A recent study led by Johns Hopkins Medicine researchers and published in Nature Cardiovascular Research examined the impact of obesity on muscle structure in patients with heart failure with preserved ejection fraction (HFpEF). HFpEF represents more than half of all heart failure cases worldwide and is increasingly occurring in patients with severe obesity and diabetes. However, effective therapies for HFpEF remain limited, with high hospitalization and death rates. Understanding the underlying causes of HFpEF is critical in developing successful treatments.
Lead investigator David Kass, M.D., explains that HFpEF is a complex syndrome involving abnormalities in many organs, despite normal heart contraction. Traditional heart failure drugs have not been effective in treating HFpEF, but drugs used for diabetes and obesity have shown promise in improving symptoms and reducing rehospitalization rates and mortality endpoints. Specifically, an SGLT2 inhibitor and GLP1-receptor agonist have been effective in treating HFpEF and have shown positive outcomes in diabetes and heart failure patients.
The study involved examining muscle tissue from 25 patients with HFpEF caused by diabetes and obesity and comparing it to heart tissue from normal donors. Ultrastructural abnormalities were found in the muscle tissue of the most obese patients with HFpEF, including swollen and disrupted mitochondria, fat droplets, and tattered sarcomeres. These abnormalities were not related to diabetes and were less prominent in less obese patients. The findings suggest a link between obesity and ultrastructural abnormalities in heart muscle.
The results of the study provide valuable insights into the impact of obesity on heart disease and offer potential targets for therapeutic interventions in HFpEF patients. The researchers hope that these findings will help in developing animal models for HFpEF and in exploring the effects of reducing obesity on reversing ultrastructural abnormalities and improving outcomes for HFpEF patients. The study sheds light on the microscopic level changes in the heart muscle of obese HFpEF patients and highlights the potential benefits of targeting obesity in treating HFpEF.
This study represents an important step in understanding HFpEF and the role of obesity in heart failure. By identifying ultrastructural abnormalities in obese patients with HFpEF, the researchers have provided valuable information for developing targeted therapies for this condition. The findings suggest that addressing obesity may help improve outcomes for HFpEF patients and highlight the importance of further research in this area. Overall, this study contributes to the growing body of knowledge on HFpEF and offers new insights into potential treatment approaches for this complex syndrome.
