wiki, endothelial dysfunction is a systemic pathological state of the
endothelium (the inner lining of blood vessels) and can be broadly
defined as an imbalance between vasodilating and vasoconstricting
substances produced by (or acting on) the endothelium. Normal
functions of endothelial cells include mediation of coagulation,
platelet adhesion, immune function and control of volume and
electrolyte content of the intravascular and extravascular spaces.
Endothelial dysfunction can result from and/or contribute to several
disease processes such as atherosclerosis and may predate clinically
obvious vascular pathology by many years.
Endothelial function can be improved significantly by exercise,
dietary changes and treatment of related conditions. Although
substantial exercise is a extremely limited option in patients with
post exertional malaise lasting more than 24-hours, other changes may
help. A study published in 2005 has determined that a positive
relationship exists between the consumption of trans fat (commonly
found in hydrogenated products such as margarine) and the development
of endothelial dysfunction. Other factors have been identified as
improving endothelial function and include cessation of smoking, loss
of weight and treatment of hypertension and hypercholesterolemia
amongst other things. Some studies have found antioxidants, potassium
and arginine supplementation to restore impaired endothelial
dysfunction. Always check with your physician before adding
supplementation to your diet.
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=E2=80=90grade inflammation and increased arter=
ial
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=E2=80=90mediated dilatation was assessed using ultrasound to measure t=
he
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=E2=80=90occlusive reactive hyperaemia was asses=
sed
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=E2=80=90mediated dilatation was significantly lower in the ME/CFS grou=
p
than in the control group (median [interquartile range]: 5.99 [3.65]
versus 9.24 [3.47]%, p<0.001).
Post=E2=80=90occlusive 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=E2=88=99min, p=3D0.012).
Furthermore, ME/CFS patients had significantly higher levels of serum
high=E2=80=90sensitivity C=E2=80=90reactive protein (p=3D0.016) and triglyc=
erides
(p=3D0.034), and lower levels of serum high=E2=80=90density lipoprotein
cholesterol (p=3D0.041), 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.
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