Researcher This diabetes drug helps with heart failure

Diabetes drug helps with heart failure

German researchers have been able to show for the first time that a particular diabetes drug affects the human heart muscle and improves cardiac function. Now there is hope for a therapy of heart failure with preserved pump function. Currently, there is no treatment that addresses the causes of this disease.

Around two million Germans suffer from heart failure

According to health experts, chronic heart failure (heart failure) is a growing challenge in Western society due to its frequency, mortality and hospitalization. It is associated with long disease, high levels of distress and poor prognosis for patients. According to experts, nearly two million people are affected in Germany alone. As a result of this disease, the heart is no longer able to provide the body with sufficient blood and oxygen. Researchers now found that sufferers could help a diabetes drug.

There is currently no causal treatment for heart failure with preserved pump function. But positive results with a diabetes drug now give hope. (Image: Robert Kneschke / fotolia.com)

What can help those affected

In recent years, new approaches to the treatment of heart failure have been reported repeatedly.

For example, researchers at the Hannover Medical School (MHH) found that some patients could use more iron because it makes the heart more resilient.

And scientists from the German Center for Cardiovascular Research (DZHK) have now shown that a diabetes drug for those affected can be of benefit.

The results of the researchers were published in the "European Journal of Heart Failure".

Drug reduced the death rate

As the DZKH writes in a communication, the drug empaglifozin in Germany is approved for the treatment of type II diabetes mellitus in adults.

The EMPA-REG OUTCOME study has now looked at the effects of empaglifozin in diabetic patients who also had cardiovascular disease.

Surprisingly, in this study, the drug reduced both the overall mortality rate and the number of deaths from cardiovascular disease by more than 30 percent each.

In addition, the number of hospitalizations fell due to a heart failure by 35 percent.

These positive effects were already apparent after two months and were reason enough for Professor Samuel Sossalla of the University Medical Center Göttingen and the University Hospital of Regensburg to assume that something happened directly to the heart muscle and to take a closer look at it.

"If empagliflozin were to act indirectly and influence secondary risk factors, such as blood pressure or cholesterol levels, it would take years to see an effect," said DZHK scientist Sossalla.

Researchers worked with explanted hearts

According to information, Sossalla and his associates worked with explanted human hearts taken from cardiac insufficiency patients when given a donor heart.

Specifically, from it prepared muscle strips, which can be imagined as a beating piece of heart in the laboratory.

"When we treated these heart muscle strips with empagliflozin, the cardiac muscle's ability to relax improved," Dr. Steffen Pabel, postdoc in the working group of Sossalla.

"The power of the heart, so its ability to contract, remained unchanged." The effect of empagliflozin on the ability to relax was regardless of whether there was also an additional diabetes disease or not.

Currently no causal therapy is available

As explained in the communication, the ability of the heart to relax is impaired in patients with cardiac insufficiency with preserved pump function. Half of all heart failure patients suffer from this form of heart failure.

The left ventricle is so thickened and stiff that in the so-called diastolic phase, it can no longer expand sufficiently and fill with blood.

As a result, in the subsequent contraction of the heart, the systolic phase, not enough oxygen-rich blood gets into the body.

For this heart failure, there are currently no therapies that fight the causes of the disease. Medicines can only alleviate the symptoms of the patients.

Effects on the human heart muscle strip

Sossalla and his research group are focusing on translational projects, ie work that helps to ensure that results from the laboratory actually reach patients.

"Here we are dealing with the opposite path," said Sossalla. "Results from the clinic lead back to the laboratory to understand the observed effect at all."

The advantage of in vitro examinations in contrast to clinical trials with patients is obvious to him:

"On isolated heart muscle cells we can see if the heart muscle is directly affected. Effects on the heart that are observed in patients may also always be indirect effects. "

The effect of empagliflozin observed on the human heart muscle strips could also be confirmed by the scientists in the hearts of mice with and without diabetes.

Mechanism for the increased ability to relax the heart muscle

In heart failure with preserved pump function, significantly fewer phosphate groups are attached to certain myocardial contractile proteins than in a healthy heart.

In their investigation of the mechanism of action, the researchers were able to show that directly after the administration of empagliflozin, the phosphorylation of precisely these contractile proteins increased significantly again.

"This first-time proven effect of empagliflozin explains why the cardiac muscle is able to relax again," says Pabel.

Another conceivable mechanism for the increased ability to relax, the change in the concentration of calcium ions in the heart muscle, the experts could exclude experimentally.

Because after the administration of empagliflozin, this concentration did not change in isolated human heart muscle cells.

The working group now wants to find out more about the mechanism of action in so-called stem cell heart muscle cells, which can be cultivated in the laboratory for months, and also on how empagliflozin acts in the long term.

For so far, they have only observed the acute effect - for more than 48 hours isolated cardiomyocytes do not survive in the laboratory. (Ad)