Thursday, December 8, 2011

Increased arterial stiffness and endothelial dysfunction contribute to high mortality due to heart disease in ME/CFS

David J. Newton a,⁎, Gwen Kennedy a, Kenneth K.F. Chan a, Chim C. Lang b, Jill J.F. Belch a, Faisel Khan a: The central finding of this study is that adult patients with ME/CFS have reduced FMD in the brachial artery and reduced post-occlusive reactive hyperemia in the forearm skin microcirculation.

These responses are both endothelium-mediated via an increase in shear stress [8,9], and the results therefore lend further support to the hypothesis that endothelial function is impaired in ME/CFS, both in large vessels and in the microcirculation.

We believe this is the first time that vascular endothelial dysfunction has been measured directly in ME/CFS patients, and these findings build on previous work reporting indirect markers of endothelial dysfunction, such as increased oxidative stress [4,10], inflammation [5,11] and arterial stiffness [5]. This evidence collectively points to increased cardiovascular risk in ME/CFS patients, which is borne out epidemiologically by their high mortality due to heart disease [12]. Read more>>

1 comment:

Unknown said...

Why myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) may kill you: disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways may explain cardiovascular disorders in ME/CFS.
Neuro Endocrinol Lett. 2009;30(6):677-93.
Maes M, Twisk FNM.

Disorders in various inflammatory and oxidative and nitrosative pathways provide explanations for the earlier mortality due to cardiovascular disorders in ME/CFS.

These pathways are:
a) chronic (low grade) inflammation with extended production of nuclear factor kappa B and COX-2 and increased levels of tumour necrosis factor alpha;
b) increased O&NS with increased peroxide levels, and phospholipid oxidation including oxidative damage to phosphatidylinositol;
c) decreased levels of specific antioxidants, i.e. coenzyme Q10, zinc and dehydroepiandrosterone-sulphate;
d) bacterial translocation as a result of leaky gut;
e) decreased omega-3 polyunsatutared fatty acids (PUFAs), and increased omega-6 PUFA
and saturated fatty acid levels; and
f) the presence of viral and bacterial infections and
psychological stressors.


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