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

A few random Googled links to what look to be similar studies:
Reduced cardiac volumes in chronic fatigue syndrome associate with plasma volume but not length of disease: a cohort study - http://openheart.bmj.com/content/3/1/e000381
Chronic fatigue syndrome: comments on deconditioning, blood volume and resulting cardiac function - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4236909/
In some patients with chronic fatigue syndrome, left ventricular function may be involved - https://www.eurekalert.org/pub_releases/2003-04/aps-isp040903.php
 
Barry said:
Is the problem because it's by Cort, or because it is unreliable?
Click to expand...
For me personally, it's because it's by Cort, for both recent history reasons and his propensity to leap to conclusions in other articles that I've read by him. That particular article though may well be accurate, I don't know as I haven't read it.

And apologies to all for taking this off-topic.
 
From the paper:
Another explanation is that the higher BNP levels are causing a diuresis (or natriuresis) and that this is depleting the plasma/blood volumes and leading to the smaller cardiac volumes. Studies from our group and others have shown smaller plasma volumes in CFS [6,7] and studies with patients with orthostatic hypotension have reported high BNP levels in some patients [18] and have been suggested as potentially causative.
Click to expand...

Low blood volume in ME/CFS patients has been suggested for decades. I don't know if anyone has rigorously tested the hypothesis in a well-characterized cohort using radioactive marker concentrations as a metric. In 2015, Dr. Bell wrote an article on low blood volume in ME/CFS at healthrising.org.

https://www.healthrising.org/forums/resources/dr-david-bell-on-low-blood-volume-in-chronic-fatigue-syndrome.234/
 
Last edited:
The physiologic actions of BNP are similar to those of ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. The net effect of these peptides is a decrease in blood pressure due to the decrease in systemic vascular resistance and, thus, afterload. Additionally, the actions of both BNP and ANP result in a decrease in cardiac output due to an overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis and diuresis.[3]
Click to expand...
https://en.wikipedia.org/wiki/Brain_natriuretic_peptide

This could certainly explain a lot of my primary symptoms, such as standing intolerance and sodium loss.
 
Interesting, ACE inhibitors can lower BNP:

Arq Bras Cardiol. 2009 May;92(5):320-6, 336-43, 349-56.
ACE inhibitors and plasma B-type natriuretic peptide levels in elderly patients with heart failure.
[Article in English, Multiple languages]
Savioli Neto F1, Magalhães HM, Batlouni M, Piegas LS.
https://www.ncbi.nlm.nih.gov/pubmed/19629285#
Abstract

BACKGROUND:
Clinical trials have demonstrated the benefits of ACE inhibitors (ACEI) in the neurohormonal activity and in the functional capacity of patients with heart failure (HF), and also that these effects are dose dependent. However, since elderly individuals have been systematically excluded from the majority of these studies, the validation and incorporation of these results in the geriatric population has been questioned.

OBJECTIVE:
To evaluate the effects of different doses of quinapril, an ACEI with a > 24-hour biological half-life, on plasma BNP levels, on the distance walked in the 6-minute walk test (6MWT) and on the incidence of adverse reactions in elderly individuals with systolic HF.

METHODS:
A total of 30 patients (76.1 +/- 5.3 years; 15 women), in NYHA functional class II-III HF, with left ventricular EF < 40% (33.5 +/- 4.5%), on diuretics (30), digoxin (24) and nitrates (13) were included. The patients were assessed at baseline and every two months, with escalating doses of quinapril of 10, 20, 30 and 40 mg.

RESULTS:
After eight months, BNP levels were 67.4% lower and the distance walked in the 6MWT was 64.9% longer in relation to baseline. Arterial hypotension with symptoms of low cerebral blood flow and/or renal dysfunction was not observed, so that the maximum quinapril dose could be used in all patients.

CONCLUSION:
The results demonstrated the benefits of ACEI on the neurohormonal profile and functional capacity of elderly individuals with systolic HF, as well as the positive relationship between dose and effect of these drugs.
Click to expand...
https://www.ncbi.nlm.nih.gov/pubmed/19629285
 
adreno said:
Interesting, ACE inhibitors can lower BNP:


https://www.ncbi.nlm.nih.gov/pubmed/19629285
Click to expand...
Just going by this, but use of ACE inhibitors doesn't look desirable
ACE inhibitors block the conversion of angiotensin I (AI) to angiotensin II (AII).[10] They thereby lower arteriolar resistance and increase venous capacity; decrease cardiac output, cardiac index, stroke work, and volume; lower resistance in blood vessels in the kidneys; and lead to increased natriuresis (excretion of sodium in the urine).
Click to expand...
https://en.wikipedia.org/wiki/ACE_inhibitor
 
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.
Click to expand...

I think this could be a failure of proprioception which is not discussed in ME the way it used to be. Many of us have a negative Romberg test where we fall over if we close our eyes. In my own case it gets worse depending on how I am. At times I stumble every time I blink.

If proprioception is not working (it is a particular set of fibres in the nerve bundle) we do not have a proper feel of where we are in space so we need to use other senses such as vision or touch to compensate. I initially used a walking stick to help me keep upright rather than for support as I began to fall whenever I walked across an open space where there was nothing to touch. I had more skinned knees than when I was 10!
 
Barry said:
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.
Click to expand...

Actually this is all done by the standard somatic sensory and motor pathways. Conscious control only kicks in for fine tuning. Spinal reflexes, cerebellum and brain stem control most automatic actions, but automatic should not be confused with autonomic. The autonomic system innervates blood vessels and sweat glands but does not control skeletal muscle action.
 
Jonathan Edwards said:
Actually this is all done by the standard somatic sensory and motor pathways. Conscious control only kicks in for fine tuning. Spinal reflexes, cerebellum and brain stem control most automatic actions, but automatic should not be confused with autonomic. The autonomic system innervates blood vessels and sweat glands but does not control skeletal muscle action.
Click to expand...
Many thanks.
 
Mithriel said:
I think this could be a failure of proprioception which is not discussed in ME the way it used to be. Many of us have a negative Romberg test where we fall over if we close our eyes. In my own case it gets worse depending on how I am. At times I stumble every time I blink.

If proprioception is not working (it is a particular set of fibres in the nerve bundle) we do not have a proper feel of where we are in space so we need to use other senses such as vision or touch to compensate. I initially used a walking stick to help me keep upright rather than for support as I began to fall whenever I walked across an open space where there was nothing to touch. I had more skinned knees than when I was 10!
Click to expand...
My wife uses a stick. Quite some time before my wife noticably suffered from ME, she seemed to develop minor balance issue that we did not really recognise at first - occasionally falling sideways off a bike when she stopped.
 
I've only just come across this as it appeared on MEA twitter feed. I wonder what this means for someone with aortic regurgitation? :unsure: Maybe I should print this off for my cardiologist when I next visit?

On the subject of ACE inhibitors, I was tried on two different types and reacted badly to both so had to stop using them. First one made me feel dreadfully ill, the second one caused chest pain. The NHS have me recorded as allergic to them.
 
Barry said:
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.
Click to expand...
I experience the exact same issue.

As an aside, I just have to pass along to you my admiration for the interest you show in your wife's illness, and the obvious support you're providing her.
 
https://tinyurl.com/y7ywdjd2
i.e.
http://www.meassociation.org.uk/201...te-with-cardiac-dysfunction-14-february-2018/

MEA Summary Review: Elevated BNP levels in ME/CFS associate with
cardiac dysfunction | 14 February 2018



________________________________

By Charlotte Stephens, 14th February 2018.

A recent study from a research group at Newcastle University has found that patients with ME/CFS have significantly higher levels of a hormone called BNP in their blood and that this also correlated with significantly lower cardiac volumes.

Structural and functional cardiac abnormalities have been reported in ME/CFS before and MRI studies have suggested subclinical cardiomyopathy in some.

Finding a cause for the cardiac abnormalities and raised BNP levels seen in patients could help in the discovery of the physiological mechanisms behind the disease and could also help to direct treatment routes.

Overview of the study

The study aimed to look at BNP levels and how these associate with the cardiac abnormalities recently identified in ME/CFS.

Cardiac magnetic resonance (MR) examinations and BNP measurements were performed on 42 patients with ME/CFS (meeting the Fukuda criteria) and 10 sedentary controls, all with an average age of 46.

BNP levels were found to be significantly higher in the ME/CFS cohort compared with controls. The authors also found that those with higher BNP levels had significantly lower cardiac volumes.

There were no relationships between fatigue severity, length of disease and BNP levels, suggesting that the findings are unlikely to be related to deconditioning.

‘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.’



________________________________

Read the full review online or as a download
https://tinyurl.com/y8c2rw42
i.e.
http://www.meassociation.org.uk/wp-...NP-and-Cardiac-Function-in-MECFS-14.02.18.pdf
 
Dolphin said:
‘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.’
Click to expand...
Anyone want to take a stab at defining "lower cardiac volume" for the layman?
 
You must log in or register to reply here.
Back
Top Bottom