Understanding the Neurohormonal Systems in Heart Failure

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The MD Magazine Peer Exchange “Managing Heart Failure Today: Current Best Practices and New Treatment Options” features a panel of physician experts discussing key factors to consider when making treatment decisions for patients with heart failure and their own clinical experiences with recently approved medications for the treatment of heart failure.

This Peer Exchange is moderated by Peter Salgo, MD, professor of medicine and anesthesiology at Columbia University College of Physicians and Surgeons, and an associate director of Surgical Intensive Care at New York-Presbyterian Hospital.

The panelists are:

• Michael Felker, MD, MHS, professor of medicine and chief of the Heart Failure Section at Duke University School of Medicine, in Durham, NC
• Milton Packer, MD, Distinguished Scholar in Cardiovascular Science, Baylor Heart and Vascular Hospital, Baylor University Medical Center, in Dallas, TX
• Scott Solomon, MD, Senior Physician and director of Non-Invasive Cardiology at Brigham and Women’s Hospital, and Edward D. Frohlich Distinguished Chair and professor of medicine at Harvard Medical School, in Boston, MA
• John R. Teerlink, MD, director of Heart Failure at San Francisco Veterans Affairs Medical Center and professor of medicine at UCSF in San Francisco, CA

Milton Packer, MD: Let’s go back to the framework that Scott [Scott Solomon, MD] proposed. There are 2 neurohormonal systems that are lethal in patients with heart failure. It is really important to block them, block them thoroughly, and block them safely.

One of those systems is the sympathetic nervous system. The mainstay of doing that is [with] a beta-blocker given at the highest-tolerated dose, because beta-blockers do lots of magical things to patients with heart failure that are really beneficial. There are some people who take a beta-blocker whose heart rate is still elevated above 70. In those patients, ivabradine can play a role in reducing hospitalizations. That sets the framework for the sympathetic nervous system.

Now, we’ll shift to the renin-angiotensin-aldosterone system. The way that we have conventionally blocked that system is with the use of an angiotensin-converting enzyme inhibitor (ACE inhibitor), or an angiotensin receptor blocker, together with a mineralocorticoid receptor antagonist and aldosterone antagonist—such as spironolactone or eplerenone. Those work on different parts of the renin-angiotensin system, but they actually do not do a completely thorough job at neutralizing the effects of that system.

There is a new drug which not only blocks the effects of the renin-angiotensin system, but also enhances the effects of compensatory peptides. The type of drug we’re talking about is an angiotensin receptor/neprilysin inhibitor.

Peter Salgo, MD: That’s the ARNI, [which is] what he was talking about earlier.

Milton Packer, MD: What is happening is [that] ARNIs are replacing ACE inhibitors and angiotensin-receptor blockers. The world has become, in many ways, much clearer than it used to be. It used to be, in the past, that you would give an ACE inhibitor, a beta-blocker, maybe a little bit of spironolactone, and you would be finished. Now, we say, “Look, we know that this has been the cornerstone of therapy, but in both systems, we can, and we must, do better.

Peter Salgo, MD: First of all, I want to thank you. That was one of the clearest descriptions of this 2-class drug system I’ve ever heard.