Elevated brain natriuretic peptide levels in chronic fatigue syndrome associate with cardiac dysfunction: a case control study, 2018, Newton et al

Abstract
Objectives To explore levels of the brain natriuretic peptide (BNP) and how these associate with the cardiac abnormalities recently identified in chronic fatigue syndrome (CFS).

Methods Cardiac magnetic resonance examinations were performed using 3T Philips Intera Achieva scanner (Best, Netherlands) in CFS (Fukuda) participants and sedentary controls matched group wise for age and sex. BNP was also measured by using an enzyme immunoassay in plasma from 42 patients with CFS and 10 controls.

Results BNP levels were significantly higher in the CFS cohort compared with the matched controls (P=0.013). When we compared cardiac volumes (end-diastolic and end-systolic) between those with high BNP levels (BNP >400 pg/mL) and low BNP (<400 pg/mL), there were significantly lower cardiac volumes in those with the higher BNP levels in both end-systolic and end-diastolic volumes (P=0.05). There were no relationships between fatigue severity, length of disease and BNP levels (P=0.2) suggesting that our findings are unlikely to be related to deconditioning.

Conclusion This study confirms an association between reduced cardiac volumes and BNP in CFS. Lack of relationship between length of disease suggests that findings are not secondary to deconditioning. Further studies are needed to explore the utility of BNP to act as a stratification paradigm in CFS that directs targeted treatments.
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Online version of the full text - http://openheart.bmj.com/content/4/2/e000697.full
 
I think this is interesting. My only disappointment is that they did not give us scatter plots for the data but only histograms. Nevertheless, the difference between patients and controls looks biologically relevant. A paradoxical relation to cardiac volume is also intriguing, since that would fit with a regulatory disturbance rather than a primary cardiac abnormality.

Some other disease controls with fatigue would be useful - something they have access to.

I think it is worth watching this space.
 
Barry said:
Given that PwME lack muscle power, and that the heart is a power-hungry muscle, is the low cardiac volume for PwME inevitable anyway? What is cause and what is effect?
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In most situations where the heart muscle is failing the cardiac volume is large. An increase in size is almost the definition of heart failure, as laid down by Starling and Bayliss a century ago. A poor heart sags into a bigger heart. What is interesting here is that the situation is the opposite.
 
Jonathan Edwards said:
In most situations where the heart muscle is failing the cardiac volume is large. An increase in size is almost the definition of heart failure, as laid down by Starling and Bayliss a century ago. A poor heart sags into a bigger heart. What is interesting here is that the situation is the opposite.
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So what would this mean for volumetric blood flow through the heart in PwME?
 
the pathogenesis of autonomic dysfunction in patients with CFS
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Since having ME my wife has had trouble with walking, that seems possibly more than just muscle issues. She told me long time back it was almost as if she had to learn to walk again. And she cannot walk with her head up for long - she has to look down at where she is going, because she has, to a degree, consciously think her way through the process of walking, whereas before of course it took no conscious effort at all.
 
Jonathan Edwards said:
The cardiac volume may not mean much at all. An athlete's heart is thick-walled but not enlarged in terms of volume capacity. A diseased heart has a bigger volume but a reduced proportion of that volume is pumped at each beat (lower ejection fraction).
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That is where I was coming from, but not being very clear. The heart is essentially a clever displacement pump I think, the fluid displacement at each stroke primarily dictated by the change in volume at each stroke. So I was wondering if we know what the displacement per beat is for PwME, compared to a healthy person, irrespective of overall volume. My wife reckons she has always had "poor circulation", mainly due to having always felt the cold very readily, especially in hands and feet ... not sure if that hangs together medically though.

When you said that heart failure results in the heart muscles slumping, I - probably mistakenly in retrospect - assumed the converse to be true, that a heart being too small would be due to the muscles being excessively tensed. But I imagine it is more likely due to the heart having simply atrophied for some reason? Or even that some people never developed full-size hearts in the first place?
 
Mij said:
@Barry this has been my experience at times, but it's not permanent. I don't know what brings this on
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Firstly, I have only a lay knowledge of medical issues, so these are just my thoughts.

My thinking is that some aspects of walking must presumably be controlled by our autonomic nervous system, being as you do not normally have to consciously think yourself through all the low level motor-control operations when you walk. Like they way when you pick up a cup of tea and drink it, although you consciously do that, there is an amazing series of low level motor control activities that occur unconsciously to achieve that. If you had to do all that at a conscious level it would be incredibly fraught and difficult.

So when observing my wife's walking, and what she describes, it feels to me like she may have lost some (certainly not all) of that low level motor control, being as she has to consciously think her way through that to some degree. The mention of autonomic dysfunction was what prompted me to comment here.
 
Lilpink said:
Didn't Cheney way back yonder find it was the 'fill' as opposed to the 'push' that was at issue in the hearts of pwme?
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Which if true, might mean that muscle(s) involved with the intake stroke are more at issue? And/or valve(s) not working properly?
 
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