CFS, heart problems, a risky procedure

Discussion in 'Fibromyalgia Main Forum' started by tansy, Jul 22, 2006.

  1. tansy

    tansy New Member

    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 (, 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 (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

    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 (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 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

    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

    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

    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.


    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

    [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

    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

    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 announcement list or see our website,, 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

    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, 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

    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

    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
  2. kholmes

    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.


    [This Message was Edited on 07/23/2006]
  3. ulala

    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!!

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