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

The amount of blood being pumped by the heart is lower than normal. I think "cardiac output" is the more common term.

 

I would think one way to approach this is via patients' ejection fractions, and I see that one of the links provided by @Andy suggests the same.

 

The heart is essentially a huge muscle with a huge energy demand. If energy production is compromised, for example with low intracellular magnesium then the pump will still work, but not as strongly as muscle strength is low.
I wondered if BNP levels have a relationship with magnesium and found this
https://www.omicsonline.org/open-ac...and-magnesium-2379-1764-1000134.php?aid=58799 , saved for bedtime reading....

 

It's a different type of muscle - much more ATP than normal (skeletal) muscle. It would be interesting to fully examine differences in skeletal, cardiac, and/or smooth muscle ... differences and similarities might be informative regarding the pathological processes of ME.

 

I think that may not be right, @Valentijn. End diastolic and end systolic volumes are the volume of the ventricular cavity, I think, not the volume pumped. I think they are saying the heart is literally small in capacity. Stroke volume (multiplied by pulse rate) is what determines cardiac output.

Stroke volume can be calculated from EDV and ESV but it does have to be multiplied by pulse rate and they say nothing about that.

 

Pre-empted my question. Presumably in principle you could have a heart that has large volume but low stroke capacity. But I think you are saying here that if you notionally started off with a "low cardiac volume" heart empty of fluid, and then measured how much it took to fill it up, that volume would be low.

Edited: For clarity.

 

Yes, the large volume heart with low stroke volume is effectively Starling and Bayliss's original definition of heart failure, drummed into the heads of all medical students. There is actually a serious flaw in Starling's concept because it does not distinguish a normal heart pushed to failure by manipulation of blood flow from a diseased heart that fails under physiological conditions but no matter.

What I think is being said here is that the heart is actually just a small bag. Athletes' hearts may be small in this sense in that the muscular wall thickens but the organ does not stretch (as it does in heart failure). I presume that the thicker wall actually limits the space inside under those conditions. But the suggestion here is that the heart has a small capacity but not because of increased muscle thickness and power.

 

Quercetin lowers BNP :

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769399/

 

https://twitter.com/user/status/994199166564827136

 

@Jonathan Edwards

I want to jump in on this one ... even before my official introduction (some of you may know me from the other site -- same screen name).

In December 2013 I was given an Rx of Trileptal (anticonvulsant) to treat nerve pain in my eyes. I had a severe Adverse Drug Reaction called DRESS Syndrome. It wasn't treated (normally, IV steroids and/or IVIG). After a few months recovery I flew to Minnesota to be seen at the Mayo Clinic. They declared me fortunate and unfortunate and sent me home.

The pathophysiology of DRESS Syndrome is understood to be a Cytokine Storm, transient immunosuppression, and the reactivation of latent viruses (sound familiar ?).

But a few months later (nine months after the DRESS Syndrome) I began having cardiac symptoms, all of which came on at once: lightheadedness, near syncope, actual syncope (fainting), arrhythmias, exercise intolerance, dyspnea (shortness of breath).

Here's where I have to really try to condense the story:

For roughly two years, three cardiologists and two electrophysiologists swore it was "just atrial fibrillation."

But I wasn't so sure.

I began poring over my echocardiogram data and believed I had heart failure. The doctors vehemently disagreed. I believed my left ventricle was small and was shrinking. The doctors vehemently disagreed. Other abnormal findings were not called out by the MDs who read the data, so the cardiologists never saw the abnormalities in the concise reports.

But it clearly looked like a form of heart failure to me.

I began to believe some disease process was "shrinking" and stiffening my heart. I'd been athletic my entire life. When I asked the cardiologists what could cause this, they all said -- in effect -- nothing, and it isn't true in your case anyway. They just kept pointing to atrial fibrillation (afib).

Stanford (Montoya) called it ME/CFS and did his usual thing with me. No improvement.

I eventually self-referred to David Systrom, the Invasive Cardiopulmonary Exercise Testing (iCPET) and ME/CFS guy at Brigham and Womens (Boston).

He Dx'd me with Heart Failure with Preserved Ejection Fraction (HFpEF) and Left Heart Failure Induced Pulmonary Hypertension (WHO Group 2).

I also self-referred to the HFpEF Clinic at Johns Hopkins (Baltimore) where I underwent an Endomyocardial Biopsy (EMB). The EMB primarily revealed myocyte hypertrophy. interstitial fibrosis, and "small vessel disease."

I was recently diagnosed with a Restrictive Cardiomyopathy (RCM) by a well-known cardiomyopathy expert (cardiologist) a few hours from my home. Perfect fit. I had been suggesting that to the last two specialists as a possibility.

My Left Ventricle DID shrink, IS too small, and IS too stiff. My Stroke Volume IS too low (particularly indexed to my body surface area). Trying to get more blood out of it causes a dramatic rise in pressures for a minimal increase in cardiac output. The pressures back up to the rest of the heart, dilating the left atria, right ventricle and right atria, and causing the arrhythmias AND the pulmonary hypertension.

Like Cheney and Lerner (and others) have said ... my cardiac output is low -- quite low. When my heart rate is too low (bradycardia -- more and more common as time goes on), my cardiac output is equivalent to cardiogenic shock.

It really isn't treatable ... until/unless the Heart Failure gets so bad that I get put on the transplant list. With my immune system, though, and history of adverse drug reactions ... doubtful. The mortality statistics are depressing. But I don't care about that. I care about the morbidity. I feel horribly ill All The Time. My exercise intolerance is shocking. My New York Heart Association Class is III-IV. I may or may not technically still be a PwME ... but ... I sure have most of the signs and symptoms.

As a lifetime athlete (and idiot) ... I spend all the energy I have to walk the dog more days than not, even "jogging" (there must be a better word for it) 200 - 250 steps at intervals. A former triathlete ... I now struggle mightily to 'jog' 400m. It feels like I am carrying a refrigerator on my back.

I'm quite sure RCM is underdiagnosed. Even when I described it perfectly and painted a comprehensive picture of my understanding of what was going on, each of my cardiologists and EPs missed it.

My doctors agree that -- particularly since I have zero risk factors and zero heart disease -- this is almost certainly all a consequence of the DRESS Syndrome.

In my case ..... it probably played out like this. In most people it resolves fairly completely, but -- as we all know -- if your immune system is banged up, bad things can happen. It seems the inflammation didn't resolve properly and resulted in fibrosis (ie, scar tissue) in all four chambers of my heart.

I still haven't ruled out a separate and similar (ie, fibrotic) process in my lungs. Working on that.

Aside from a handful of heart meds (with no proof of efficacy), I am being pushed to have a pacemaker implanted, and to undergo Radio Frequency Catheter Ablation (RFCA). But those would treat symptoms ... symptoms which are only weakly contributing to my symptoms.

RCM is among the known chronic causes of Cardiogenic Shock.

I think some sort of myocarditis ... and/or some sort of RCM ... is probably among the phenotypes of ME/CFS. How you would arrive at that diagnosis is a difficult question, as is the possible upside OF arriving at that diagnosis. Europe seems far more broad minded on this one than the States. If I'd had the money I would have flown to Berlin to be seen by Dr. Carsten Tschöpe early on.

I have no end of information on this particular issue ... having done years of research on it. I'll gladly share what I know ... as I can.

One of The Most Important Things I Have Learned is .... negative findings don't mean anything. Only positive findings are diagnostic. In my case, the combination of the echocardiograms, cardiac event monitors, iCPET, and EMB painted the picture.

And just like So Many of Us: I was right and the doctors were wrong ;-)

All the best to you all ... and ... Hi there

TG

 

It is disappointing that we seem to have heard nothing more on this line of research. Has anyone heard of anything?

 

Maybe the approx 1/3 of PWME are 'just' pre-diabetic?

Brain natriuretic peptide and cardiac autonomic function in type 2 diabetic patients

https://www.diabetesresearchclinicalpractice.com/article/S0168-8227(05)00361-X/pdf

 

Metabolic syndrome (linked to pre-diabetes) is considered a co-morbidity by the CFIDS Association, I think. Some of the symptoms may overlap: https://en.m.wikipedia.org/wiki/Metabolic_syndrome