Duke Health

Skip to main content

News & Media

News & Media Front Page

Small Study Suggests a New Way to Treat Fluid Buildup in Heart Failure

Duke team challenges the paradigm about fluid as a symptom of heart failure

Contact

Sarah Avery
Sarah Avery
Director
919-724-5343 Email

DURHAM, N.C. – One of the key features of heart failure is an accumulation of fluid in the heart and lungs that causes life-threatening symptoms, including shortness of breath, lightheadedness and an elevated heart rate.

This fluid buildup has long been considered a symptom of heart failure, but researchers at Duke University Medical School have explored a new theory: It might be a key contributor, and a fairly treatable one, at that.

Led by cardiology fellow Marat Fudim, M.D., the researchers performed a small proof-of-concept study among five acute heart failure patients at Duke University Hospital. The researchers performed a simple procedure essentially shutting off the spigot causing the fluid buildup, immediately improving other heart failure symptoms.

The study is being presented May 26 at the European Society of Cardiology’s Heart Failure 2018 meeting and is also published in the journal Circulation.

“Obviously, this is a small study, but the results from these five patients suggest that this approach has potential for one of the most common heart conditions in the world,” Fudim said, noting that more than five million people in the United States have heart failure and it is one of the leading causes of hospitalizations and death. 

Fudim and colleagues, including Manesh Patel, M.D., chief of Duke’s Division of Cardiology and member of the Duke Clinical Research Institute, designed the study to address a curious observation around the fluid buildup that accompanies heart failure: If the buildup were the result of a person simply retaining water, patients would see weight gain in the days and weeks before an acute episode. This isn’t the case. 

Instead, Fudim said, the fluid is a spilling of the natural stockpile that the body stores in the belly region for emergencies such as stress or trauma. The release of this extra blood, driven by an activation of nerves by hormones, is a welcome boost to the organs in fight-or-flight events.

With heart failure, however, the body appears to be stuck on alert, flooding the heart and lungs with fluid beyond the organs’ capacity to manage it. Controlling this process is a bundle called the splanchnic nerves.

What if, Fudim and colleagues surmised, they could turn off the portion of the splanchnic nerve bundle that controls the flood of fluid to the heart and lungs? The procedure is actually relatively simple and is not uncommon -- a similar procedure has been used for decades to ease abdominal pain among cancer patients. 

One side effect of the procedure among cancer patients was lower blood pressure as blood shifts into the belly region -- “which is exactly what we want to achieve for heart failure patients,” Fudim said.

The Duke study only briefly numbed the over-active area of the nerve bundle using a temporary anesthetic that lasted 90 minutes. Among the five heart failure patients who underwent the procedure at Duke, all showed a marked reduction of pressures inside the heart and increases in cardiac output. This was primarily driven by a significant reduction in vascular resistance and improved arterial vascular storage space. 

“The splanchnic vascular compartment may be a key player in the fluid imbalance that is a hallmark of acute and chronic heart failure” Patel said. “These findings suggest that continued research into therapeutic use of splanchnic nerve block for the treatment of acute and potentially also chronic heart failure is of interest.”

Patel and Fudim said larger studies are already planned and will include a control group to compare outcomes, which was not part of the current study.

In addition to Patel and Fudim, study authors include W. Schuyler Jones, Richard L. Boortz-Marx, Arun Ganesh, Cynthia L. Green and Adrian F. Hernandez. 

The study received funding support from the American Heart Association (17MCPRP33460225).

News & Media Front Page