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CFS, heart problems, a risky procedure

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CFS, Heart Problems, and a Risky Procedure: A Warning from Dr. Cheney

by Carol Sieverling, reviewed and edited by Paul R. Cheney, M.D., Ph.D.

I had a relatively brief appointment with Dr. Cheney at the end of June. He is
very concerned that the CFS community will hear that he has detected a heart
problem called Patent Foramen Ovale (PFO) in a significant number of his
patients, and that as a result, many CFS patients will pursue a corrective
procedure that is potentially very dangerous. He asked me to write an article
informing CFS patients about the risks of undergoing a catheterization procedure
to close a PFO or Atrial Septal Defect (ASD).

Background - Virtually All CFS Patients Have Diastolic Dysfunction

As most are already aware, Dr. Cheney has found that the cellular energy deficit
at the core of CFS results in diastolic heart dysfunction. This heart condition
does not trigger CFS. However, the heart is affected as CFS progresses and
cellular energy disturbances mount. About 100 of his patients have been tested
in his clinic via echocardiography (a sonogram of the heart) and all but one
were positive by one or more parameters indicative of diastolic dysfunction. The
exception is a 21-year-old patient and her age may have been a factor.

For those who want more technical details on testing for diastolic dysfunction,
all patients (except the 21-year-old) evidenced diastolic dysfunction by their
pulmonary vein D/S ratio. In addition, Dr. Cheney is finding that his older
patients, typically over 50, manifest diastolic dysfunction by the classical
reversal of the mitral in-flow E/A ratio. This E/A reversal accounts for 40% of
all the patients he's tested so far. This ratio jumps to 60% if the TDI e'/a'
reversal is also used as either/or criteria for diastolic dysfunction. Younger
patients manifest diastolic dysfunction primarily as left atrial cavitation
during 70-degree head-up tilt. (The tilt is part of his echo protocol). Seventy
percent of his patients are in this category. Except for a small group of
middle-aged patients, the E/A or e'/a' reversal as compared to atrial cavitation
is usually mutually exclusive. However, both aberrations can exist together in
the middle-aged patient.

There have been other online postings that discuss Dr. Cheney's understanding of
diastolic dysfunction in CFS (Co-Cure.org), as well as the three-hour video of
Dr. Cheney's presentation to our support group just over a year ago. A few of
those videos are still available from dfwcfids.org. (A new Cheney video and/or
DVD should be available this fall).

What is a PFO?

In most people, the right and left sides of the heart have no opening between
them. Circulated blood flows into the right side of the heart. It then goes to
the lungs to pick up oxygen, dump carbon dioxide, and has mini-clots filtered
out as well as potential portal vein toxins and toxic gases produced by
fermentation in the gut. From the lungs it goes to the left side of the heart,
which sends it on to the brain and body.

When the fetus is in the womb, however, it relies on its mother for clean,
oxygenated blood from the umbilical cord blood and does not use its lungs. As a
result, the fetal heart has an opening known as the Patent Foramen Ovale (PFO).
This opening allows blood to take a short cut from the right atrium (upper
chamber of the right heart) to the left atrium, which sends it on its usual path
through the left ventricle and out the aorta to the rest of the body. The PFO is
formed by two overlapping tissues or septi, the septum primum and the septum
secundum.

Typically, when the lungs kick into action at birth, pressure in the right heart
substantially decreases relative to the left side and the PFO slams shut and the
two tissues grow together, forming a permanent seal. But in up to 20 to 30
percent of the general population, the flaps of both tissues press together but
never fuse. This can potentially allow unfiltered blood to escape into the left
side of the heart from the right, depending on the difference in pressure
between the right and left sides. However, the normal pressures in a healthy
heart (left side greater than right) keep the flap valve from opening, so the
vast majority of people with a PFO experience no problems.

A PFO opens when more pressure is created in the right side of the heart. This
can be produced acutely by a Valsalva maneuver, and can occur when people cough,
sneeze, lift something heavy, or strain at stool. If the pressure is enough to
open the PFO, blood can flow from the right atrium to the left.

Dr. Cheney demonstrates the basics of a PFO visually with his hands. Hold your
hands as if in prayer against your chest. Tilt your hands down and point them
away from you, but keep them against your chest. (They represent the wall
separating your atria, the two upper chambers of your heart.) Slide the left one
down so that your left index finger is aligned with your right ring finger. Your
right hand stays stationary. Your left hand is the "valve" that moves. Keep your
little finger still - it's the hinge - while tilting your left hand away from
your right. This is a rudimentary representation of a PFO.

With your hands in this position, you should be able to feel why higher pressure
on the left keeps the PFO shut. (Your left hand pushes against your right.)
Conversely, higher pressures on the right cause the valve of the PFO to open.
(Your left hand tilts away from your right.)

For excellent diagrams and a good description of the development of a PFO in
utero and after birth see
www.oucom.ohiou.edu/dbms-witmer/Downloads/Witmer%2008-21-02%20Heart%20defects.pdf. (See pages 7-9, Atrial Partitioning II-IV).

Most (Perhaps All?) CFS Patients Have a PFO

In late April Dr. Cheney began looking for PFOs in his patients based on
evidence of high right-sided pressures and low left-sided pressures in CFS
patients. To date he has administered contrast echos to 24 patients.
Seventy-eight percent of those not on the treatment protocol for his current
research study were positive - a PFO opened and visibly shunted blood from one
atrium to the other. A Valsalva maneuver is used to induce the PFO to open while
the contrast IV saline with micro-bubbles of air flow through the heart. This is
called a saline bubble test. (Actual echo photos of a positive test result will
be posted on dfwcfids.org in our "Cheney section".)

One published study found that when contrast IV saline was administered in the
arm as opposed to the groin area during this test, a false negative rate of 30%
occurred. Since the groin area cannot be used for the IV in the setting of Dr.
Cheney's clinic, and the arm is typically used by most physicians, it's possible
that virtually all of his patients have (or had) PFOs that shunt blood from one
atrium to the other. This obviously assumes that those who tested negative
actually have PFOs that went undetected (i.e. false negatives).

Dr. Cheney suspects that the PFOs of most CFS patients open only transiently,
not chronically. In other words, the flap valve only opens occasionally.
However, the size of the PFO and how often it opens varies from patient to
patient. During the contrast echo, some patients clearly had a large opening,
allowing more bubbles to cross into the left atrium. Others only had a very few
bubbles moving across, indicating a much smaller opening or less pressure
difference between the right and left atria.

Consequences of a PFO

In adults, this two-flap valve (PFO) between the right and left atrium allows
blood to flow either way, though it tends to flow predominantly in one direction
in any one person. A right to left shunt (flow) increases the risk of a stroke,
since the lungs have not filtered out mini-clots. (Taking low-dose aspirin three
times a week along with a daily supplement of Nattokinase or Lumbrokinase, is
not a bad idea. For a comparison of the latter two, see
www.allergyresearchgroup.com/faq/index.php?article=182.)

Dr. Cheney suspects that these mini-clots explain why so many CFS patients (up
to 50%) have punctate lesions or Unidentified Bright Objects (UBOs) on their MRI
brain scans. Each UBO may actually be a very tiny area damaged by a mini clot.

Migraines have also been linked to PFOs that shunt right to left. Clinical
trials are underway to close PFOs in patients with severe migraines that are
non-responsive to medication. Dr. Cheney pointed out that carbon dioxide levels
in the blood rise with a right to left shunt since unoxygenated blood from the
right side gets dumped into the left arterial circulation. Since carbon dioxide
is a vasodilator it would cause arteries in the brain to dilate, which could
trigger a migraine.

The increased carbon dioxide could also cause slight brain swelling, which could
be mistaken for Chiari I Malformation. Many will remember all the publicity that
this defect received a few years ago as it mimics CFS, and the brain surgery
that some underwent with mixed results.

Higher levels of carbon dioxide would also explain some patients Dr. Cheney has
seen through the years whose symptoms seemed to mimic carbon monoxide poisoning.

There are different risks if the PFO primarily shunts from left to right,
sending blood from the left atrium to the right atrium. From there it's pumped
through the right ventricle into the pulmonary artery and into the lungs.
Increasing the amount of blood in the right atrium can increase the pressure of
the blood moving into the lungs. If the pressure on the right side of the heart
is high enough, pulmonary hypertension can develop and eventually become life
threatening if it rises too high. (Pulmonary hypertension is a disorder in which
the blood pressure in the pulmonary artery rises far above normal levels.)

A left to right shunt also reduces the efficiency of the heart as oxygenated
blood is returned to the right heart, going in the wrong direction. The heart
has to work harder to overcome this inefficiency.

Cause of PFOs and ASDs in CFS Patients

Researchers state that between 20% and 30% of the general population has a PFO,
yet Dr. Cheney's findings as of July 19th indicate that 78% of his "non-study"
CFS patients have one. Are people with PFOs at risk for CFS, or does CFS create
PFOs? Though there is no definite answer as yet, Dr. Cheney strongly suspects
the latter.

There is evidence in CFS patients that right-sided pressures are higher than
normal and left-sided pressures are lower than normal. There's a complex
explanation for this that I'm not sure I fully understand - see the note at the
end for my attempt at an explanation (thankfully heavily edited by Dr. Cheney).
The bottom line is that when the pressure on the right side of the heart rises
high enough in relation to the pressure on the left side, it's possible that a
PFO sealed after birth could pop open. Thus CFS could conceivably create PFOs.

Once a PFO exists, whether it never sealed after birth or was later blown open
by the pressure differential of the two sides of the heart, CFS can enlarge it
through the following process: (1) The cellular energy deficit of CFS leads to
diastolic dysfunction of the heart. (2) Textbooks state that diastolic
dysfunction leads to dilation (enlargement) of the left atrium and increased
right ventricular systolic force. (3) Referring to the diagrams on the website
given above or to the arrangement of your hands described above, imagine the two
opposing flaps that make up the PFO being pulled farther and farther apart by
the left atrial enlargement. (The lower hand being pulled down). The flap that
moves and is considered to be the valve is the lower one and is structurally
part of the left atrium.

The combination of left atrial enlargement and a high right to left pressure
difference could explain why nearly 80% of CFS patients have tested positive for
PFOs, and why their primary shunting is typically from right to left.

As the left atrium expands over time, the PFO may gradually transition from a
flap valve to an actual hole. Cardiologists then call it an ASD and usually
insist that it has existed since birth, which may or may not be the case in CFS
patients. In the context of CFS, with left atrial enlargement and a high right
to left pressure differential, the difference between a PFO and an ASD is simply
a matter of degree - a distinction without a difference. When the flaps can no
longer oppose each other, the PFO becomes an ASD.

There is precedent for a disorder in which left atrial enlargement can lead to
the formation of an ASD. It's called Lutembacher Syndrome. This disorder is
defined as a combination of mitral stenosis and an ASD shunting left-to-right
and even bi-directionally. (Mitral stenosis is a narrowing of the valve that
lies between the left atrium and left ventricle.) Classic Lutembacher Syndrome
is usually described as a congenital mitral stenosis and an acquired ASD.
Recently, several variants have been described.

Dr. Cheney's research into this subject revealed that left atrial enlargement is
part of Lutembacher Syndrome and that left atrial enlargement could produce an
ASD by enlarging a PFO or enlarging a pre-existing small ASD. It's worth noting
that less than one percent of the general population has an ASD, but that people
with mitral stenosis have a much higher incidence rate of ASDs, suggesting that
something (such as left atrial enlargement) is actually creating the ASD.

Why Not Close the PFO or ASD?

Until a few years ago, all PFO and ASD closures involved open-heart surgery and
the use of a heart-lung bypass machine. In 2000 the FDA approved a device called
CardioSeal. In 2002 the Amplatzer device was approved. CardioSeal contains a
nickel-cobalt-chromium-molybdenum alloy. Amplatzer contains nickel and titanium.
Both devices are collapsible discs that are threaded though the femoral vein
into the heart. Once in place, they open up like umbrellas and anchor to the
wall of the atrium with hooks. The ASD or PFO is sandwiched between the two
connected metallic mesh discs.

Approximately a year ago a patient of Dr. Cheney's with a 15-year history of CFS
had a device implanted in his atrial wall via a catheter threaded up the femoral
vein. His story is very enlightening.

He had several echos done from 2001 to 2004 that showed pulmonary hypertension,
but there was no mention of a PFO or ASD in the echo reports. (After recently
examining some of those earlier echos, Dr. Cheney noted the classic E/A reversal
that denotes diastolic dysfunction.) During that same period the patient was
also having brief, unsustained bouts of atrial fibrillation that were gradually
becoming worse.

In the spring of 2005 the patient had another echo done in his hometown that
revealed a 50% ejection fraction (above 55% is normal), mild regurgitation in
the tricuspid and mitral valves, a slightly enlarged left atrium, pulmonary
hypertension of about 50 mm Hg (normal is 16 mm Hg, primary pulmonary
hypertension is anything above 25 mm Hg at rest), and most disconcertingly a
very large ASD.

The cardiologist emphasized the size of the hole in the atrial wall and told him
he'd probably had it since birth. The patient isn't sure he's had the ASD since
birth, given his previous health history and the large size of the ASD. It's
highly unlikely such a large hole in the heart would go undetected for nearly 60
years.

A procedure to close it was done about a year ago. He is the first and only
patient of Dr. Cheney to undergo this procedure - at least so far. After a short
bout of atrial fibrillation immediately after the procedure, he experienced
three weeks during which he felt as if he had been cured. In the last 20 years
he'd never felt that good.

Then his atrial fibrillation recurred, soon becoming chronic and unresponsive to
therapy. Months went by and nothing could control it. His left atrium further
enlarged and he deteriorated clinically. Atrial fibrillation is very poorly
tolerated when one also has diastolic dysfunction.

In February of this year, he went to a nationally renowned clinic for a
consultation about his chronic atrial fibrillation. This national clinic is well
known for its expertise in a laser procedure called a Mini-Maze used to cure
atrial fibrillation. They did an echo and discovered that his heart had nearly
been destroyed. Both atrio-ventricular valves were now severely leaking and his
ejection fraction was down to 30%. They told him he would die without urgent
open-heart surgery. His diagnosis was changed from "chronic atrial fibrillation
following ASD closure" alone to now include "valvular heart disease", a
diagnosis he'd never had before.

He had both valves repaired and the Mini-Maze laser procedure was ultimately
successful at stopping the atrial fibrillation. Dr. Cheney credits the surgeon
and clinic with saving the patient's life. They told him that with the
fibrillation halted, his left atrium would reduce in size. They also told him
that the ASD closure device appeared to have "traumatized" tissue growing over
its metallic mesh surfaces. (It's normal for endothelial cells to gradually
cover the implanted device, though it's not normal for them to become
"traumatized".)

In May, the patient made several trips to the ER, most for tachycardia (rapid
beating of the heart). His fourth trip was prompted by trouble breathing and
feeling faint. They found he was experiencing cardiac tamponade - the heart was
being compressed by fluid accumulating in the space between his heart muscle and
the outer covering of the heart, known as the pericardial sac. That day and the
next they used a syringe to draw out a total of over 3 liters of fluid from that
space. (That's over 3 quarts!).

The patient stabilized enough to finally see Dr. Cheney the last week of June.
(I saw Dr. Cheney two days later, after he'd had time to start processing all
that he had learned from this patient.) Dr. Cheney noted that the echo done at
the patient's June visit looked "pretty good", except that his left atrium was
larger than ever, and he still had a significant pericardial effusion (fluid
gathering in the pericardial sac) and continued evidence of diastolic
dysfunction. His ejection fraction was normal and his heart valves were no
longer leaking. In many ways, his situation was pretty stable considering all
that had happened.

Conclusions

Dr. Cheney spent much time describing this case to me, and in turn I have
devoted much space to it here because it illuminates some very important points.
While it's very likely that some elements of his story are unique to this
patient, there is much that suggests that implanting these devices in a CFS
patient carries significant risks of which cardiologists may be unaware.

His shunting before the closure was likely in both directions. Now, without the
ability to shunt blood over to the left side, too much pressure might build up
in the right side. He no longer has the safety of the pop-off or release valve
effect of the ASD. Some cardiologists are hesitant to close some ASDs for this
very reason. The problem is a conundrum because failure to close a large ASD
could also result in increased right-sided pressure if the shunt is
predominantly left to right under high pressure.

The traumatized tissue on the implanted device is what concerns Dr. Cheney the
most. The device used for this procedure contains nickel, a heavy metal, and Dr.
Cheney believes that the tissue could be reacting to it. (A friend of mine with
CFS once mentioned that some of her earrings caused her ear lobes to swell and
turn red. She finally figured out that this only happened when the earrings
contained nickel.) Nickel poisoning could set in motion Fenton chemistry that
could increase his diastolic dysfunction, which would further enlarge his left
atrium. Therefore, the use of nickel could be contributing to the very disease
process that made its use seem necessary in the first place. (Nickel testing may
reveal if he is, in fact, reacting to it).

The diastolic dysfunction itself most likely started the enlargement of his left
atrium, which may have widened an existing PFO or smaller ASD, and even
contributed to the development of atrial fibrillation. Dr. Cheney is convinced
that CFS created or interacted with the patient's ASD, especially in light of
the new data on CFS and PFOs. His cognitive complaints were slowly developing
after CFS onset and may have been connected to or even caused by the evolving
ASD and increased right to left shunting.

Dr. Cheney's major concerns:

[1] If the left atrium is enlarging due to CFS associated diastolic dysfunction,
should you even consider implanting a device into it? The continued enlargement
expected in untreated diastolic dysfunction might simply cause the tissue
growing over the device to stretch and tear. The resulting damage and
inflammation might cause the heart to react by building up fluid around it that
may result in tamponade (compression of the heart with fluid) or evoke chronic
atrial fibrillation. Needless to say, Dr. Cheney has serious reservations about
implanting a device to close a PFO in a CFS patient if the left atrium has not
yet been stabilized by treating the underlying diastolic dysfunction.

[2] Dr. Cheney is also very concerned about the interaction of nickel and the
pathophysiology of CFS. Implantation of the closure device containing nickel
puts CFS patients at risk for the induction of Fenton chemistry, which will
exacerbate the underlying CFS pathophysiology and further enlarge the left
atrium.

[3] Dr. Cheney suspects that we do not really understand the implications of the
presence of the PFO/ASD in the setting of such a complex disorder as CFS, and
all the interrelationships that exist. The pop-off valve effect of a PFO/ASD
that releases pressure is an example. He is concerned that if the PFO/ASD is
closed, a lot of physiology could be changed abruptly, and because it is so
complex and interrelated the patient could get worse.

Signs of Hope

I have saved this final point for last because it's hopeful. Dr. Cheney is very
intrigued that the patient described above, who clearly has CFS associated
diastolic dysfunction, felt cured for three weeks after his ASD was closed.
Obviously, there were problems that would have surfaced eventually, given the
state of the tissue over the device and the development of chronic atrial
fibrillation.

But his "three-week cure" raises the possibility that if it were possible to
restore normal pressures to the heart and keep PFOs from opening, or to
stabilize the left atrium and keep PFOs from developing into larger PFOs or
ASDs, a significant positive clinical transformation might be possible. Dr.
Cheney wonders how many of our symptoms are totally, or at least partly, derived
from a PFO. He doesn't yet know for sure, but the possibilities are intriguing.

Other than open-heart surgery or the implantation of a device containing nickel
through a femoral vein, cardiologists have little to offer. However, Dr.
Cheney's current study protocol is yielding very interesting early results. And
it is early - the study will not be fully completed until late this year or
early next year. There are two distinct stages of treatment, and the second has
two different dosage groups. There are about 20 participants and they are at
different points on the study timeline. Many are just starting the second phase
of treatment, so the full benefits of the study protocol have yet to be seen.

Two early hopeful indications from the study relate to PFOs and suggest that the
treatment protocol is leading to an improvement that is normalizing pressures in
the heart and keeping PFOs closed.

First, the numbers change as more patients are tested, but currently 67% of
study patients test positive for a shunting PFO versus 78% of those not on the
study treatment protocol. And it's possible many study patients who are testing
positive now will test negative after they've been treated for a longer time.

The hope is that those study patients who tested negative are not false negative
(i.e. actually have a shunting PFO that was not detected), but have been on the
treatment protocol long enough to have improved their cardiac function to the
point of keeping a PFO shut. Unfortunately at the time the study began, PFOs
were not even on the radar thus making a true baseline for a shunting PFO
impossible to determine for many study patients.

If this data holds true over time and with larger numbers, this could represent
an alternative to open-heart surgery or having a device implanted, at least for
many CFS patients.

Second, my own experience suggests that the treatment does indeed normalize
heart pressures and may keep a PFO closed. I am in the study and have been on
the second phase, the porcine heart cell signaling factors, since May 24th.
While it was not possible to test me early enough to get a true baseline for a
shunting PFO, there is evidence that I have a PFO that was shunting, albeit
perhaps only to a mild degree, until just recently.

I was negative on the contrast echo at my June 30th appointment, indicating that
no shunting was taking place, which is great news and matches my overall
improvement.

Indications that I may have a PFO that was shunting right to left and is now
likely staying closed are:

*Increased pressure on the right side of the heart (TRmaxPG on the echo). A
high pressure in September of 2005 dropped 35% into the normal range on both my
2006 April and June echos.

*Venous blood gas testing showed low PO2 levels in March (possible
shunting), but normal levels in May (no shunting).

*The echo sonographer described the area of my left atrium where a PFO would
be located as "very thin". Dr. Cheney said that's how a PFO typically looks,
though this is far from definitive.

*I have a history of migraines that do not respond to medication, but have
not had any recently.

*I had "punctate lesions" or UBOs on an MRI done several years ago.

*While wearing a pulse-oximeter clipped to my finger in Dr. Cheney's office
in April of this year, my oxygen saturation suddenly and inexplicably dropped to
81% and then rose back to normal (98%). I have been monitoring it since May, and
it has not dropped into the 80's (except during intentional breath holding) at
any time that I have been aware of.

With few study participants even at the halfway point yet, Dr. Cheney is not
comfortable giving out treatment protocol information. And even if adjustments
in the protocol are not made at the conclusion of the study, his primary concern
is that no treatment protocol is ever one-size-fits-all. It's always
individualized for each patient. So the treatment protocol needs to be presented
in a setting that allows him to provide a context and go into more detail.

Dr. Cheney is light years ahead of where he was a year ago when he spoke to our
support group here in the Dallas - Fort Worth area. He wants to come speak again
and we are working to arrange a date in late August or September. A DVD of the
presentation should be available some time after the seminar. Watch for online
announcements on the Co-Cure.org announcement list or see our website,
dfwcfids.org, for details as they become available.

In the meantime, if you are a CFIDS patient and discover you have a PFO or ASD,
please think twice before allowing the implantation of a device containing
nickel into an atrial wall that is, or will likely be, expanding. Please wait
until more is known about these complex issues and until we see what benefit Dr.
Cheney's current research study protocol has to offer.

*********************************************************************
Note from the section on the cause of PFOs and ASDs in CFS patients:

The increased pressure on the right side of the heart may in part be a result of
a left shift on the oxygen-hemoglobin dissociation curve observed in most CFS
patients. Interestingly, babies in the womb are left-shifted due to fetal
hemoglobin and therefore have higher pressure on the right side of the heart,
and of course they have a PFO. All of this is normal, even necessary, for
fetuses - but not for adults. In a sense, the left shift and higher right-sided
pressures the left shift produces are telling our bodies that we are back in the
womb and therefore a PFO is necessary for life - a fact that is not true for
adults.

The left shift on the oxygen-hemoglobin dissociation curve and the resulting
reduction in oxygen transfer into the cells of the body is actually a defense
against the redox (reduction-oxidation) problem described in my 2004 article on
the heart which can be found on our website, dfwcfids.org. It describes Martin
Pall's work, particularly the production of energy (ATP) which generates
superoxide in the mitochondria, which under normal circumstances is safely
reduced to water by enzymes embedded in the mitochondria and just outside the
mitochondria.

However, in CFS the enzymes do not seem to function effectively due to a variety
of reasons, most of which are the subject of speculation. This allows superoxide
to leak out of the mitochondria where it can combine with nitric oxide to form
peroxynitrite, a very deadly free radical. Because it takes one superoxide
molecule combining with one nitric oxide molecule to produce one molecule of
peroxynitrite, the levels of peroxynitrite in the body can be significantly
reduced if there isn't much superoxide available to combine with nitric oxide.
And in CFS that's exactly how the body defends itself against terrible damage
from peroxynitrite - it cuts back on energy production which in turn lowers the
production of superoxide.

Note: Increasing the energy of a CFS patient is extremely dangerous unless you
first restore the enzymes in the mitochondria and the supporting co-factors they
need to work well. If superoxide cannot be safely broken down into water and/or
peroxynitrite neutralized, inducing energy in a CFS patient will likely result
in a major relapse, perhaps worse than any state previously experienced. Be very
cautious with any product on the market designed to increase cellular energy in
CFS if you haven't first restored the function of the enzymes needed to handle
the by-products of such energy production. Of course Dr. Cheney's current study
protocols are intended to address this very problem.

The push-crash phenomenon, whether on the small day-to-day scale or on a much
broader scale, is actually part of the CFS case definition and the principle
cause of CFS disability. In effect, the fatigue of CFS is a defense mechanism,
and push-crash is simply a way to enforce this mechanism and protect the
patient.

To summarize, the redox problem in CFS causes the body to actually put
mechanisms in place to lower the amount of oxygen getting into cells. This is a
protective, compensatory measure. This acute reduction in oxygen to the cells is
caused by a left shift on the oxygen-hemoglobin dissociation curve. This results
in increased right-sided pressures in the heart. When these pressures are high
enough, they can pop open a PFO that was previously sealed at birth.

The diastolic dysfunction of CFS also plays into this picture by causing left
atrial dilatation and by increasing the right ventricular systolic squeeze.
Unfortunately, a PFO with a right to left shunt forces a shift to the right on
the oxygen-hemoglobin dissociation curve and can therefore cause serious redox
problems by driving oxygen into the cells. PFOs in a CFS patient are therefore a
serious menace as they effectively evoke oxygen toxicity throughout the body. In
a curious way, CFS and newborns are both supersensitive to oxygen toxicity and
for similar reasons.

Edited by Paul R. Cheney MD, PhD
 

kholmes

New Member
For some reason, reading Cheney--or Carol Sieverling's take on Cheney--is always like reading a horror novel, though Cheney does seem knowledgeable, and I hope patients considering the operation are aware of the problems he's discovered.

Is Cheney finding these PFOs in his CFS patients through standard echocardiograms? I thought that his recent theory involved a decrease in blood volume in severe CFS patients that could only be detected through a cardiac impedence test.

I am also wondering how many people on here with CFS have had standard echocardiogram's that have shown heart problems.

I am severely disabled with CFS, but my echo showed no problems, though I've suspected some problems in that area. I tried the British doctor, Dr. Sarah Myhill's protocol, using COQ10, B12, alpha-lipoic acid, and magnesium, but I didn't notice any difference.

I hope Cheney is starting to find some treatments for improved mitochondrial function.

Kholmes


[This Message was Edited on 07/23/2006]
 

ulala

New Member
I'll have to come back to it tomorrow and print it. I have an appt. with an electrophysiologist in several weeks and will also give it to her.

I hope some of the scholars here weigh in on this!!
 

Aliston

Member
Body with anti-bacterial soap. An associate of the medical team could want to shave the individual’s chest area till they are able to get the anaesthetic.
 

johnswick

Member
Thanks for share,
I'll have to come back to it tomorrow and print it.
Many people ask me a website good about Word unscrambler. So give me share this good and free online tool. .
An update for prohealth members: Word unscrambler without download, installing or register.
 
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