Researchers have shown through a study published in Nature Scientific Reports a new gene therapy that could help couple non-excitable cells to undamaged heart cells to dramatically reduce post-infarction arrhythmias.
According to researchers at Cornell University they have managed to create a sort of bridge that enables non-heart cells to become electrically active and bring back normal pattern of electrical conduction in a damaged heart. Scientists point out that the most common and potentially lethal complication following a heart attack is the heart’s inability to do one of its most basic jobs: beat at a normal rate.
Following myocardial infarction, heart muscle cells are replaced by fibroblasts and new blood vessels, which do not conduct electricity and leave the heart susceptible to ventricular tachycardia – an excessive heart rate that can result in sudden death. These non-heart cells disrupt the normal pattern of electrical conduction that is critical for effective pumping.
The new work demonstrates a dramatic reduction of post-infarction arrhythmias in mice following the transfer of a single gene, Connexin43, which electrically couples non-excitable cells to undamaged heart cells.
The team’s excitement is tempered by the reality that these are mouse hearts, with induced, regularly shaped infarctions that are fractions of the size of those in humans. The spatial difference is not trivial, according to the lead author of the study.
Scientists still need to answer whether their technique will work in humans or even in larger animals and that’s an investigation underway. What’s most exciting about this is the ease with which this procedure could be done, if tests on larger animals prove successful, said the lead author.
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