Mechanical hearts can regenerate some heart tissue
Pilot study opens new avenue for development of heart regeneration
therapies

Date:
February 7, 2022
Source:
UT Southwestern Medical Center
Summary:
Mechanical hearts spur some regeneration in dormant parts of
failing hearts, according to a pilot study that shows promise for
developing regenerative heart therapies.



FULL STORY ========================================================================== Mechanical hearts spur some regeneration in dormant parts of failing
hearts, according to a UT Southwestern pilot study that shows promise
for developing regenerative heart therapies.


========================================================================== "This is by all accounts a small study, but it represents the first
evidence that mechanical hearts, which are tried and true, approved
treatments for end- stage heart failure patients, can generate new muscle tissue in the failing human heart," said lead author Hesham Sadek, M.D.,
Ph.D., Professor of Internal Medicine, Biophysics and Molecular Biology.

His findings, published in the American Heart Association flagship journal Circulation, found that left ventricular assist devices (LVADs), widely accepted in cardiology as life-saving interventions, showed metabolic reactivation in myocardial areas that had little or even no activity.

"What we need to do now is replicate these results in larger studies," Dr.

Sadek said. "If this holds true in larger studies, mechanical hearts
might emerge as a regenerative therapy to reverse heart failure, which
is the holy grail in heart failure treatment." Dr. Sadek has broken
extensive ground in this area of cardiology research with studies of
heart regeneration in mice that were published in the journals Nature
and Science.Cell reported his findings that oxygen metabolism causes
DNA damage in heart cells that shuts down their ability to regenerate.

Vlad Zaha, M.D., Ph.D., Assistant Professor of Internal Medicine, co-led
the study with Dr. Sadek.

"This study found evidence of regeneration in the parts of the heart that
would be considered dead," Dr. Zaha said. "It's a promising finding that
will lead to further investigations to replicate the results at larger
scale, and -- if confirmed -- to explore potential new therapies to
amplify this process in the context of LVAD support." The pilot study
of four patients, ages 39-59, who were taking medications for heart
failure measured metabolic activity by tracking a radiolabeled sugar
molecule called F-fluorodeoxyglucose (FDG) in the heart. This FDG signal
is considered a marker of "viable," or alive, heart tissue.

Positron emission tomography (PET) imaging tracked FDG uptake every six
months for up to 18 months. All participants exhibited some degree of
increase in FDG uptake in areas of previous metabolic inactivity at their baseline, which is suggestive of possible myocardial regeneration. Among
the four patients, the increase in FDG uptake from their baseline ranged
from 1.87% to 23.80%.

The study was funded in large part by UT Southwestern's Hamon Center for Regenerative Science and Medicine and the Leducq Foundation. Other UTSW researchers who contributed to the study include Mark Drazner, M.D.,
Pradeep Mammen, M.D., and Chao Xing, Ph.D.

========================================================================== Story Source: Materials provided by UT_Southwestern_Medical_Center. Note: Content may be edited for style and length.


========================================================================== Journal Reference:
1. Tiberiu A. Pana, Jainy Savla, Ingrid Kepinski, Adam Fairbourn,
Aneela
Afzal, Pradeep Mammen, Mark Drazner, Rathan M. Subramaniam, Chao
Xing, Kathryn A. Morton, Stavros G. Drakos, Vlad G. Zaha, Hesham
A. Sadek.

Bidirectional Changes in Myocardial 18 F-Fluorodeoxyglucose Uptake
After Human Ventricular Unloading. Circulation, 2022; 145 (2):
151 DOI: 10.1161/CIRCULATIONAHA.121.056278 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/02/220207155656.htm

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