Heart Failure Pathways and the Role of Beta Blockers

2017-05-10 21:09:02
Tags: heart failure,Retail


Peter L. Salgo, MD: Let’s talk about some of the evidence-based care that we know works, we know we apply to heart failure patients, and we know where we’re going to go with that. We have the renin-angiotensin aldosterone (or RAAS) system. We’ve got the sympathetic nervous system (SNS) pathways. They’re both associated, in complex ways, with HFrEF (heart failure with reduced ejection fraction). Why don’t you put this puzzle together for us a little bit?
Akshay Desai, MD: I think we’ll focus on the HFrEF population, or the population with low ejection fraction. We all understand, in our neurohormonal model, that heart failure begins with a cardiac insult that results in the decline in cardiac output that initiates a sequence of sustained neurohormonal activation. And, initially, that neurohormonal activation, which is activation of the systems you talked about (renin-angiotensin and aldosterone, the sympathetic nervous system), are adapted. They help us to maintain blood pressure, to maintain cardiac output, and to augment forward flow. But over time, that sustained activation in the system promotes deleterious processes in the heart. The heart gets bigger and the heart gets stiffer. More salt and water are held on to when it’s not needed. That’s what precipitates the heart failure syndrome. So, sustained neurohormonal activation, we think, is the crux of heart failure progression, and most of our therapies interrupt that neurohormonal activation.
Peter L. Salgo, MD: If these are auto regulatory mechanisms that are there to correct problems with the physiology, low blood pressure, low oxygen delivery, whatever you would like to say, when you start to turn these things off, why is it not intuitive that you make things worse, not better?
Akshay Desai, MD: I think that’s actually one of the difficult things to understand about heart failure management. These systems are valuable and corrective to a point, but they’re not intended to be activated in an unfettered or unrestricted way.
Scott Solomon, MD: It’s also really important, Peter, to remember that they didn’t evolve to help us with heart failure. They evolved to help us with exsanguination—with bleeding. When we start to bleed out, we have to have systems that allow us to clamp down. That’s what the renin-angiotensin system is.
Peter L. Salgo, MD: As you pointed out, you want the SVR (systemic vascular resistance) to go up.
Scott Solomon, MD: Exactly. But what happens in heart failure is that your kidneys and your vasculature believes that’s happening, and so, these systems get activated, but incorrectly.
Peter L. Salgo, MD: What can we do to interrupt some of these vicious cycles, if you will? Is that a fair description of some of these pathways? And what can we do to get at the heart of HFrEF so that we can correct the pharmacologic abnormality and maybe help the heart do a better job? I would think that anybody listening to this broadcast, or watching it, would think, “Ahh, heart failure. Too much water, wrong place, diuretics.” Orly, what about that?
Orly Vardeny, PharmD, MS: There’s 2 different strategies for treating patients with HFrEF, and one is to treat the symptoms. That’s where diuretics come in. But diuretics don’t have any sort of effect on prolonging survival or anything beneficial in terms of disease progression. They actually worsen things. They lead to an activation of the renin-angiotensin aldosterone system. They’re a necessary evil. We use them because we have to treat the congestion, but in terms of the disease itself, or the syndrome, they’re not beneficial. What is beneficial is the other strategies that are geared toward blocking both the renin-angiotensin aldosterone system and the sympathetic nervous system.
Peter L. Salgo, MD: You’re telling me that if I’m squishing and I’m wet, I’m going to use a diuretic, but it’s not going to help because it’s just going to make things worse? It’s going to empty me out and potentiate all these other mechanisms that are bad. So, let’s take a look at these other mechanisms. If you say that some of them are not designed to do what they’re trying to do, let’s talk about the SNS. We have beta blockers here. Now, to me, at least on first pass when I first heard this, for someone who has a reduced ejection fraction, you’re going to give him/her an anticatecholamine, a beta blocker. That’s as counterintuitive as it gets, and yet, it works. Why does that work, Akshay?
Akshay Desai, MD: I think that, acutely, that is what happens when you give a beta blocker, and this is one of the reasons that, in patients who are in the throws of cardiogenic shock or patients who have acute decompensated heart failure, we tend not to give beta blockers because the negative inotropic effects dominate the effects. But in long-term application, and when the dose is titrated gradually, there is receptor downregulation. There’s a modification of secondary messenger streams, and there are effects on remodeling of the heart that actually become beneficial. So, we see ejection fraction acutely drop on administration of a beta blocker, but in chronic application, the ejection fraction goes up.
Peter L. Salgo, MD: That’s fascinating. You’re going to get at this long term. It’s not the acute phase that you’re looking at.
Sheryl Chow, PharmD, BCPS: Although I wanted to also add here, and I completely agree with you, but in patients that have been on beta blockers chronically and then have an acute episode, generally, you wouldn’t want to discontinue it unless the beta blocker uptitration is the cause of the acute heart failure.
Scott Solomon, MD: You know, Peter, it’s interesting. When I was in medical school, it was considered malpractice to give a patient with heart failure beta blockers.
Peter L. Salgo, MD: I was alluding to this.
Scott Solomon, MD: Yes. And the only reason we changed is because of well-designed clinical trials that challenge this conventional wisdom.
Peter L. Salgo, MD: And they were based on underlying understanding of the pathophysiology.
Scott Solomon, MD: Exactly.
Peter L. Salgo, MD: In other words, “It should work. Let’s try it and look at that.”
 

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