For decades, about half of all patients with heart failure appear to have hearts that contract normally—a syndrome now known as heart failure with a preserved ejection fraction (or HFpEF).
This type of heart failure was first seen primarily in slim, elderly women with high blood pressures and thicker heart muscle.
But as the incidence of obesity and diabetes has increased, many patients with HFpEF are now found to be severely obese with blood pressures not as high and heart muscle not as thick as seen in previous patients.
In a new study, researchers found that greater obesity seems to make muscle contraction much weaker in this very common form of heart failure.
The research was conducted by a team from Johns Hopkins Medicine.
Traditionally, this form of heart failure has been treated with medicines that often reduce contraction strength while improving the heart’s relaxation.
Further research will need to determine if this approach needs to be modified.
As part of the evaluation of patients with HFpEF, a tiny piece of the heart muscle is collected using a standard heart biopsy procedure.
In the study, the biopsy samples taken from patients who were less obese but had high blood pressure and thick heart muscle were compared with those with severe obesity but lower blood pressure and less thick heart muscle.
The team teased out single muscle cells from these samples and studied their function.
When the researchers added calcium to stimulate the cells to contract, those from the less-obese group responded normally.
However, the force response to high calcium was reduced by 40% in cells from patients with obesity.
In the third group of patients who had both high blood pressure and thicker hearts, as well as severe obesity, the force response in the cells given calcium was similarly reduced as in the most obese group.
The researchers believe this points to obesity as the key factor.
HFpEF was previously called diastolic heart failure, emphasizing the idea that although the heart could contract normally, it didn’t properly fill with blood when the heart relaxed in preparation for the next beat (called diastole).
While preserved contraction appears still true for less obese patients with high blood pressure and thick heart muscle, it doesn’t appear to hold true when they also have severe obesity.
The team says severe obesity alters underlying human biology—most recently brought in focus with the COVID-19 pandemic as obesity has been shown to be an independent risk factor for more severe disease and worse outcomes.
Many of COVID-19’s effects on artery function, the immune system and inflammation, and metabolism and heart stress may also be relevant to HFpEF.
One author of the study is David Kass, M.D.
The study is published in Circulation.
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