RELAX-AHF: Results and Implications

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The HCPLive Peer Exchange “Advances in Heart Failure Management” features expert opinion and analysis from leading physician specialists on the latest developments in heart failure research, diagnosis, and management.

This Peer Exchange is moderated by Peter Salgo, MD, professor of medicine and anesthesiology at Columbia University and an associate director of surgical intensive care at the New York-Presbyterian Hospital in New York City.

The panelists are:

• Michael Felker, MD, MHS, Professor of Medicine, Chief of the Heart Failure Section, Director of the Heart Center Clinical Research Unit, and Director of the Advanced Heart Failure Fellowship at Duke University School of Medicine
• Jim Januzzi, MD, Roman W. DeSanctis Endowed Distinguished Clinical Scholar in Medicine at Massachusetts General Hospital and Hutter Professor of Medicine at Harvard Medical School
• Christian Schulze, MD, PhD, Associate Professor of Medicine, Division of Cardiology at Columbia University Medical Center, and Director of Research for the Center of Advanced Cardiac Care at Columbia University Medical Center

In this Peer Exchange segment, the panelists discuss the RELAX-AHF trial of serelaxin and why its results surprised and confused the cardiac community.

Human relaxin-2 is a naturally occurring vasoactive peptide hormone that mediates cardiovascular changes that accompany pregnancy. The recombinant form of this hormone, serelaxin, has shown promise for the treatment of acute heart failure. The RELAX-AHF trial studied serelaxin in hospitalized patients with acute heart failure. These patients were treated within 16 hours of arriving in the emergency room, says Felker, and dyspnea was improved in one way but not in another.

“The most striking finding,” Felker says, “was that when you looked out to 180 days, there was a 35% risk reduction in cardiovascular mortality with serelaxin,” although this was a tertiary endpoint built in for safety. But, despite this “substantial effect on mortality, we saw no effect on hospitalizations,” which was an important area of focus. “On the one hand, people were really excited by the results. On the other hand, they were confused by the results,” he says.

To try to explain the confusing results, Januzzi says, “rehospitalization is a very challenging endpoint in some ways because there are a lot of factors beyond cardiovascular mechanisms that lead to re-hospitalization for heart failure.” They range from treatment consequences to worsening renal function to purely social reasons, he says, “So a drug for acutely decompensated heart failure may or may not necessarily have as direct an effect on re-hospitalization as we might hope.”