Newton en kollega's hebben de 24-uurs bloeddruk vergeleken van
mensen met ME/CVS, gezonde proefpersonen en mensen met PBC
(primaire biliaire cirrose:
chronische ontsteking van de kleine galkanaaltjes in de lever, waardoor de
galvloeistof niet goed afgevoerd wordt, met als gevolg littekenvorming van de lever).
Zoals U uit onderstaande tabel kunt aflezen,
is de bloeddruk van ME/CVS-patiënten
beduidend lager dan die van gezonde mensen (ca. 20 mmHg).
De variatie van de bloeddruk over een etmaal
(de bloeddruk is 's nachts lager en neemt enige tijd voor het ontwaken toe)
is juist weer iets groter dan die van gezonde mensen (12 versus 14 mmHg).
Er was een duidelijk verband tussen "vermoeidheid" en de bloeddrukvariatie,
zowel bij ME/CVS- als bij PBC-patiënten.
M.b.t. de oorzaak van de bloeddrukafwijkingen,
schetsen de auteurs aan het eind van de studie drie scenario's (zie hieronder)
- De lage bloeddruk is een gevolg van inaktiviteit:
niet erg waarschijnlijk volgens de auteurs.
- Een verminderde werking van de HPA-as leidt tot ontregeling van de bloeddruk.
- De ontregelde/lage bloeddruk (en de daaruit voortvloeiende
hypoperfusie: verminderde doorbloeding) veroorzaakt de vermoeidheid.
Three scenarios can be envisaged.
The first scenario is that low BP is secondary to fatigue,
reflecting the decreased amount of physical activity
(and resulting decrease in any exercise-associated increase in BP)
undertaken by patients who perceive themselves to be fatigued.
Two observations could argue against this interpretation.
First, the effect is principally expressed at night,
when physical activity is obviously low, rather than during the day;
and second, studies have shown that physical activity in fact
explains only a small part of BP and HR variability.
There is now extensive literature
describing day-night ambulatory BP differences
with some studies suggesting that in fact
night time BP is a more important parameter when considering outcomes than daytime BP.
Our finding of a relationship between increased diurnal variation and fatigue
would suggest that those with more exaggerated BP variation
are at increased risk of cardiovascular and cerebrovascular events.
Further work is needed to explore whether
the association between BP dipping and outcomes in those with fatigue
and whether the exaggerated diurnal variation in BP that associates with fatigue
is indicative of a generalized disordered circadian regulation or specifically related to AD.
A second potential mechanism which could give rise to
both fatigue and BP dysregulation is dysfunction of the hypothalamic-pituitary-adrenal axis
which has been demonstrated to occur in animal models of cholestasis
- one of the underlying pathophysiological processes in PBC
and also hypothesized as a potential abnormality in those with CFS.
This potential hypothesis is supported to a degree
by the observation of weak benefit in two randomized control trials in CFS
involving the use of the glucocorticoid hydrocortisone.
The third scenario is that
BP dysregulation is causally linked to fatigue expression.
Suggestions that this might be the case have come from population-based studies
confirming a relationship between symptom expression and low BP.
Lower BP could give rise to fatigue through either or both of
central nervous system and peripheral muscle hypoperfusion.
Were there to be a direct link between dysregulation and fatigue,
it would explain earlier observations that
the AD present in a significant proportion of CFS and PBC patients,
and which in other clinical settings has been shown to impinge on BP regulation,
is itself strongly associated with the presence and degree of fatigue.
AD (autonome disfunctie):
ontregelde aansturing door de hersenen
van onbewust plaats vindende processen in het lichaam.
Lower Ambulatory Blood Pressure in Chronic Fatigue Syndrome.
Psychosom Med. 2009 Mar 17. [Epub ahead of print]
Newton JL, Sheth A, Shin J, Pairman J, Wilton K, Burt JA, Jones DE.
Objective:
To examine blood pressure circadian rhythm
in subjects with chronic fatigue syndrome (CFS)
and appropriate normal and fatigued controls
to correlate
parameters of blood pressure regulation
with perception of fatigue
in an observational cohort study.
The cause of CFS remains unknown
and there are no effective treatments.
Methods:
To address whether inactivity was a confounder,
we performed a 24-hour ambulatory blood pressure monitoring
in the following three subject groups:
CFS patients (Fukuda Diagnostic criteria) (n = 38);
normal controls (n = 120); and
a fatigue comparison group (n = 47)
with the autoimmune liver disease primary billiary cirrhosis (PBC).
All patients completed a measure of fatigue severity (Fatigue Impact Scale).
In view of the different demographics between the patient groups,
patients were age- and sex-matched
on a case-by-case basis to normal controls
and blood pressure parameters were compared.
Results:
Compared with the control population,
the CFS group had
significantly lower systolic blood pressure (p < .0001) and
mean arterial blood pressure (p = .0002)
and exaggerated diurnal variation (p = .009).
There was a significant inverse relationship
between increasing fatigue and
diurnal variation of blood pressure
in both the CFS and PBC groups (p < .05).
Conclusion:
Lower blood pressure and
abnormal diurnal blood pressure regulation
occur in patients with CFS.
We would suggest the need for a randomized, placebo-controlled trial
of agents to increase blood pressure
such as midodrine in CFS patients with an autonomic phenotype.
PMID: 19297309 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/19297309
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