Germany.

Recently, Bengel and his colleagues were investigating whether whole body positron emission tomography (PET) could help predict a long-term heart failure after an acute heart attack. As a bonus, they also found a potential link between heart and brain dysfunctions in the body’s signs of inflammation after a heart attack. The results appeared in the Jan. 23 issue of the Journal of the American College of Cardiology.

To start, the researchers gave a group of mice an acute surgical heart attack and left another group as a control with a placebo surgery. They then gave the mice whole body-PET scans and looked for the mitochondrial translocator protein (TSPO), a biomarker produced in large amounts throughout the body after inflammation.

“The stronger the inflammation signals are very early after the myocardial infarction, the higher the likelihood that the heart failure will develop later on,” said Bengel.

In the first week after the heart attack, the researchers found both the animals’ hearts and brains had significantly elevated levels of TSPO, indicating strong inflammation of these particular organs. The excess TSPO production was caused by infiltrating immune cells and muscle cells of the heart, and local immune cells called microglia in the brain.

Four weeks after the first heart attack, the researchers found the TSPO levels plummeted to normal both in brain and heart. However, the initial heart TSPO levels were enough to set the stage for later progressive heart failure. When they followed up on the mice around the eighth week, the researchers found the heart was again inflamed, and so was the brain. So heart failure and brain inflammation appear to go hand in hand, even when the heart starts to fail much later than the initial heart attack, explained Bengel.

“The more inflammation you have in the heart, the more inflammation you have also in the brain,” he said. “This may be an important connection, since other studies have shown that inflammation in the brain supports the progress of cognitive dysfunction.”

In a small substudy on human patients who survived a heart attack, the researchers found strong inflammation in their hearts and brains in the first week, but they did not follow up with subsequent tests. Also, the researchers did not give a cognitive assessment to either the mice or the human subjects, although Bengel hopes to pursue this in the future to further substantiate the results.

Jeremy Pearson, the associate medical director at the British Heart Foundation in London, said the imaging study sets a working hypothesis for larger studies to investigate the link between heart attack and dementia. “The two conditions share a number of risk factors, but this research strengthens the idea that there could be a direct link,” he said.

Pearson, however, did caution that the research is in too early a stage to suggest specific therapeutic implications. “The researchers suggest inflammation could be the key link, but it’s still too early to say whether anti-inflammatory medicines might lower the risk of developing dementia after a heart attack,” he said.