Three different US studies in mice have given insights into heart attacks, including how to repair heart tissue and the benefits of sleep in recovery.
In work at the Icahn School of Medicine at Mount Sinai, New York, researchers induced heart attacks in mice and then analysed the animals’ brain signals and sleep patterns.
They found that after a heart attack, a deep stage of sleep increases (with slow brain waves and reduced muscle activity), caused by immune cells entering the brain from the blood, and activating a brain region that causes an increase in sleep.
The findings revealed that this communication between the heart and brain during sleep helps to reduce stress on the heart, promote healing and reduce inflammation - the findings were also mirrored in heart attack patients.
Senior author Cameron McAlpine said the work: “..supports including sleep as part of the clinical care of patients after a heart attack”.
Two other separate studies from the University of California, Los Angeles (UCLA), looked at how to repair the heart after a heart attack, as there are currently no treatments that can do this.
It has been known that a protein (GPNMB ) released by immune cells in bone marrow is linked to human heart failure, but its role in heart injury and function has been unclear.
One study showed that mice, lacking GPNMB, fared significantly worse after a heart attack (for example by having a higher incidence of heart rupture), whereas mice given an additional GPNMB dose showed improved heart function and less scarring.
GPNMB could therefore not only be a possible treatment option for the repairing the heart, but possibly other organs.
The other study developed an experimental treatment, based on monoclonal antibodies, that blocks the protein (ENPP1) responsible for increasing inflammation and scarring in the human body, that in turn worsens damage to the heart.
The treatment helped improve heart repair in mice, prevented excessive tissue damage and reduced scarring. Four weeks after a heart attack, only five per cent of the animals developed severe heart failure, compared to more than half the mice not given the treatment.
Arjun Deb, at UCLA, said: “Based on its effect on heart repair, this could represent a new class of tissue repair-enhancing drugs.”