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A group of researchers managed to embed a naturally-occurring protein into a patch which can help heal muscles damaged by heart attacks.
After they attached the patch on the muscle of lab animals, scientists learned that it can also improve cardiac function and survivability in the wake of a heart attack.
The patch has yet to be tested on humans, but the experiments on mice and pigs showed promising results. Scientists wrote in their report that lab animals regained almost full cardiac function within one to two months after the heart attack.
The research team hope to use the patch in clinical trials in two years’ time. Lead author of the study Pilar Ruiz-Lozano of Stanford University and her fellow researchers from the University of California and UC San Diego published a research paper on the findings Wednesday in the journal Nature.
Mark Mercola, one of the study authors, explained that the patch doesn’t require additional drugs to trick the immune system into believing that the device is a natural component of the body. Plus, the patch can be mass produced, and doesn’t cost as much as other technologies on the market do.
The team learned form laboratory tests that a protein called Follistatin-like 1 (FSTL1) has a positive effect on heart muscle tissue, forcing it to regenerate faster after a heart attack. Next, they came up with the idea of embedding it to a flexible patch that can be glued to the hearts of lab animals that were subdued to a forced myocardial infarction.
Surprisingly, the miracle protein helped the cells within the animals’ heart muscle to regenerate at amazing rates and rebuild the affected organ in relatively little time. Scaring was also kept to a minimum, the team noted.
Dr. Ruiz-Lozano explained that current medical technologies used to treat damaged heart muscle after a major cardiac event cannot address muscle regeneration and scaring. As a result, patients gradually lose cardiac function and become impaired and even face risk of premature death.
Although, patients usually survive a first heart attack, the event leaves scares on the heart muscle and weakens it. As a consequence, the muscle can no longer work at maximum capacity when trying to pump blood. Moreover, the local pressure forces the scarring to expand which often results in heart failure.
Heart failure can be deadly and is often tied to a low survival rate since half of patients die within six years. Current drugs that try to offset heart attacks’ outcomes try to help the damaged heart to pump blood easier and eventually prolong the patient’s lives. But none of these drugs can rebuild damaged heart muscle.
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