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A Paradigm Shift in the Treatment of Heart Failure?



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A small preliminary study could trigger a paradigm shift in the treatment of heart failure. The latest research is published today in Circulation and presented at Heart Failure 2018 and the World Congress on Acute Heart Failure, a congress of the European Society of Cardiology. The study suggests that heart failure may be caused by inappropriate fluid shifts in some patients and not by excess fluid.

Heart failure is a global pandemic affecting at least 26 million people worldwide and increasing their prevalence. Despite the significant advances in therapy and prevention, mortality and morbidity are still high and quality of life is poor.

It is currently believed that heart failure is caused by excess salt and fluid in the heart and lungs. However, 50% of patients with acute heart failure have no fluid overload when in hospital.

In these patients, an alternative mechanism might be that the fluid was inappropriately distributed from the abdominal cavity (splanchnic duct) to the heart and further to the lungs. It is believed that this leads to increased pressure in the heart, leading to impaired cardiac function (decompensation). It has been suggested that this redistribution is partly caused by hyperactivity of the splanchnic nerves, which causes a constriction of the vascular system in the abdomen.

This first proof-of-concept human trial attempted to prove that this fluid redistribution exists in patients with acute heart failure and could be a target for treatment. The study included five patients with acute heart failure admitted at Duke University Hospital in Durham, North Carolina, USA.

Splanchnic blockade was performed by injecting lidocaine on both sides of the spine under X-ray control. This is an established method of relieving abdominal pain in patients with pancreatic and duodenal cancer. Right ventricular catheterization was performed to measure pressures in the cardiac and pulmonary artery.

After lidocaine injection, the pressures on the right and left sides of the heart and pulmonary artery decreased rapidly, indicating that blood was moving from the heart and lungs to the abdomen. The pressure decrease started 1

5-20 minutes after the nerve block and reached the maximum effect after 30 minutes. The pressure returned to baseline after 90 minutes, which is the expected duration of the lidocaine effect. There were no adverse events.

Before and after the procedure, patients underwent a six-minute walk test and were asked about shortness of breath, a typical heart failure symptom. Both measures improved, but the differences were only statistically significant for the shortness of breath questionnaires, probably due to the low number of patients.

The main researcher Marat Fudim of the Duke Clinical Research Institute said: "This study supports the idea that volume redistribution is a cause of heart failure. When the splanchnic nerve is blocked, the abdominal vessel is no longer constricted and space is created, and the fluid shifts from the heart and lungs to the abdomen, where it should be in the heart and lungs, and patients feel better. "

Diuretics are a cornerstone of treatment for acute heart failure, but often cause kidney damage. "This may be because these patients do not really have extra fluids," Dr. Fudim. "Our study suggests that relocating fluid from the chest to the abdomen, rather than getting rid of fluid with diuretics, may be the appropriate treatment for some patients with acute heart failure."

Dr. Fudim noted that the nerve block in this study was transient. Future studies will need to investigate the influence of longer-acting drugs or even kill the splanchnic nerves. The latter was used to relieve pain in cancer patients. The nerve block must also be tested in patients with chronic heart failure.


Further information:
What is heart failure?

Further information:
Marat Fudimet al. Splanchnic Nerve Block for Acute Heart Failure, Circulation (2018). DOI: 10.1161 / CIRCULATIONAHA.118.035260

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Provided by:
European Society of Cardiology


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