Cardiac issues in Myalgic Encephalomyelitis
The more we know…
One of the systems that myalgic encephalomyelitis affects is the cardiovascular system. This, along with immune and brain dysfunction, can help differentiate ME from many other conditions.
A recent paper by Jean M. Nunes, Douglas B. Kell and Etheresia Pretorius brought together much of what we know about the cardiovascular issues seen in ME.
I have made an attempt to offer highlights of this in-depth paper. I would love to see the cardiology field embrace what we already know so we would all have access to educated cardiologists & electrophysiologist (EP) cardiologists.
I have only covered some of what is in the paper, but I hope this overview empowers patients to seek the care of cardiologists and EP cardiologists who are willing to learn about ME.
I realize this is a long article. If you aren't up to reading, maybe just take note that this covers a recent paper that explains some of the cardiac issues seen in ME. If you get an opportunity to see a cardiologist who is willing to learn, this may be useful information for that appointment.
If you are not up to reading the entire article now, maybe skip down to the CoQ10 section that explains why this may be a supplement worth considering. It has been recommended for people with ME for decades and is listed in the “Replenish Nutrients, Restore Homeostasis, and Relieve Symptoms” section of the ME International Consensus Primer (pg 16).
The recent paper, Cardiovascular and haematological pathology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): A role for viruses, consolidated some of the information we know about the cardiac issues seen in ME. It underscores the importance for people with ME being evaluated for known cardiac issues. It states:
“individuals exhibit an increased risk for premature heart failure and earlier all-cause mortality”
Treatment for many of these cardiac issues can improve quality of life, but we need much more research into this area to confirm which findings apply to ME as a distinct disease and which are downstream effects of many conditions.
About the Authors
Jean M. Nunes is listed in the paper as being in the Department of Physiological Sciences, Faculty of Science, Stellenbosch University, in Matieland South Africa.
Douglas B. Kell is listed in the paper as also being in the Department of Physiological Sciences, Faculty of Science in Matieland South Africa as well as in the Department of Biochemistry and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool in the UK and in The Novo Nordisk Foundation Centre for Biosustainability in Denmark.
Etheresia Pretorius is listed in the paper as also being in the Department of Physiological Sciences in Matieland South Africa as well as the Department of Biochemistry and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool in the UK.
This interview of Resia (Etheresia) Pretorius by Amy Proal of PolyBio lists her as the Department Head and a Research Professor in the Physiological Sciences Department, Faculty of Science at Stellenbosch University in South Africa. This is a good interview to learn more about the microclots found in Long COVID and ME patients.
Overview of the Paper
The paper covers various cardiac abnormalities that have been documented. These findings include reduced cardiac output, deficits in blood flow to the brain and dysregulation of the vascular system.
It includes discussion about the recent finding of microclots in blood, clotting dysregulation as well as endothelial dysfunction. The following from the paper helps clarify the importance of the endothelial cells:
“Endothelial cells are important for vessel regulation whereby nitric oxide and endothelin synthesis and release modulate constriction and dilation activity… Furthermore, the endothelium is responsible for enabling the transfer of substances across the vessel wall; a damaged endothelium is expected to lead to impairments in substance exchange in localised areas.”
The paper also discusses viral reservoirs which likely contribute either directly or indirectly to the cardiovascular and haematological dysfunction.
Practice points for clinicians:
The paper includes a section that covers important points for clinicians, including that symptoms do not seem to be caused by deconditioning, disease is biologically driven, characterized by vascular pathology and is not psychosomatic. I appreciate that they included the following statement about the importance of cardiovascular assessment.
“Assessment of cardiovascular (specifically cardiac functioning) and haematological health [dealing with the blood and related structures, such as bone marrow] are necessary steps in the clinical evaluation of ME/CFS patients.”
Cardiac Issues
The paper is very in depth, but here are a few of the cardiac issues covered:
“Arterial wave reflection is inversely associated with left ventricular systolic function (as determined by tissue Doppler imaging techniques) and is involved in the pathogenesis of heart failure.”
This underscores the importance of assessing cardiac function to determine cardiovascular risk.“Reduced stroke volume in ME/CFS has since been corroborated, and decreases in end-diastolic volume and cardiac output have also been reported “
“Plenty of recently published studies are demonstrating significant platelet hyperactivity and endothelial dysfunction in ME/CFS, as well as anomalous clotting processes.”
“Significantly increased levels of fibroblast growth factor 21 (FGF21) and the N-terminal prohormone of brain natriuretic peptide (NT-proBNP)”
“Positive correlations between NT-proBNP concentrations and that of proinflammatory cytokines (namely, IL-1β and IL-6) were noted. NT-proBNP is positively and independently associated with cardiovascular risk [113] and FGF21 is involved in glucose and lipid metabolism”
“Elevated levels of autoantibodies against adrenergic and cholinergic receptors have been found”
Highlighting a Few Findings
Red Blood Cell Deformability
As we have known for decades, there are issues with our red blood cells. I was not surprised they included this well known finding. If doctors would take note of this basic finding about how the oxygen exchange is impaired at the cellular level, there might be better recognition of the biological (not psychological) aspects of ME. The paper states:
“Red blood cells from ME/CFS individuals exhibit reduced deformability, accompanied by diminished membrane fluidity [168]. This makes erythrocytes less pliable and stiffer, hindering efficient traversal through microcapillaries. This will impact the supply of oxygen to and retrieval of carbon dioxide from tissues and hinder blood flow (especially in capillaries where erythrocytes flow in a single file), which in turn might give rise to some symptoms associated with ME/CFS. Low erythrocyte volume might also contribute to shortcomings in circulation and oxygen delivery to tissues”
Fibrinaloids
The paper discussed the more recent findings of microclots in the blood of people with ME (also seen in Long COVID).
“We have published findings of small amyloid fibrin clots, called fibrinaloids or microclots, as well as hypercoagulation and hyperactivated platelets, in Long COVID patients…”
“results show that ME/CFS PPP [platelet-poor plasma] samples contain significantly greater levels of fibrinaloids when compared to controls… however, seems to be lower than that of Long COVID.”
This is a promising line of research that could lead to treatments involving H.E.L.P. apheresis.
NOTE: H.E.L.P. apheresis is a special kind of apheresis that is not readily available to many of us. The treatment is explained in the paper, Heparin-induced extracorporeal LDL precipitation (H.E.L.P.), as:
“H.E.L.P. procedure (heparin-induced extracorporeal LDL precipitation) is a selective and sophisticated apheresis procedure. By means of heparin and lowering the pH level, lipoproteins and fibrinogen are reduced by 50-60%. In addition to lipoprotein (a) reduction (50- 60%) adhesion molecules (ICAM- 1, VCAM-1, P selectin), which play a major role in the development and progression of atherosclerosis, are significantly lowered.“
CoQ10
The paper includes discussion about the importance of CoQ10 and how a reduction in plasma levels has been observed in patients which can lead to cardiovascular issues and reduced mitochondrial function. It is also a risk predictor of mortality in chronic heart failure.
“Decreases in CoQ10 reduce antioxidant capacity and might account in part for the increases in O&NS [oxidative and nitrosative stress] observed in ME/CFS. Furthermore, CoQ10 might hold potential as a useful predictor of heart failure in ME/CFS patients. CoQ10 supplementation increases cellular resistance to lipid peroxidation, and may therefore prove useful against the lipid peroxidation observed in ME/CFS.”
I have been taking CoQ10 (with Hawthorn) for years as it was recommended by ME experts in the early 1990s. It seems to improve my energy levels and hopefully my cardiac function.
Deconditioning is NOT a primary cause of issues in ME
This cardiovascular paper includes the following important point:
“deconditioning due to the ME/CFS-induced lifestyle does not account in significant part for the cardiovascular abnormalities observed in this disease population, and increases the plausibility of cardiac involvement in ME/CFS pathogenesis and symptom manifestation.”
Viral component
This paper also includes information about the role various viruses play in the cardiovascular issues and the chronic nature of ME.
“A recent study has identified significant levels of EBV and HHV-6 microRNA in the central nervous system of deceased ME/CFS individuals, which points at active infection in the brain and spinal cord.”
We need more awareness by all specialists about the viral aspect of myalgic encephalomyelitis.
Clarification
This paper discusses a vast increase in prevalence numbers of “ME/CFS” due to Long COVID. We do not yet know how many of those with Long COVID will have ME as defined by the International Consensus Criteria (ICC). Also the diagnosis of Long COVID is very broad and encompasses many different patient groups including those with organ damage that explains their ongoing symptoms. The ME/CFS criteria (no matter which one they mean) is broader than the ME-ICC.
The 2012 ME IC Primer states that the term myalgic encephalomyelitis should be used for patients who fit the ICC. Not all of the research cited in this paper uses patients who were selected using the ICC. Follow-up research is needed to know which of these findings applies to people with ME.
ME/CFS has several meanings including:
ME and CFS (separate conditions under umbrella label of ME/CFS)
ME/CFS as defined by Canadian Consensus Criteria (precursor to the ICC)
ME/CFS as defined by the IOM report (what is on the CDC website)
ME/CFS as defined by the NICE guidelines in the UK
In any conversation about myalgic encephalomyelitis, we need to know which criteria is being used. ME is a distinct disease and anyone diagnosed with ME/CFS or CFS needs to be thoroughly screened to rule out other diseases and be adequately tested to confirm an ME diagnosis.
I am looking forward to more doctors understanding the reality of Myalgic Encephalomyelitis… the sooner the better!
Colleen
Information provided here or in comments is not to be considered medical advice.
Sources:
Cardiovascular and haematological pathology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): A role for viruses published in Blood Reviews - Volume 60, July 2023, 101075 by Elsevier
Horstkotte, D, and K-P Mellwig. “Heparininduzierte extrakorporale LDL-Präzipitation (H.E.L.P.)” [Heparin-induced extracorporeal LDL precipitation (H.E.L.P.)]. Zeitschrift fur Kardiologie vol. 92,Suppl 3 (2003): III1-5. doi:10.1007/s00392-003-1304-x
The National Library of Canada Cataloguing-in-Publication Data: Myalgic Encephalomyelitis – Adult & Paediatric: International Consensus Primer for Medical Practitioners. ISBN 978-0-9739335-3-6