New gene therapy to help damaged human hearts beat
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. If there were a way to make these cells electrically active, one could bridge the conduction block to a certain degree, and greatly decrease dangerous post-infarction complications.
Michael Kotlikoff, provost of Cornell University and a professor of molecular physiology, is part of an international collaboration that is aiming to bridge that gap in damaged hearts with a simple gene-therapy approach.
Their work demonstrates a dramatic reduction of post-infarction arrhythmias following the transfer of a single gene, Connexin43, which electrically couples non-excitable cells to undamaged heart cells.