Tony Breu

Tony Breu



1/18 🤔Why does heart failure with preserved ejection fraction (HFpEF) lead to sodium retention? With reduced ejection fraction (HFrEF), decreased cardiac output (CO) leads to neurohormonal activation and sodium avidity. If CO is preserved in HFpEF, what's the inciting event?

2/ Let's start with cardiac output (CO) and cardiac index (CI). 💡At rest, most patients with HFpEF have normal CO/CI. But, these patients lack cardiac reserve. With exercise, their heart rate and CO/CI do not rise as much as in those without HFpEF.

3/ I suspect that the normal CO/CI at rest doesn't leave patients with HFpEF as at risk for the neurohormonal activation we see in HFrEF. Let's look at this next. More specifically: 🤔Is the neurohormonal axis increased in HFpEF?

6/ Taken as a whole, I interpret the data as indicating that: ☞ In HFrEF, neurohormonal activation is central, with studies consistently supporting this mechanism ☞ In HFpEF, neurohormonal activation may play a role though the data is less consistent and less convincing

7/ Support for this interpretation can be found in the negative trials aimed at neurohormonal blockade in HFpEF. ❌ β-blockers ❌ ACE inhibitors ❓ Aldosterone antagonists

8/ It's worth wondering why we see ANY neurohormonal activation in HFpEF. Though values aren't as high as in HPrEF, some studies suggest they are higher than in controls. And remember, it's hard to invoke CO/CI. Obesity may provide an answer in some patients.

11/ Collectively, these studies show that in obesity-associated HFpEF, aldosterone isn't simply a result of cardiac dysfunction but is also a product of adipose tissue. I'm excited to see how this mechanism of sodium avidity plays out in the years ahead.

12/ Note that adipocyte-medicated increases in aldosterone can't explain the mild elevations in renin and norepinephrine noted earlier. But it does demonstrate that there is more than one path to elevated aldosterone. It also highlights the complex pathophysiology of HFpEF.

13/ Before closing, we still must ask: 🤔If the neurohormonal axis is NOT the main mechanism of sodium retention HFpEF, what else might be going on?

14/ Some argue that primary renal sodium retention plays a central role in HFpEF. One proponent of this theory, @JamesCFangMD, wonders: could HFpEF sit at the RENAL end of the cardiorenal syndrome spectrum?

16/ In one study in HFrEF, sodium retention was seen even when renin and aldosterone were appropriately suppressed by a high-salt diet. 💡This highlights that neurohormonal activation isn't the only mechanism, even in HFrEF.

18/18 🫀HFrEF is associated with ↓CO/CI and neurohormonal activation leading to sodium retention 🫀HFpEF is associated with preserved CO/CI at rest and less neurohormonal activation 🫀HFpEF may be associated with primary renal sodium retention and obesity-mediated ↑aldosterone

I want to extend a huge THANK YOU to... 🥇@MKIttlesonMD 🥇@ramontgo For providing peer review of this tweetorial.

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