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January 25, 2025 – Cedars-Sinai Medical Center, Los Angeles – A groundbreaking study conducted at Cedars-Sinai has revealed that a specially designed drug, PR-364, could potentially prevent heart failure in heart attack survivors. The study, which was recently published in the European Heart Journal, demonstrates that the drug successfully prevented heart failure in laboratory mice that had experienced a heart attack. This promising discovery opens up possibilities for new treatments for heart failure, a condition that affects up to 30% of heart attack survivors within a year.
Heart failure occurs when the heart is unable to pump enough blood to meet the body’s needs, causing symptoms like fatigue, shortness of breath, and swelling. It is often a result of heart attacks, which damage the heart muscle. Despite the survival of heart attack victims, many develop this debilitating condition, which drastically affects quality of life and shortens life expectancy.
The study focused on adult male laboratory mice that had undergone a heart attack (myocardial infarction). The administration of PR-364, a small molecule, showed remarkable results in preserving the heart’s pumping power and mitigating the progression of heart failure. In comparison, untreated mice showed significant deterioration in heart function.
To better understand why PR-364 had such a profound effect, the researchers examined the drug’s impact on mitochondria, the powerhouses of cells that generate the energy necessary for various cellular functions. The data revealed that PR-364 improved mitochondrial health in multiple ways:
- Enhanced Mitophagy: PR-364 boosted the process by which damaged mitochondria were cleared away, aiding the repair of heart muscle.
- Increased Mitochondrial Production: The drug stimulated the creation of new mitochondria.
- Improved Mitochondrial Function: PR-364 enhanced the overall performance of mitochondria, further contributing to heart repair.
These results suggest that PR-364 could help prevent heart failure by enhancing the heart’s ability to recover from the damage caused by a heart attack.
“Taken together, these effects suggest how PR-364 helped prevent the development of heart failure after heart attacks in laboratory mice,” said Dr. Jennifer Van Eyk, a professor of Cardiology and the director of the Advanced Clinical Biosystems Institute at Cedars-Sinai. “While our data does not prove that PR-364 would have the same impact on human patients, it points to a promising path for future heart failure treatments for survivors of heart attacks.”
The next steps for the research include investigating whether a second-generation version of PR-364 may be more effective, exploring gender-specific responses to the drug, and delving deeper into the mechanisms through which PR-364 works.
Eduardo Marbán, MD, Ph.D., the executive director of the Smidt Heart Institute at Cedars-Sinai, emphasized the significance of these findings. “More people than ever are surviving heart attacks. This study is particularly exciting because it demonstrates that the drug was effective even when administered two hours after the heart attack, making it a potential treatment option for patients after the event.”
Disclaimer: Although the findings are promising, it is important to note that this research was conducted on laboratory mice and further studies are required to determine if PR-364 will have the same effect in human patients. The drug’s safety and efficacy in people have yet to be established.
For more details, refer to the study titled “Enhanced Parkin-mediated mitophagy mitigates adverse left ventricular remodelling after myocardial infarction: role of PR-364,” published in the European Heart Journal (2024). DOI: 10.1093/eurheartj/ehae782.
