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A paradigm shift in heart failure treatment?

Heart failure may be caused by inappropriate fluid shifts in some patients rather than excess fluid

Heart Failure

Vienna, Austria – 26 May 2018:  A small, preliminary study could trigger a paradigm shift in the treatment of heart failure. The late-breaking research is published today in Circulation and presented at Heart Failure 2018 and the World Congress on Acute Heart Failure, a European Society of Cardiology congress(1,2). The study suggests that heart failure may be caused by inappropriate fluid shifts in some patients rather than an excess of fluid.

Heart failure is a global pandemic affecting at least 26 million people worldwide and is increasing in prevalence. Despite the significant advances in therapies and prevention, mortality and morbidity are still high and quality of life poor(3).

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 do not have fluid overload when they present to hospital.

In these patients, an alternative mechanism could be that fluid has been inappropriately redistributed from the abdominal (splanchnic) compartment to the heart and lungs. It is thought that this leads to increased pressure in the heart, resulting in impaired heart function (decompensation). It has been proposed that this redistribution is partly caused by overactivity of the splanchnic nerves, which cause the vasculature in the belly to constrict(4).

This first proof of concept study in humans sought 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 to Duke University Hospital in Durham, North Carolina, US.

Splanchnic nerve block was performed by injecting lidocaine on either side of the spine under X-ray guidance. This is an established procedure that is used to relieve abdominal pain in patients with pancreatic and duodenal cancer. Right heart catheterisation was conducted to measure pressures in the heart and pulmonary artery.

Following lidocaine injection, pressures in the right and left side of the heart and pulmonary artery reduced rapidly, suggesting that blood shifted from the heart and lungs to the belly. The reduction in pressures began 15–20 minutes after the nerve block and reached the maximum effect at 30 minutes. Pressures mostly returned to starting levels at 90 minutes, which is the expected duration of lidocaine action. There were no adverse events.

Before and after the procedure, patients performed 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, likely due to the small number of patients.

Principal investigator Dr Marat Fudim, of Duke Clinical Research Institute, said: “This study supports the notion that volume redistribution is a cause of heart failure. When the splanchnic nerve is blocked, the belly vasculature is no longer constricted and space is created. Fluid then shifts from the heart and lungs to the abdomen, where it should be. This normalises pressures in the heart and lungs and patients feel better.”

Diuretics are a cornerstone of treatment in acute heart failure but often cause kidney damage. “This may be because these patients do not actually have extra fluid,” said Dr Fudim. “Our study suggests that shifting fluid from the chest to the belly, instead of 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 temporary. Future studies will need to examine the impact of longer-acting medications or even killing the splanchnic nerves. The latter has been used to alleviate pain in cancer patients. The nerve block will also need to be tested in patients with chronic heart failure.



Notes to editor

Authors: ESC Press Office
Tel: +33 (0)4 8987 2499
Mobile: +336 (0) 2314 5784


SOURCES OF FUNDING: The study was sponsored by an American Heart Association Grant, 17MCPRP33460225 (PI Marat Fudim).


DISCLOSURES: M.F. is supported by an American Heart Association Grant, 17MCPRP33460225 and NIH T32 grant 5T32HL007101; he consults for Coridea, and Axon Therapies. Other authors have nothing to disclose.


References and notes

1Fudim M, Jones WS, Boortz-Marx RL, Ganesh A, Green CL, Hernandez AF, Patel MR. Splanchnic Nerve Block for Acute Heart Failure. Circulation. 2018. 10.1161/CIRCULATIONAHA.118.035260. [Epub ahead of print].

2The abstract ‘Splanchnic nerve block for acute heart failure’ will be presented during the session Late breaking trial I – Acute heart failure which takes place on 26 May from 08:30 to 10:00 CEST in room Berlin.

3Savarese G, Lund, LH. Global Public Health Burden of Heart Failure. Card Fail Rev. 2017;3:7–11.

4Fudim MHernandez AFFelker GM. Role of Volume Redistribution in the Congestion of Heart Failure. J Am Heart Assoc. 2017;6(8). pii: e006817. doi: 10.1161/JAHA.117.006817.

About Heart Failure 2018 and the World Congress on Acute Heart Failure

Heart Failure and the World Congress on Acute Heart Failure are annual congresses of the Heart Failure Association (HFA) of the ESC.


About the Heart Failure Association

The Heart Failure Association (HFA) is a branch of the ESC. Its aim is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.

About the European Society of Cardiology

The European Society of Cardiology brings together health care professionals from more than 150 countries, working to advance cardiovascular medicine and help people lead longer, healthier lives.


Information for journalists attending Heart Failure 2018

Heart Failure 2018 and the World Congress on Acute Heart Failure will be held 26 to 29 May at the Messe Wien in Vienna, Austria. Read the full scientific programme.

  • To register on-site please bring avalid press card or appropriate letter of assignment with proof of three recent published articles (cardiology or health-related, or referring to a previous ESC Event).
  • Press registration is not available to industry or its public relations representatives, event management, marketing or communications representatives.