Research: endothelial dysfunction in Chronic Fatigue Syndrome, International Journal of Cardiology, 10 November 2011

November 21, 2011


From the International Journal of Cardiology, 10 November 2011.

Large and small artery endothelial dysfunction in chronic fatigue syndrome

David J Newton, Gwen Kennedy, Kenneth KF Chan, Chim C Lang, Jill JF Belch, Faisel Khan
Vascular and Inflammatory Diseases Research Unit and Department of Clinical Pharmacology, Institute of Cardiovascular Research, University of Dundee, Dundee

Background and aim:

There is accumulating evidence that myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is associated with increased cardiovascular
risk. Autonomic dysfunction, impaired blood pressure regulation, raised oxidative stress, low‐grade inflammation and increased arterial stiffness have all been reported in ME/CFS patients. However, measurements of endothelial function in the disease have had conflicting results, which are probably due to the methodology used.

The aim of this study was to assess vascular endothelial function directly in the forearm macro and microcirculations of patients with ME/CFS.

Methods:

Flow‐mediated dilatation was assessed using ultrasound to measure the percentage increase in brachial artery diameter during the hyperaemia following 5 minutes of ischaemia in 30 ME/CFS patients and 27 healthy controls. In addition, post‐occlusive reactive hyperaemia was assessed in 9 ME/CFS patients and 9 healthy controls using laser Doppler flowmetry to measure the increase in forearm skin microcirculation after 5 minutes of ischaemia. Venous blood samples were taken for the laboratory measurement of haematological markers.

Results:

Flow‐mediated dilatation was significantly lower in the ME/CFS group than in the control group (median [interquartile range]: 5.99 [3.65] versus 9.24 [3.47]%, p<0.001). Post‐occlusive reactive hyperaemia in the forearm microcirculation was also significantly lower in ME/CFS patients (area under the response curve: 19.76 [15.46] versus 38.70 [18.14] AU∙min, p=0.012). Furthermore, ME/CFS patients had significantly higher levels of serum high‐sensitivity C‐reactive protein (p=0.016) and triglycerides (p=0.034), and lower levels of serum high‐density lipoprotein cholesterol (p=0.041), compared with healthy controls. Conclusion:

These findings provide direct evidence of endothelial dysfunction in both the large and small vessels of patients with ME/CFS, which may warrant a large prospective trial of cardiovascular outcomes in the disease.

3 thoughts on “Research: endothelial dysfunction in Chronic Fatigue Syndrome, International Journal of Cardiology, 10 November 2011”

  1. So in terms of function what dose this mean? sounds interesting? dose it mean that the blood vessels don’t carry the blood as they should and how dose this lead to heart attacks?
    I very much enjoy reading all the research results coming in and I understand quite a bit of them, by looking up the words I don’t understand, but so much goes over my head, would it be possible as well as posting it to have a simple none medical explanation of what it means and how it affects the body? like this means the blood is not getting all the places in the body it should or what ever they are talking about? please for us less medical people thankyou As well as ME and POTS I also have dyslexia, so while I’m not “thick” I do struggle with big words and medical terms.

  2. This study above points directly at what Dr. Charles Stratton’s work from Vanderbilt University with a bacterial infection called c. pneumonaie which he has been researching for the past decade and c.f.s. patients have higher loads of this infection than all other chronic illnesses he is working on! This also could explain why the recent Norway study has success in c.f.s as well as other studies done on arthritis because that medicine reduces inflamation…Dr. stratton is now convinced that c. pneumonaie survives on inflamed areas and injuries…It is also transmitted through blood contact as well as airborne such as cough/saliva…I believe his work will hold major keys in all chronic illnesses of today but I do not believe that this latest Norway medicine will kill c. pneumonaie in full but could be reducing c. pneumonaie numbers…I tested positive to his lab methods…As he has explained the cure is worse than the illness…I would like to hear Dr. Stratton’s response to Norway trial here and also would be of utmost importance to exactly see in his lab what this latest medicine does against c. pneumonaie and even some blood samples from Norway patients before medicine and after for Dr. stratton to test against his findings just to see what it shows on c. pneumonaie…Dr. Stratton believes he has found the cause and is worth it for all these teams to work together to end these chronic health issues once and for all…cfs/m.e. is a serious physical illness and has no space whatsoever in funding phycological comedy…If c.pneumonaie is the cause then let’s really see what this latest study shows with these patients and who knows maybe possible they both have major keys to unravel these devastating illnesses…

  3. I am also convinced if these Norway researchers decided to send before/after blood samples to Dr. Stratton he would welcome these samples with open arms! The Norway research team would have never tried to search for XMRV in patients if they did not think an infection could be involved and besides Dr. Stratton has already enough data collected on cfs patients and his testing methods would be of importance to the Norway team and it is also quite possible that by combining both teams could bring a possible answer. I am 100% behind Dr.Stratton’s findings and his important research and here is a website devoted to that vital research… cpnhelp.org

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