Preliminary research suggests increasing cardiac ketones may benefit heart failure with preserved ejection fraction in mice.
Increasing ketone supply to the heart in mice with HFpEF allowed their hearts to utilize more ketones and produce more energy, potentially offering a new treatment approach.
HFpEF is a type of heart failure with signs of high left ventricle filling pressure and normal or near-normal ejection fraction, for which there is currently no evidence-based treatment.
Healthy hearts require a high rate of ATP production for continuous pumping, which comes from a balance of glucose and fats.
Study found that increasing ketone supply to hearts with HFpEF led to higher ATP production without interfering with glucose or fat use.
Research suggests that identifying key proteins involved in cardiac energy metabolism could lead to potential drug targets for treating HFpEF in the future.
Preliminary research presented at the American Heart Association’s Basic Cardiovascular Sciences Scientific Sessions in 2024 suggests that increasing ketone supply to the heart in mice with heart failure with preserved ejection fraction (HFpEF) can enhance the heart’s ability to utilize ketones and produce more energy. The study found that when HFpEF hearts were given more ketones, overall ATP production increased, leading to improved pumping ability without interfering with glucose or fat utilization. Heart failure with preserved ejection fraction is a common type of heart failure characterized by high left ventricle filling pressure despite normal ejection fraction.
Heart failure with preserved ejection fraction is a significant challenge in cardiovascular medicine, with no established evidence-based treatments currently available. The study highlights the importance of understanding the role of ketone use in HFpEF and suggests that increasing the ketone supply to the heart may optimize heart energy production and potentially improve cardiac function. While the study conducted on mice presents promising findings, further research involving different subgroups of HFpEF and experimental models closely aligned with human physiology is needed to advance the development of potential treatments for this condition.
