Heart Failure
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A clinical study led by scientists at Karolinska Institute and Karolinska University Hospital in Sweden reveals how the hunger hormone ghrelin can increase cardiac pump function in patients with heart failure.

According to the Heart Failure Society of America, nearly seven million Americans over the age of 20 suffer from heart failure. The disease causes the heart muscle to weaken, leaving it incapable of providing the body with sufficient oxygen and nutrients. Current treatments slow down progression of the disease but are unable to increase cardiac pump function.

Reporting in the European Heart Journal, researchers at Karolinska Institute were now able to directly increase the heart’s pump function by targeting a hormone called “ghrelin.” According to the researchers, the hormone has many receptors in cardiac tissue and is normally responsible for increasing appetite and releasing growth hormones, making it a promising target for stimulating the heart muscle.

“Heart failure is the most common cause of hospitalisation in older generations and is associated with a poor quality of life and high mortality. If we can find ways to increase the heart’s pump function, we can potentially improve life quality and prognosis for these patients,” said Lars Lund, professor at the Department of Medicine at Karolinska Institute and first author of the study in a press statement.

In the double-blind clinical study, 30 patients with chronic heart failure were randomly divided into two groups, receiving either a modified version of the ghrelin hormone as active treatment or a placebo. Both compounds were administered intravenously for two hours and the participants of the study were followed up after a two-to-five days.

The researchers were able to show that after two hours of active treatment with ghrelin, the volume of blood pumped by the heart in one minute (i.e. cardiac output) had increased by an average of 28 percent, compared to a small reduction in the placebo group.

According to the scientists, the reason for the increase in cardiac output was that more blood was pumped from the heart per heartbeat, whereas the heart rate remained unchanged or even slightly slower. After the follow up, the pump capacity in the ghrelin group remained 10 percent higher compared to the patients that had received placebo treatment.

By studying isolated mouse heart cells in the laboratory, the scientists were able to identify a possible underlying mechanism for the improvement of cardiac pump function using ghrelin. The hormone increased the contractile function of the heart cells without mobilizing calcium ions, which are normally essential for muscle contraction.

The researchers say that none of the patients experienced adverse side effects such as hypotension, tachycardia, arrhythmia, or ischaemia. However, due to the small size of the patient group and the relatively short follow-up, the researchers believe that larger clinical studies will be needed to estimate the effectiveness of the treatment in the long run.

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