- A new study suggests severe obesity may weaken heart muscle cells in people with heart failure with preserved ejection fraction, or HFpEF.
- Researchers found that people who lost the most weight showed better heart muscle contraction, suggesting some of the problem may be reversible.
- The findings may help explain why HFpEF in severe obesity can behave differently from the traditional form of the disease.
Heart failure with preserved ejection fraction, or HFpEF, has long been seen mainly as a problem of stiffness.
The heart appears to pump normally on standard measures, but it relaxes poorly and does not fill properly.
A new study suggests that in people with severe obesity, that is not the whole story.
Researchers examined heart muscle cells from people with HFpEF and found that those with the highest BMI had weaker contraction at cell level.
That is striking because preserved ejection fraction can give the impression that pumping function is intact.
The researchers found that heart muscle cells from the most obese HFpEF group behaved more like cells from patients with classic heart failure and reduced ejection fraction.
They also identified a chemical change in a muscle protein called troponin I.
This change was more prominent in patients with severe obesity and seemed to weaken contraction.
That makes troponin I a possible treatment target in this subgroup.
The study also included a smaller group of patients who underwent weight loss treatment, mostly with GLP-1 drugs.
Those who lost the most weight showed improved contraction of heart muscle cells.
In people who lost at least 10% of body weight, peak force came close to normal.
That does not prove weight loss is a cure.
But it does suggest that some of the cellular damage linked to severe obesity in HFpEF may be reversible.
The broader message is important.
HFpEF is not one single disease.
In people with severe obesity, it may involve weaker muscle, not just stiffer muscle, and that may call for a different treatment approach.
