Preventing Heart Failure Readmissions Through Better Care - Episode 4
Peter L. Salgo, MD: Tell me if I’m getting this right. The definition of heart failure is the inability of the heart to produce an adequate cardiac output without the expense of a very high preload on the left side. Your left atrial pressures go up, your pulmonary venous pressures go up, and the transient BNP (B-type natriuretic peptide) pressures go up. Is that fair?
Scott Solomon, MD: Exactly.
Peter L. Salgo, MD: What’s BNP? How does BNP measure any of that? That’s a test that we’re using. What is BNP?
Sheryl Chow, PharmD, BCPS: BNP is released in response to ventricular stretch, which occurs in the event of increased preload. So, it’s going to be released. It actually counteracts a lot of the deleterious effects of the RAAS (renin—angiotensin aldosterone system) and the sympathetic nervous system.
Peter L. Salgo, MD: You’re telling me that I have an increased presystolic wall tension somewhere deep in the bowels of the heart. I don’t know if the heart has bowels.
Scott Solomon, MD: That’s a mixed metaphor, Peter.
Peter L. Salgo, MD: Yes, it is, and I love it. BNP is coming out, right?
Sheryl Chow, PharmD, BCPS: Absolutely.
Peter L. Salgo, MD: You’re telling me that my residents, now, don’t even have to listen for rattles or an S3 heart sound? They don’t have to examine the patient? They just get a blood test and check for BNP and that’s it, yes?
Scott Solomon, MD: No.
Orly Vardeny, PharmD, MS: It’s only one piece of the puzzle, if you will. Because there’s, first of all, other conditions or other things that can raise BNP. It’s not necessarily just BNP, but it’s BNP in addition to the constellation of symptoms the person presents with.
Peter L. Salgo, MD: But there wasn’t a blood test before. Now there is.
Akshay Desai, MD: That’s sort of a challenge. I think all of us want to reach for a blood test and make a diagnosis or reach for radiologic imaging. But heart failure is not like that. And, in fact, many of us who treat heart failure patients have trouble recognizing it. I think that the more tools we have to make the diagnosis, the more useful it is. BNP is one of those tools. Like any diagnostic test, Peter, if you’re uncertain about the diagnosis, that’s where BNP is useful. There are some patients where it’s obvious you have heart failure. They come in, they can’t breathe when they lie flat, they’re swollen, and their heart function is weak on the echocardiogram. That patient has obvious heart failure. Then there are other people who are clearly short of breath because they have pneumonia. So, it’s the patient in the middle where you’re a little uncertain whether it’s the lung or the heart or something else that’s making them short of breath. That’s where a high BNP helps you.
Scott Solomon, MD: Peter, I think what you’re hearing is that we all believe you have to take a history first. You do a physical exam, and then, maybe, you can measure the BNP. I’m being facetious, but obviously, you need all of these things. We have to be able to incorporate all of this evidence.
Sheryl Chow, PharmD, BCPS: I just want to also underscore everything that you’ve been saying. I know a good friend of mine has always said, “BNP makes bad physicians worse and good physicians better, and it should be used as a tool, not a crutch.”
Scott Solomon, MD: I think that’s worth making clear, because there is some confusion about the difference between the BNP assay and NT- (or N-terminal) proBNP. These can sometimes be confusing, and it’s worth at least bringing this out.
Peter L. Salgo, MD: So, how would you parse that out? What is the difference?
Scott Solomon, MD: There are 2 separate assays, and it turns out that it’s dependent on which one you have access to at your hospital—you may use the BNP assay, you may use the NT-proBNP assay. The numbers are different. NT-proBNP tends to be 4 to 6 times higher than BNP in general. BNP is a hormone; it’s actually there for a reason. As Sheryl said, when BNP goes up, it’s one of the endogenous systems that we have to counteract the deleterious effects of renin—angiotensin system activation.
Peter L. Salgo, MD: It isn’t there by accident.
Scott Solomon, MD: Right. Now, NT-proBNP is actually broken off the pathway earlier on. It’s inert; it doesn’t actually do anything. It can still be measured, and it’s still a measure of the severity of heart failure. They’re both very good predictors of outcome. They’re both very good predictors of all sorts of things in heart failure. But they’re different, and it’s worth being clear about this. It will come up when we talk later, about some of the therapies, because the effect is different.
Sheryl Chow, PharmD, BCPS: To add to what Scott was saying about the difference between NT-proBNP and BNP, it’s not really a 1:1 ratio that we’re looking at. You would think it is because it’s cleaved off the BNP to form the NT-proBNP. But the issue is that BNP has a much shorter half-life (about 23 minutes), where NT-proBNP has a much longer half-life (about 120 minutes). It hangs around longer, and it takes longer to clear.
Peter L. Salgo, MD: Is that better or worse?
Sheryl Chow, PharmD, BCPS: It depends on how you look at it.
Transcript edited for clarity.