Post by beebs on Jul 29, 2011 17:05:23 GMT -5
I met many on CFS forums suffering from heart failure. Some had typical symptoms of heart failure, were refused tests by their GPs. Others were told its all in their heads, there is nothing wrong with them. Many committed suicide, or died!! Outrageous, cruel and barbaric!!
Various triggers for CFS such as post medications, post vaccines, post surgery, post infections. Regardless of the trigger, and despite thousands of papers published concerning serious malfunctions such as autonomic nervous system, cardiovascular, mitochondrial, hypthyroidism, diabetes, and many other symptoms, severe weakness to the point of being bedridden for many years on/off, severe photosensitivity, etc.. discarded by the medical establishment, to protect their own self interests.
A few years go, could be ten years ago, Dr Bell or Dr Cheney, wrote a paper linking CFS with a type of diastolic heart failure difficult to detect.
It was ignored by main stream medical establishment.
This paper (published a few days ago) uses an MRI to assess heart function in CFS patients and a control group.
Will they now ignore the most recent study showing heart failure in those who meet the CFS/ME Fuduka criteria?
J Intern Med. 2011 Jul 27. doi:
10.1111/j.1365-2796.2011.02429.x.
[Epub ahead of print]
Impaired Cardiac Function in
Chronic Fatigue Syndrome
measured using Magnetic
Resonance Cardiac Tagging.
Hollingsworth KG, Hodgson T,
Macgowan GA, Blamire AM, Newton JL.
Newcastle Magnetic
Resonance Centre, Institute of
Cellular Medicine, Newcastle
University, Campus for Ageing
and Vitality, NE4 5PL, UK
Institute for Ageing and
Health, Newcastle University,
Campus for Ageing and
Vitality, NE4 5PL, UK
Department of Cardiology,
Freeman Hospital, Newcastle
upon Tyne, NE7 7DN and
Institute of Human Genetics,
Newcastle University, NE2
4HH, UK
Abstract
Objectives:
Impaired cardiac function has
been confirmed in patients
with chronic fatigue syndrome
(CFS).
Magnetic resonance cardiac
tagging is a novel technique
that assesses myocardial wall
function in vivo.
We hypothesized that CFS
patients may have impaired
development and release of
myocardial torsion and strain.
Methods:
Cardiac morphology and
function was assessed using
magnetic resonance imaging
and cardiac tagging
methodology in 12 CFS
(Fukuda) and 10 matched
controls.
Results:
Compared to controls the CFS
group had substantially
reduced LV mass (reduced by
23%), end diastolic volume
(30%), stroke volume (29%),
and cardiac output (25%).
Residual torsion at 150% of
the end-systolic time was
found to be significantly
higher in the CFS patients
(5.3±1.6(o) ) compared to the
control group (1.7±0.7(o),
p=0.0001).
End diastolic volume index
correlated negatively with
both torsion to endocardial
strain ratio (TSR) (r =-0.65,
p=0.02) and the residual
torsion at 150% end systolic
time (r=-0.76, p=0.004), so
decreased end diastolic
volume is associated with
raised TSR and torsion
persisting longer into
diastole.
Reduced end diastolic volume
index also correlated
significantly with increased
radial thickening (r=-0.65,
p=0.03) and impaired
diastolic function represented
by the ratio of early to late
ventricular filling velocity (E/A
ratio, r=0.71, p=0.009) and
early filling percentage
(r=0.73, p=0.008).
Conclusion:
CFS patients have markedly
reduced cardiac mass and
blood pool volumes,
particularly end diastolic
volume:
this results in significant
impairments in stroke volume
and cardiac output compared
to controls.
The CFS group appeared to
have a delay in the release of
torsion.
Various triggers for CFS such as post medications, post vaccines, post surgery, post infections. Regardless of the trigger, and despite thousands of papers published concerning serious malfunctions such as autonomic nervous system, cardiovascular, mitochondrial, hypthyroidism, diabetes, and many other symptoms, severe weakness to the point of being bedridden for many years on/off, severe photosensitivity, etc.. discarded by the medical establishment, to protect their own self interests.
A few years go, could be ten years ago, Dr Bell or Dr Cheney, wrote a paper linking CFS with a type of diastolic heart failure difficult to detect.
It was ignored by main stream medical establishment.
This paper (published a few days ago) uses an MRI to assess heart function in CFS patients and a control group.
Will they now ignore the most recent study showing heart failure in those who meet the CFS/ME Fuduka criteria?
J Intern Med. 2011 Jul 27. doi:
10.1111/j.1365-2796.2011.02429.x.
[Epub ahead of print]
Impaired Cardiac Function in
Chronic Fatigue Syndrome
measured using Magnetic
Resonance Cardiac Tagging.
Hollingsworth KG, Hodgson T,
Macgowan GA, Blamire AM, Newton JL.
Newcastle Magnetic
Resonance Centre, Institute of
Cellular Medicine, Newcastle
University, Campus for Ageing
and Vitality, NE4 5PL, UK
Institute for Ageing and
Health, Newcastle University,
Campus for Ageing and
Vitality, NE4 5PL, UK
Department of Cardiology,
Freeman Hospital, Newcastle
upon Tyne, NE7 7DN and
Institute of Human Genetics,
Newcastle University, NE2
4HH, UK
Abstract
Objectives:
Impaired cardiac function has
been confirmed in patients
with chronic fatigue syndrome
(CFS).
Magnetic resonance cardiac
tagging is a novel technique
that assesses myocardial wall
function in vivo.
We hypothesized that CFS
patients may have impaired
development and release of
myocardial torsion and strain.
Methods:
Cardiac morphology and
function was assessed using
magnetic resonance imaging
and cardiac tagging
methodology in 12 CFS
(Fukuda) and 10 matched
controls.
Results:
Compared to controls the CFS
group had substantially
reduced LV mass (reduced by
23%), end diastolic volume
(30%), stroke volume (29%),
and cardiac output (25%).
Residual torsion at 150% of
the end-systolic time was
found to be significantly
higher in the CFS patients
(5.3±1.6(o) ) compared to the
control group (1.7±0.7(o),
p=0.0001).
End diastolic volume index
correlated negatively with
both torsion to endocardial
strain ratio (TSR) (r =-0.65,
p=0.02) and the residual
torsion at 150% end systolic
time (r=-0.76, p=0.004), so
decreased end diastolic
volume is associated with
raised TSR and torsion
persisting longer into
diastole.
Reduced end diastolic volume
index also correlated
significantly with increased
radial thickening (r=-0.65,
p=0.03) and impaired
diastolic function represented
by the ratio of early to late
ventricular filling velocity (E/A
ratio, r=0.71, p=0.009) and
early filling percentage
(r=0.73, p=0.008).
Conclusion:
CFS patients have markedly
reduced cardiac mass and
blood pool volumes,
particularly end diastolic
volume:
this results in significant
impairments in stroke volume
and cardiac output compared
to controls.
The CFS group appeared to
have a delay in the release of
torsion.