If there is a factor in the serum, why is plasma exchange not working?

@Mithriel ever seen an older person with a heart condition ? Ive seen so many ppl with NYHA 4, global heart failure. They would outrun me everyday. A diastolic dysfunction is maybe a side symptom that worsen things but by far is anything profound in Cfs.

 

When heart issues were being looked at in ME, Paul Cheney examined all his patients and found that they all had diastolic heart failure, which makes sense as that is an active process and could well be involved with the problems found by Workwell.

He was interested as he had systolic heart failure and had to have a heart transplant. He speculated why his heart had given out while his patients' hearts did not and decided that his heart failed in the background so he carried on overloading it till it failed completely but in his patients they became fatigued so rested their hearts.

I use a heart rate monitor and am not alone in finding that when I am in particularly bad PEM my heart rate drops drastically. I also see the effect with my blood pressure when my diastolic becomes very low (<50).

People with ME have been known to die from heart attacks when they exercise too much - an MP died in the House of Commons gym - and it was seen as a problem 40 years ago, but heart issues are one of the neglected areas because of the dubious concentration on fatigue.

Many people with ME have small hearts, can't remember the details but we are not like other heart patients, the heart is not damaged just not working the same as everything else in ME.

 

I think there are subsets who will respond differently. Systrom/Oaklander believe there is a small fiber neuropathy subset (based on skin biopsy) where whatever has gone wrong in the biological process has damaged nerve fibers. So if you are in a subset where there is physical damage, it is going to be a long process to repair that damage when the "factor in the blood" is removed. They associate SFN with impaired cardiac return and hypoxia.

Statement in abstract from Oaklander about SFN, hypoxia, and impaired cardiac return.

Source : Chapter 10 - Dysimmune small fiber neuropathies - 1 May 2020

 

I think we’ve had other studies showing hypoxia in the brain even in the absence of PoTS (30% drop in oxygen compared to controls if I remember correctly?). Is there no treatment that already exists, for this type of issue?

So is the hypothesis that there’s a problem with the blood vessels and so there’s less oxygen - in that case is it a problem with blood vessel constriction? But wouldn’t that cause in all cases continuous high blood pressure (Isn’t that what high blood pressure is - vessel constriction)?