The type in question, “heart failure with preserved ejection fraction” (a measure of the percentage of blood leaving the heart each time the heart muscle contracts), accounts for more than half of all heart failure cases worldwide.
This form of heart disease has been linked to high blood pressure, as well as excess muscle growth (hypertrophy) to help cope with the stress.
Over the past two decades, “heart failure with preserved ejection fraction” (HFpEF) has been occurring more frequently in patients with obesity and diabetes, according to the Journal of the American College of Cardiology.
The lack of human heart tissue studies to determine exactly what is abnormal has been a major challenge in developing treatments, the researchers explained.
“Heart failure with preserved ejection is a complex syndrome, involving abnormalities in many different organs,” said lead researcher David Kass, MD, professor of medicine at the Johns Hopkins University School of Medicine. “In HFpEF, the heart appears to contract well, but symptoms of heart failure persist. While many previous efforts to treat the condition with standard heart failure medications have been unsuccessful, success has since been found with diabetes and obesity medications.”
The study found that a drug used to treat diabetes, known as an SGLT2 inhibitor (sodium-glucose cotransporter 2 inhibitor), is currently the only evidence-based treatment for HFpEF that not only improved its symptoms, but also reduced long-term rehospitalization rates.
The weight loss drug GLP1-receptor agonist has also been tested and found to improve symptoms in patients.
In the new study, the research team obtained a small piece of muscle tissue from 25 patients diagnosed with varying degrees of HFpEF caused by diabetes and obesity, and compared it to heart tissue from 14 organ donors whose hearts were considered normal.
They examined the muscles using an electron microscope, which showed the muscle structure.
“Unlike looking at the heart with a conventional microscope, an electron microscope allows us to magnify the image up to 40,000 times its size,” says Dr. Maryam Meddeb, a cardiovascular specialist at the Johns Hopkins University School of Medicine who conducted the study. “This provides a very clear picture of the inside of the muscle cell, or what we call the microstructure, such as the mitochondria that act as power plants, and the sarcomeres (a unit of muscle fiber) that generate force.”
The researchers found that the microstructural abnormalities were particularly present in the tissues of the most obese patients, those with HEpEF, where the mitochondria were swollen, pale and ruptured, had many lipid droplets, and their sarcomeres appeared torn.
“The findings raise the key question of whether reducing obesity, as is now being done with many drug treatments, will reverse these microstructural abnormalities and thus improve HFpEF outcome,” Kass said.
The study was published in the journal Nature Cardiovascular Research.
Source: Medical Express
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2024-08-04 21:06:06
