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A study has shown that some patients with artificial hearts have the ability to regenerate heart muscle, a discovery that could transform the treatment of heart failure. Published in Circulation, this research provides the strongest evidence yet that human heart cells can regenerate under certain conditions.
The study, co-led by Dr. Hesham Sadek of the University of Arizona Sarver Heart Center, investigated whether artificial heart devices, such as left ventricular assist devices (LVADs), enable heart muscle cells to regenerate. Researchers analyzed tissue samples from LVAD patients using an innovative carbon-dating method developed by collaborators at the Karolinska Institute. They found that patients with artificial hearts regenerated heart muscle cells at a rate more than six times higher than that of individuals with healthy hearts.
“This is the strongest evidence we have, so far, that human heart muscle cells can actually regenerate,” said Dr. Sadek, adding that the study highlights the heart's latent ability to repair itself under the right conditions.
The research builds on Sadek’s earlier findings that resting the heart might enable regeneration. LVADs provide this rest by pumping blood directly into the aorta, allowing the heart to function with less strain—a state analogous to a muscle recovering after an injury.
Heart failure currently has no cure, and treatments primarily focus on symptom management and slowing disease progression. Artificial hearts are typically used as a bridge to transplantation or as a last resort in advanced cases. However, this study suggests these devices might also trigger biological changes that promote heart recovery in some patients.
Notably, only about 25% of LVAD patients experience significant regeneration, which researchers term “responders.” Understanding why some patients respond while others do not is a critical next step. “The exciting part now is to determine how we can make everyone a responder, because if you can, you can essentially cure heart failure. ,” said Dr. Sadek.
This discovery could shift the paradigm of heart failure treatment, moving from symptom management to potential regeneration and recovery. By targeting molecular pathways that govern cell division, researchers hope to enhance this regenerative capacity, paving the way for innovative therapies.