Cardiac Insufficiency

Printer Friendlier Version

<<< back to [Home]


CFS and Cardiomyopathy

Compensated Idiopathic/Diastolic Cardiomyopathy theory
     Dr Paul Cheney Source Material
     Sacrificial Prioritisation
     Proposed Causes of CICM
     Patent Foramen Ovale (PFO)
     RNA Phenotype Encoding of CFS
     Preload Strategy
     Afterload Strategy
     Other Treatments
     Dr Sarah Myhill's Comments on CICM
     General Comments on Dr Cheney's Cardiac Insufficiency Hypothesis
           Mitochondrial Function
           Sacrificial Prioritisation
           Evolving Ideas and Past Recommendations

Dysautnomia and Abnormal Spontaneous Brainstem Activation (ASBAs)
Short Term Strategies for Alleviating Chest Pains and Palpitations (Cardiac Arrhythmia)
     Chest Pains


As many CFS sufferers will be able to verify, CFS affects not just the hormonal patterns, energy levels, the digestive tract, and general biochemical function of the body, but also seems to affect the heart and blood flow. In some patients, the heart feels like it feels overstrained (beats fast) with gentle exercise, prolonged periods of mental concentration or even when deprived of sleep for a short time; sometimes even generally sensitive or uncomfortable and perhaps prone to frequent palpitations. Patients may often feel short of breath. Low blood pressure affects some but not all patients, or at least a propensity for blood pressure to drop more readily. Some CFS patients may also feel better when lying down than when standing up, on account of postural hypotension, whilst others may feel better when sitting up than when lying down (on account of poor O2 diffusion in the supine position). Some patients may feel better after gentle stretching (that does not involve too much exertion) as more blood circulates and also seems to reach the brain. So what is actually going on here?

back to top

CFS and Cardiomyopathy:

Cardiomyopathy literally means 'heart muscle disease' and is the deterioration of the function of the heart muscle, or myocardium, itself for a variety of reasons. With respect to CFS, we are concerned with specific types of cardiomyopathy, meaning specific causes or routes to cardiomyopathy.

The focus of much of Dr. Paul Cheney's current work on Cardiac Insufficiency hypothesis and its connection to CFS, which is considered on this page in conjunction with the work of other specialists, is based on the groundwork laid out by the following publication:

'Abnormal Impedance Cardiography Predicts Symptom Severity in Chronic Fatigue Syndrome.' Peckerman, et al; The American Journal of the Medical Sciences. 2003; 326(2):55-60.

A (recent) related paper by Dr Vegard Bruun Wyller is listed below:

'Usefulness of an Abnormal Cardiovascular Response During Low-Grade Head-Up Tilt-Test for Discriminating Adolescents With Chronic Fatigue from Healthy Controls.' Vergard Bruun Wyller MD, Reidar Due MD, J. Philip Saul MD, Jan P. Amlie MD PhD and Erik Thaulow MD PhD; American Journal of Cardiology 2007;99:997-1001.

This page shall consider the cardiac aspects of the Diastolic Cardiomyopathy theory, with the related areas of Tissue Oxygenation and Peroxynitrite considered elsewhere.

back to top

Compensated Idiopathic/Diastolic Cardiomyopathy theory:

back to top


In his studies, Dr Cheney has linked significantly decreased values of Cardiac Output in Litres per Minute (a.k.a. 'Q') to CFS cases and post-malaise fatigue (up to 30%), more closely than any other high level determinand. Dr Cheney hypothesises that Compensated Idiopathic Cardiomyopathy (a.k.a. Idiopathic Dilated Cardiomyopathy or IDCM) is a heart condition or heart failure that goes undetected by cardiologists. Idiopathic cardiomyopathy literally means heart condition of unknown cause or origin. According to Cheney, Compensated Idiopathic Cardiomyopathy in CFS is the body's response to protect the heart from complete failure on account of its low levels of available energy. This lack of energy is a result of poor mitochondrial function. The heart, having less energy available and being less capable of fulfilling its normal output requirements, and the body in general requiring less oxygen because of reduced mitochondrial function, reduces its output in order to prevent total heart failure. The body defends the blood pressure, which should not be allowed to drop below a certain level or life cannot be sustained. It does this by restricting the blood flow to some of the organs by closing valves within the circulatory system (this combined with the slightly lowered blood pressure having a corresponding negative effect on the lymphatic system and circulation). The body initially tries to mask this deficit according to Cheney by increased adrenaline and stress hormone outputs, which puts a strain on the endocrine system, but eventually these will become overburdened and deficient, resulting in further decreases in cardiac function and metabolic rate. The systematic sacrifice or shutting down of the body's organs results in the progression of the condition of CFS according to Cheney, and simply aiming to boost blood circulation to these organs and their oxygen requirements puts more strain on the heart and potentially makes the whole condition worse. Cheney's hypothesis works on the basis of boosting mitochondrial function and the factors that are holding back mitochondrial function, in order to bring the heart and other organs functions back to normal in the right sequence.

What other symptoms are there of cardiomyopathy in CFS patients besides lower cardiac output and a decreased propensity for heavy exercise? Other symptoms can include elevated pulse rate (during rest, standing up from a reclining posture - known as Postural Orthostatic Tachycardia Syndrome (POTS) - see links below, or indeed during light exercise), a heavy heart beat, palpitations and even chest pains (if not enough oxygen or ATP is available for the cardiac muscle) when fatigued or when lieing down on the left side.

POTS may also be accompanied by Neurally Mediated Hypotension (NMH), which is a drop in blood pressure that occurs after being upright, e.g. a drop in systolic BP of 25mm Hg). It occurs when too little blood circulates back to the heart when people are upright and triggers an abnormal reflex interaction between the heart and the brain. It is also known as the fainting reflex, delayed orthostatic hypotension, neurocardiogenic syncope, vasodepressor syncope and vaso-vagal syncope. Syncope is the medical term for fainting.

What is the mechanism of the cardiomyopathy? How is heart function impaired exactly? Diastolic Dysfunction is the result of this low mitochondrial function. The heart has two phases, the relaxation/expansion phase, where the left venticle fills with blood (known as the diastolic phase); and the contraction or systolic phase. The expansion/relaxation (diastolic) phase is said to require more energy than the contraction phase, so this part of the cycle is not executed as well, resulting in only partial filling of the left ventricle. This creates a larger pressure difference than normal. This puts additional strain on the heart muscle.

back to top

Dr Paul Cheney Source Material:

Cheney's theory is summarised briefly in the links below.

Currently the most comprehensive article on the internet on Cheney's theory is shown below which was written by Carol Sieverling, based on a series of patient interviews with Paul Cheney between September and November 2004.

This article however does not go into sufficient detail in a number of areas, including the role of PFOs, the effects of oxygen on the heart, other treatments to support enzyme production (including animal stem cells) and promote heart function etc., which have been elaborated on by Cheney in his actual seminars and talks (and indeed more recent research papers), which were captured on video, and are listed below.

A 2003 video talk by Dr Cheney can be seen at the link below.

To purchase a 2 DVD set of Dr Cheney's seminar from 9 September 2006, University of North Texas, Health Science Center, Fort Worth, Texas, visit the links below. It appears that one batch of these DVDs features a corrupted section of the seminar which cannot be viewed properly.

A summary of Dr Cheney's Fairfax, Virginia seminar from 25 April 2009 can be read at the links below.

I have attempted to integrate all of the above Cheney sources into one overall high level summary below, with my own commentary and critique. This was first written in January 2009, but I have since integrated a wide variety of other material and split the article into 3 pages, as mentioned above.

Cheney seems to have consistently changed the emphasis of his theory over the years, and refined it, and each year he seems to come up with new ideas for protocols, based on the studies of the patients at his clinic, whom do not seem to be truly representative of the diversity of CFS cases elsewhere. There are various areas of discrepency and contradiction in the ideas presented, which are discussed on this page and the other two related pages.

The related topic of homocysteine metabolism and glutathione production, and elevated homocysteine levels, which can contribute to an increased risk of heart attack in some CFS patients, is discussed elsewhere on the Nutritional Deficiencies page.

back to top

Sacrificial Prioritisation:

Cheney theories that the body has a special sequence of sacrificial prioritisation, sacrificing blood flow (perfusion) to organs in a sequence, rather than in an equal manner. This is a result of CFS patients having a low blood pressure, and the blood supply to the organs being shut down one by one, in order to maintain sufficient blood pressure (and effectively raise the blood pressure). The order of this proposed sequence is summarised below.

So to summarise, Cheney's theory is that CFS is a set of symptoms of Compensated Idiopathic Cardiomyopathy, that without it would otherwise mean those affected would likely die very young of a heart attack. The degree of compensation is said to vary hence showing variations in CFS severity and degree of symptoms. This does not mean that CFS patients will not develop fatal heart conditions, but that the onset is much later than it otherwise would be, at a slightly younger age than the rest of the population.

back to top

Proposed Causes of CICM:

In the 2004 document, Cheney states that the cause of the Compensated Idiopathic Cardiomyopathy (CICM) or decreased cardiac output is a loss of muscle power on account of mitochondrial inefficiency. This is attributed to a number of causes:

However, in his 2006 seminar, Cheney's overall argument is that viral and bacterial infections are a result of poor mitochondrial function (and the knock on effects of lower oxygen requirements/levels). He does not focus so much on heavy metal toxicity as a cause of mitochondrial dysfunction.

He does however examine DNA damage from elevated RNase-L levels (a cellular anti-viral response) as a cause of CICM and oxidative damage from free radicals from excessive oxygenation (which is a circular argument as this is a result and not a cause of mitochondrial dysfunction, i.e. a deficit of energy to actually produce protective antioxidants against the free radicals produced by metabolism). He did not really mention peroxynitrite or the roots causes of mitochondrial function at all, but rather their downstream effects and how to address mitochondrial dyfunction, how to accelerate reverse phenotype adaptation and how to boost the heart output.

Cheney states that reduced oxygen levels in the body and a more anaerobic metabolism results in lower oxygen levels in the cells, which attracts facultative anaerobes, e.g. candida, Lyme Disease (bacteria of the Borrelia genus) and Chlamydia bacteria etc. Thus Cheney postulates that they are the result and not the cause of CFS. Cheney postulates that the low oxygen levels and consumption are an adaptation to poor mitochondrial function, which 'cause' the CFS. There are of course other reasons for Candida overgrowth besides low oxygen levels, and these may include diets high in simple carbohydrates, excessive ingestion of mouldy-type foods, stress and a variety of other factors. Low oxygen levels are of course irrelevant to viral infections, which often play a part in CFS cases.

Cheney stated that for many years he believed that viral infections were the cause of CFS, rather than just the trigger, and that too high RNase-L levels were also party to blame. RNase-L production is an anti-viral response by the body to a viral trigger, which indiscriminately destroy viral RNA as well as human RNA (by inhibiting ability to replicate). Excess RNase-L production in CFS cases is thought to explain much of the cellular damage that occurs. Excessive RNase-L damages cellular and mitochondrial RNA and also impairs ATP production and according to Cheney is even thought to induce intracellular acidosis (through excessive lactate build up). RNase-L is examined in more detail on the Stealth Viruses page.

However, he stated in the 2006 seminar that he believes that the viral infection is merely a symptom of low mitochondrial function, and that fighting the viruses will not cure CFS. He believes that if the body does not have enough energy, then it cannot address all the other downstream issues that result from a lack of energy, i.e. enzymatic efficiency etc. Whilst in many patients, the viral and bacterial infections work synergistically with the low energy levels/availability to produce a more adverse situation, if one fixes the energy issue, Cheney believes the other issues will correct themselves. His logic being that all people have viruses floating around in the bloood stream and in the tissues, but not everyone has CFS. However, this slightly contradicts what he said in 2004 and also the 2006 recommendation he has given for the anti-viral drug Nexavir, discussed in the Other Treatments section.

One example given of the energy argument is taking the actual required vitamins in the form the body uses them rather than the precursors of those vitamins, as the body requires energy to convert them, and amino acid and other chemical conversion in the body in a CFS patient is already flawed, i.e. better to take folate rather than folic acid, as the body has to convert folic acid to folate (requiring ATP which is in short supply). How significant this actually is given the quantities involved is a matter of debate.

This logic is however somewhat flawed, and contradicts the 'synergistic' argument; as treatment may indeed require tackling all issues, including downstream effects (like viral or bacterial infections) as well as 'initial causes'; as the downstream effects of viral or bacterial infections put a strain on the immune system and require additional energy and ATP to combat, 24/7, which makes the job of fixing the energy deficit that much harder, as the energy requirement is much higher because of them. In addition, I believe that it is also a chicken and egg question, as to which was the initial cause, and they likely worked together synergistically from the start (in terms of the trigger).

Cheney states that by treating energy production (mitochondrial function), the thyroid and cardiac function will sort themselves out, but by targetting the thyroid and cardiac function and not the energy production issue, the patient may not make significant progress, or if he does, may be in a dangerous position (in terms of putting too much pressure on heart output and 'over oxygenation'). Clearly there is some merit to these statements, but logic would dictate treating all areas rather than just one.

A detailed look at Peroxynitrite formation and methods of restraining Nitric Oxide and Peroxynitrite formation is found on the Nitric Oxide & Peroxynitrite page.

A detailed look at insufficient tissue oxygenation and oxygen management is found on the Insufficient Tissue Oxygenation and CFS page.

back to top

Patent Foramen Ovale (PFO):

In Cheney's 2006 seminar, he postulates that in extreme cases of Diastolic Dysfunction in CFS patients, a Patent Foramen Ovale (PFO) may be present and exaccerbating the cardiac dysfunction. A PFO is a tiny hole in the heart, utilised in foetal physiology.

Let us examine what a PFO is first of all.

During a foetus' development, the heart's two atria chambers are connected by a hole through the wall of the muscle (formed roughly in the fourth week of gestation), which allows blood to be diverted away from the lungs.

In the primitive atrium it is known as the foramen ovale, the formane in the septum secundum. A drawing of the septum secundum in a foetal heart is shown below.

'The foramen ovale begins forming late in the fourth week of gestation. Initially the atria are separated from one another by the septum primum [shown below] except for a small opening in the septum, the ostium primum.'

'As the septum primum grows, the ostium primum narrows and eventually closes. Before it does so, bloodflow from the inferior vena cava wears down a portion of the septum primum, forming the ostium secundum...The ostium secundum provides communication between the atria after the ostium primum closes completely. Subsequently, a second wall of tissue, the septum secundum, grows over the ostium secundum in the right atrium. Bloodflow then only passes from the right to left atrium by way of a small passageway in the septum secundum and then through the ostium secundum.'

'This passageway is called the foramen ovale [ie. the foramen in the septum secundum]. Normally this opening closes in the first three months of life. When the lungs become functional at birth, the pulmonary pressure decreases and the left atrial pressure exceeds that of the right. This forces the septum primum against the septum secundum, functionally closing the foramen ovale. In time the septa eventually fuse, leaving a remnant of the foramen ovale, the fossa ovalis.'

In a foetus, the lungs are not working and are full of fluid in the womb, and are only used once the baby is born. Up to that point, the foetus relies on oxygen being supplied in the umbilical cord, which diffuses into the baby's own blood. At the point of birth, when emerging from the womb, the baby takes its first breath and this PFO valve shuts. The umbilical cord is cut and tied off shortly afterwards.

In most infants it grows shut, using scar tissue, but in 15-20% of the population it does not. i.e. in 15-30% of the population the PFO valve never grew shut, but opens and closes depending on the partial pressure of oxygen in the blood. This is the foramen ovale, specifically the foramen in the septum primum. 'Patent' literally meaning 'open'. This can potentially result in heart difficulties, e.g. laboured breathing or recurrent respiratory infections. Please see the link above for further details. The article is spread over 8 pages.

'Atrial septal defect (ASD) is a form of congenital heart defect that enables blood flow between the left and right atria via the interatrial septum. The interatrial septum is the tissue that divides the right and left atria. Without this septum, or if there is a defect in this septum, it is possible for blood to travel from the left side of the heart to the right side of the heart, or vice versa.'

The article 'Atrial Septal Defect, Ostium Secundum' by Ira H. Gessner, is shown at the link below.

'Fusion of the septum primum and the septum secundum closes the foramen ovale. Complete closure occurs in most individuals. In 25-30% of normal adult hearts, however, a probe can be passed from the right atrium to the left atrium via the foramen ovale and ostium secundum. This patent foramen ovale allows a tiny left-to-right shunt that can be detected by sensitive techniques, such as color Doppler echocardiography, in 15-20% of adults.'

A Cardiologist friend of mine, Dr Tatinha, has stated, in 2009:

'There are three major types of interatrial complications: ostium secundum, ostium primum and sinus venosus defects. Secundum Atrial Septal Defect (ASD), [i.e. a PFO], is by far the most common type. Adult patients with simple congenital heart disease, such as isolated atrial septal defects are rapidly becoming a relatively large population with a variety of clinical problems...more recently, MRI are mandatory to assess types and significance of ASDs. Standard echocardiography is the first-line imaging modality to confirm suspicion of such defects and 3D echo and MRIs are the most modern and more promising techniques in case of difficult diagnosis. Surgical or percutaneous repair should be offered at any age unless associated with pulmonary vascular disease, whereas surgery remains the only option for primum and sinus defects. Follow-up of operated patients is based on Holter ECG and echocardiography. Adults with isolated ASD are more likely to reach adult age without being diagnosed. This diagnosis should be kept in mind in presence of symptoms and signs of pulmonary overload. Unfortunately, I do not have any clear recommendations and some indications can be retrieved from the literature. Percutaneous device-based closure or conventional or mini-invasive surgery should be proposed on the basis of types of defects (secundum, primum or sinus defects). In case of secundum ASD, decision about surgery or device-based closure should be made on the basis of anatomical characteristics of the defect. Currently, percutaneous closure seems to be the first choice in uncomplicated defects, whereas mini-invasive surgery seems indicated in some cases (e.g. difficult control's arrhythmia, difficult anatomy, defects larger than 40 mm, etc.)'

Cheney suggests that it is one of the primary drivers behind cardiac insufficiency and the mechanism of CFS within severe CFS patients. A PFO may indeed exaggerate the symptoms of mitochondrial cardiac insufficiency in CFS patients. Cheney likens the PFO, an impaired cardiac function, to the foetal circulation, which is an immature function, the difference being that the foetus is not able to use its lungs but relies on the umbilical cord, whereas the adult with a PFO has no umbilical cord and relies on his lungs for oxygen requirements.

Cheney hypothesises that CFS sufferers (with no PFO) may actually rip/blow open this Formane Ovale valve, having formerly been sealed shut with scar tissue after birth, when sufficient pressure builds up in the right atrium. This valve thus remains open for much of the time, depends on the oxygen levels and pressure inside the right atrium. Cheney believes that Diastolic Dysfunction/CICM may greatly increase the likelihood of ripping open one's foramen ovale, if one does not already have a PFO. The further down the line of CICM is, and the weaker the heart function is (i.e. a reflect of poor mitochondrial function), then the more likely this scenario is to develop. One should take into account the decreased strength of the heart muscle, heart muscle wasting, decreased blood pressure being compensated for by sequential sacrifice of blood supply to the organs and increased heart rate; but also the increased pressures inside the heart resulting from diastolic dysfunction.

Dr Tatinha has also confirmed with me that it is indeed possible to blow/rip open one's Foramen Ovale and thus develop a PFO at any point in one's life. How frequent this actually is however is not fully understood. If one assumes that having a PFO in the vast majority of cases is a congenital (birth) defect which will never grow shut, then is it possible that those patients who are claimed to rip open a Foramen Ovale may be able to grow it shut again (with scar tissue) as they once did when they were infants? Is there a difference between doing so as an infant and as an adult? Clearly the adult heart is operating at much greater pressures. It is probably unlikely that it will self-correct in an adult.

In Cheney's clinic, he has observed the prevalence of PFOs to be approximately 80-90%, in contrast to the 15-30% of the population with one. There appears to be a little 'back pedalling' or at least more accurate quantification in Cheney's figures in 2006, as in his 2003 seminar video he states that 99% of his patients had a PFO, which is quite different. Has the demographic of his patients changed? Were these figures based on a very small number of patients? Or just a moment of generalisation to emphasise the point? It would make sense to take his latest figures more seriously. Clearly not everyone who has a PFO develops CFS during his lifetime. And not every CFS patient has a PFO (yet). One can speculate as to the reason for this, whether these CFS cases simply arose from that 15-20% sub-segment of the population, or whether they blew/ripped open their Foramen Ovales in the course of Diastolic Dysfunction as a result of a progressed state of CFS.

Cheney has in his own research admitted that perhaps he receives only the most extreme and far gone (cardiac-related?) CFS cases in his clinic (i.e. those that have progressed to severe diastolic dysfunction and have 'developed' PFOs), and his own research and hypotheses, based upon those patients that visit his clinic, may indeed reflect this. Is it possible therefore that his test subjects are not representative of the CFS community as a whole? And that his hypotheses are based often on a small subset of the many routes and 'configurations' that CFS can manifest itself in? If Cheney is correct that ripping open one's Foramen Ovale is indeed one of the latter stages of CFS, which many/most CFS cases will progress to in less than ideal circumstances (lack of treatment, lifestyle/diet/environment/biochemical status conducive to deterioration of one's condition), then he is really looking at the worst case scenario of CFS. Otherwise, he is merely looking at a small cross section of cases that bear no relevance to the types and progression of CFS in most patients in general. - 'Oxygen Toxicity as a Locus of Control for Chronis Fatigue Syndrome' by Dr Paul Cheney, 27 May 2008'

'The missing piece to this puzzle may be that we see a super-select group of CFS patients at our clinic.'

Cheney has observed the effect of oxygen on the PFO as described in the section above. Supply of oxygen enriched mixtures or oxygen under pressure as in hyperbaric oxygen therapy has shown mixed results. Whilst low oxygen doses (i.e. slightly enriched oxygen mixtures) has shown to improve most CFS patients with a PFO at Cheney's clinic, high oxygen doses (i.e. pure oxygen or oxygen mixtures under pressure) has resulted in a larger percentage of patients getting worse. Cheney claims that the cardiac muscle has an oxygen threshold, and below this the PFO stays shut, but above certain partial pressures of oxygen, the PFO opens and stays open. He therefore concludes that too much oxygen is not a good thing and can simply worsen the diastolic dysfunction of a person with a PFO. Of course, it is one thing breathing 90% O2 at atmospheric pressure, but it is quite another breathing O2 enriched air or pure O2 under pressure, and Oxygen becomes toxic and inflames the lungs at 1.6 and can cause CNS toxicity, and may also displace Nitrogen and CO2 in the blood, so it is not surprising that some problems can be observed with O2 under pressure in CFS patients. Without knowing the exact nature of the adverse symptoms from afflicted patients when additional oxygen is delivered, it is hard to comment. However, it could also be a possibility that a Herxheimer effect was occurring, on account of pathogenic microbe die off under high oxygen pressures - and nothing to do with a PFO at all.

Besides minor complications and constraints on one's lifestyle, there are more serious consequnces of having a PFO, both for younger and older patients (whether they have CFS or not), including an increased risk of a stroke from a paradoxical embolism is a cause of stroke in both age groups. The prevalence of a PFO has been shown to be much greater amongst patients who have had a cryptogenic stroke than amongst those with stroke of known cause in all age groups. There is also a very strong connection between the presence of a PFO with concomitant (simultaneous) atrial septal aneurysm and cryptogenic stroke (a stroke of unknown origin), compared with incidences of known/identifiable types of stroke.

A PFO also has a potential impact on scuba divers. If one does have a PFO, then one is at considerable risk of getting the 'bends' or decompression sickness from a non-decompression dive well within the non-decompression limits, let alone a very deep dive or decompression dive. During a scuba dive one is breathing in air or other gases at a pressure equal to the surrounding water (i.e. at a greater pressure the deeper one goes). This pressure forces nitrogen into the blood which is then absorbed by the tissues of the body. The lungs are the place where nitrogen under pressure is absorbed into the blood, but also where nitrogen escapes from the blood and is removed from the body during one's ascent. Depending on the depth and bottom time, the ascent has to be adjusted accordingly, to allow the nitrogen to escape from the tissues at a controlled rate and be removed from the body without forming too big bubbles which can occur if one ascends too quickly. If a diver has a PFO, then some blood full of fine bubbles of nitrogen bypasses the lungs and goes directly to the brain and onwards to the rest of the body, where a bubble getting stuck in a blood vessel will cause the symptoms of DCS and at worst death.

The usual method for testing for a PFO is a transthoracicechocardiogram with a a saline bubble infusion. This is performed by aggitating a saline solution with air bubbles by squirting saline with air in it from one syringe to another, both connected via a tube. This aggitated saline, containing very fine air bubbles, is injected into a vein in the arm. The patient is then required to perform the valsalva manoevre (i.e. blowing into a closed tube), which increases the pressure in the heart and will open up the PFO if it present. The heart is monitored on the echocardiogram (ultrasound) on the screen and any bubbles that pass directly from the right atrium to the left can be observed on the screen. The exact method of counting/recording bubbles that do pass through a PFO varies. Clearly it depends on the competence of the cardiologist, and evidently many people have been misdiagnosed because the practitioner was not paying attention to he bubbles properly and perhaps missed a few that passed across. The procedure is not painful and is akin to a slightly aggressive scuba diving ascent in terms of bubble formation. If no PFO is present, all the bubbles in the blood will be transported to the lungs for removal.

Other methods for PFO testing include a transesophageal echocardiogram, transcranial doppler (TCD) and even MRI. The exact method used will depend on the consultant in question.

I myself have been involved in recreational scuba diving and technical/decompression diving, and one of the recommended practices in certain fields of the technical diving (DIR) community is to have a PFO test, to check that one definitely does not have a PFO before embarking on any serious decompression diving. So if one is found to have a PFO, then one should desist from diving immediately and write off one's diving career. Knowing one does not have a PFO also gives one assurance that doing aggressive but accurate decompression dive profiles will not result in the bends. Some technical divers argue that if a diver has gone to the stage where he is performing deep diving and decompression diving, and has not had the bends, then in all likelihood he does not have a PFO and thus a test is not necessary. However this is not strictly true in all cases.

I had a PFO test performed by a private specialist in London in 2000 and his results were negative. Please see the links page for details. My CFS developed around the end of 2002, however, I had always had minor mitochondrial, endocrine, digestive and immune system problems for many years prior. The onset of my condition cannot therefore be explained by a PFO, although it is possible according to Cheney that I may have ripped open his foramen ovale when my CFS condition deteriorated, although I consider this unlikely. As a PFO does not necessarily lead to CFS, then having a PFO concurrent with CFS does not necessarily mean that one cannot overcome one's CFS and get back to how one was before, i.e. a non-CFS suffering person who happens to have a PFO.

Most doctors do not bother to test for PFOs as it is not regarded as important, and finding a doctor or specialist who is willing to get involved or knows anything about it is quite difficult.

There are two medical procedures for PFO closure, transcatheter closure and surgical closure. Transcatheter closure involves having a 'plug' pushed up one of your blood vessels until it reaches the heart, where it is pushed into the hole of the foramen ovale to effectively plug it shut. The exact shape and size of the plug will depend on the individual. The surgical closure involves open heart surgery and 'sewing' the foramen ovale shut. I have heard of one of two DIR technical divers that have had their PFOs sewn up as they refused to give up diving. So if you do have a PFO and want to have it plugged or sewn up, then it is really no big deal. Do not write yourself off as 'doomed' if you have bad CFS and a PFO as both can be corrected (independently or together).

back to top

Phenotype Encoding of CFS:

In his 2006 seminar, Cheney stated that he believes that over time, a process of phenotype adaptation occurs to embed the characteristics of CFS into one's genes.

The adaptation is genetically coded as a DNA and RNA phenotype shift. This tends to happen over 2-3 years. This locks in the dysfunction (or metabolic function and level of enzymatic activity etc.) at the genetic level, and means that the longer one's condition goes on for, or the worse it becomes, the harder it is to recover as the mechanisms and biochemical problems becoming increasingly coded on a genetic level. This does not mean that one is genetically programmed to develop CFS, or that one's CFS is incurable, but that one's body adapts, and it is not solely the hypothalamic dysfunction that is driving the problems. Of course, as one treats CFS, the genetic coding and phenotype adaptation will work in reverse, to return to 'normal', but this process may slow down one's recovery that would otherwise have been much swifter. According to Cheney, it may take up to 2-3 years for one's body to readjust back to normal, even after one has seemingly removing all the barriers to full health and is supplementing the body. This he cites is not a disease issue any longer but an adaptation issue, and the more one can do to help the adaptation process along by providing optimal conditions for the body, and indeed to accelerate it the better, rather than keeping the adaptation locked in by continuing to abuse the body or over-stress it. He also believes that a rapid recovery from a body that was phenotypically adapted to CFS or a very severe state of CFS is in an 'unstable state', and one may either be suppressing the body's natural defence mechanism which will come back to exert its purpose to protect the body again; or equally (my comment) that the body's natural tendency is to return to the previous state of adaptation (if it has not had time to phenotypically adapt to a new, healthy pattern) with the slightest 'push'. As stated, in the latter case, it is important not to overdo it as soon as one starts to feel better, but let the body naturally adjust over time to this healthy state.

Cheney cites his heart transplant operation, that took place during 2003/2004 at the peak of his CFS condition (and diastolic failure), presumably having been extremely ill with CFS himself in the many years of his research prior to this, when he still felt fatigued after receiving a new heart; although of course this was in part due to his mitochondrial function still being poor and being unable to 'fuel' his 'new' heart, as well as phenotype shift (the body not being used to a stronger, more youthful heart with a higher potential peak output).

Cheney in his 2006 seminar was rather vague as to whether it was reflected in the RNA or DNA, and mentioned both.

In the Other Treatments section below, Cheney cites stem-cell related treatments or compounds that promote stem cell growth and production may assist in accelerating the reverse of this phenotype adaptation to CFS.

How much truth is there in this theory? Clearly the results speak for themselves, but is phenotype encoding just another way of saying that the longer the symptoms persist for, the more complex the underlying biochemical problems become underneath, and thus take more unravelling and time to address?

One might argue that herbal medicine, diet, emotional state and indeed energetic state (in terms of 'qi') are also very important, and may greatly progress the rate of one's recovery. Are oriental medicine and energetic therapies in general describing the same thing? Or is Cheney pointing to the wrong/different cause, both of which are acting on the rate of recovery? Can energetic therapies like oriental medicine etc. actually speed up phenotype adaptation?

Some miscellaneous medical and cardiac information web site links are listed below, containing up to date medical news and articles.

back to top

Preload strategies:

Cheney (in 2004) has suggested some other approaches to assist in our Cardiac function, day to day, increase one's 'Preload (blood volume)' in the heart and reduce one's 'Afterload blood volume' (reducing the resistance the blood encounters). This is not intended as a 'cure' but more as a way of alleviating symptoms associated with cardiac insufficiency. The trick to preloading is not to 'preload' too much or the effect is counterproductive in absolute terms.

back to top

Afterload strategy:

This may perhaps explain why patients with related conditions like Fibromyalgia and Multiple Chemical Sensitivities (MCS) have been shown in recent studies to have less blood flow to certain parts of the brain.

However, Dr Cheney believes that a problem with 'Q' is what differentiates CFS and PVFS from Fibromyalgia and MCS, as the latter groupings do not have a problem with Q according to him - unless the patients also have CFS. Dr Cheney has historically not differentiated between CFS and ME.

Perhaps this is a circular argument (a chicken and egg situation), as many of the diosorders, imbalances and deficiencies in question actually have an impact/are active agents in both. All Fibromyalgia and ME cases in my experience have some component of mitochondrial inefficiency, endocrine system dysfunction and also toxicity behind them.

back to top

Other Treatments:

In Cheney's 2006 seminar, he additionally recommends the following treatments.

back to top

Dr Sarah Myhill's Comments on CICM:

Dr Sarah Myhill believes that 'CFS is Heart Failure Secondary to Mitochondrial Malfunction', which is broadly in line with what Dr Paul Cheney has proposed.

Dr Myhill has suggested that although cardiac function and output capability in CFS patients is impaired, the traditional tests such as ECG, ECHOs and angiograms used by cardiologists will produce normal results. Dr Peckerman has proposed to the USNIH that an Impendence Cardiography type test for CFS be developed based on the principles of decreased 'Q' (cardiac output in litres per minute).

Dr Myhill's recommendations for mitochondrial and cardiac support are based on the cardiologist Dr Sinatra's recommendations. These are similar to Dr Cheney's suggestions, but also include D-ribose and L-Carnitine (of course other animo acids or organic acids may be deficient causing the problems rather than just Carnitine). Beta blockers, tricyclic antidepressants and phenothiazines actually block CoQ10 production in the body and way worsen the situation.

The book 'The Sinatra Solution: Metabolic Cardiology' by Dr Stephen T. Sinatra can be viewed at on line by clicking here.

Dr Myhill is also a strong advocate of cellular detoxification, particularly using methods such as phospholipid therapy and FIR saunas. She views toxicity as one of the major stumbling blocks in proper mitochondrial function in CFS patients. These techniques are explored more on the Toxicity page.

Additional Articles about Cardiac Insufficiency and CFS:

A list of related research articles by Dr Peckerman, Dr Martin Lerner, Dr Myhill and Dr Paul Cheney and many others, some of which have already been listed on this page, are available at the link below.

The article below examines possible links between viral infections and cardiomyopathies.

A number of articles about Dr Paul Cheney's treatment protocols (old and new) in general (not just relating to Cardiac Insufficiency).

back to top

General Comments on Dr Cheney's Cardiac Insufficiency Hypothesis:

back to top

Dysautonomia and Abnormal Spontaneous Brainstem Activation (ASBA)

An analysis of autonomic system profiling, and the types of parameters and reflex mechanisms of the sympathetic (fight or flight) and parasympathetic (rest and digest) nervous system that can be tested, can be found on the Tests page in the Neurophysiological Tests section. It is worth reading through this section in order to put this discussion of Abnormal Spontaneous Brainstem Activation into context.

Dysautonomia in general can be regarded as a shift in the body's normal automatic, unconscious regulatory functions that control many adaptations of the body that we do not consciously have to concern ourselves with regulating with our minds to ensure we stay alive throughout the day, in response to changing demands on the body. Fluctuations or instability in the baroreflex (Blood Pressure maintenance) and heart rate affect the provision of a steady and reliable blood flow to the organs and muscles of the body which can result in fatigue, dizziness, difficulty in exercising, quick depletion of energy and other symptoms.

During severe illness, especially infections, the body's autonomic system undergoes a shift in its normal baseline of functioning in order to prepare the body to fight off the infection. The brain stem and hypothalamus are involved in the body's immune system response. The problem lies when the autonomic nervous system does not return to its original equilibrium and normal baseline - it seemingly having 'forgotten' where or what it is, and being trapped in a pattern of dysautonomia or misregulation of the body. The autonomic functions of the brain are generally controlled by the Brainstem and the Pituitary Gland in the Hypothalamus. After a severe viral episode, or other mechanism, the brainstem itself can become overstimulated and over-interpret stimuli from the nervous system and also behave erratically itself.

'The brain stem (or brainstem) is the lower part of the brain, adjoining and structurally continuous with the spinal cord.'

As well as abnormal fluctuations or instability in the blood pressure and heart rate, Dr Peter Julu argues that the actual heart beat itself may be impaired. The heart beat may take the form of a 'stop-start' cycle, where the cardiac muscle receives energy and inotropics (compounds that help to strengthen the heart beat), which run out half-way through the beat cycle. This prevents a smooth heart beat and may be comparable to what Paul Cheney describes in his Diastolic Cardiomyopathy theory.

Abnormal Spontaneous Brainstem Activation (ASBA) is a condition whereby the brainstem is inflamed, irritated or overstimulated, and the neurons are 'misfiring' and sending signals to the nervous system, including the heart, in an abnormal or erratic manner. This can result in what we observe as cardiac arrhythmia and instability. This cardiac arrhythmia of the blood pressure and heart rate is manifested in random fluctuations in the heart rate and blood pressure, within certain limits, and abnormal responses to various physiological changes in the body, e.g. posture, bodily movements etc. (i.e. dysautonomia). ASBAs can be indirectly measured by abnormal spontaneous cardiac behaviour.

According to Dr Peter Julu, ASBAs are generally found in:

In the context of CFS and related conditions, it is the Allergic function that appears to be operating.

There are various possible causes of ASBAs in CFS patients. These could be:

Dr Peter Julu believes the emphasis is on Allergies rather than Heavy Metal Toxicity, which he believes has other types of effects on the body.

Those marked with a '*' above are all tied to the Nitric Oxide / Peroxynitrite cycle and the self-perpetuating cycle of free radical production and oxidative stress. These tend to inflame the nervous system, and upregulate the allergic response, which itself generates more Peroxynitrite (via Nitric Oxide and Superoxide). Excessive immunity activation is just one cause of the Peroxynitrite cycle, and there are many others, including stress and toxicity. In my opinion, ASBAs, caused by brainstem inflammation and improper brainstem functioning, are largely a result of excessive Peroxynitrite formation. This is a characteristic of inflammatory diseases in general. More information on this topic can be found on the Nitric Oxide/Peroxynitrite Cycle page.

Thermoregulatory Vasomotor Function (TVF) is the ability of the nervous system to control body temperature in response to changes in the external environment. It relates to the regulation of the blood vessels in the body. In a healthy person, if the left hand is exposed to cold, then the blood vessels in both hands are expected to constrict to stop heat loss, rather than each hand operating independently. Abnormal TVF may result in no response in the blood vessels in the rest of the body to a cold input one one of the extremities, or even the opposite response, e.g. vasodilation in both hands when vasoconstriction is expected. Examples of poor or abnormal TVF function include temperature sensitivity and maladaptation to temperature changes, e.g. a sensitivity to drafts. TVF problems can also result in the body running slightly too warm during certain times of the day, burning off more energy than it should be for heat, which is badly needed in the organs or tissues of the body. Certain individuals with TVF problems may find that they do not need such thick blankets at night, for example. TVF problems may arise for a number of reasons. One of these could be damage to the valves in the blood vessels in question by toxins. These valves can however repair once the sources of the toxicity is removed from the body. Another parallel mechanism for poor thermoregulatory problems may be decreased thyroid function. Another possible cause of systematic cellular temperature increase is the accumulation of Lipofuscin deposits in cells.

It is of interest that the Brain Stem and Hypothalamus have been identified by Neurologists such as Dr Peter Julu as being responsible for much of the dysautonomia observed in CFS patients and patients of related disorders. These parts of the brain are inflamed and irritated, and overstimulated. In contrast, the NLP practitioner Ashok Gupta, who treats CFS patients himself, has identified the Amagdala, in the Pre-Frontal Cortex, as being responsible for the problems of CFS. The Amagdala is the primitive part of the brain involved in interpretation of external conscious stimuli and dealing with the baser emotions, often associated with digust, fear and the fight or flight response. Ashok Gupta argues that this part of the brain is overstimulated and 'burnt out' and proposes a series of brain calming measures in order to calm the Amagdala and restore better quality sleep patterns and general relaxation. Please see the Stress Management and CFS page for more information.

A programme geared towards treating dysautonomia depends on the exact cause.

back to top

Short Term Strategies for Alleviating Chest Pains and Palpitations (Cardiac Arrhythmia):

back to top


Palpatations (Extrasystole or Cardiac Arrhythmia) can take the form of fluttering in the chest, skipped beats, heavy, thumping or pounding heart beats. It is not a fault with the heart per se, but a fault with the electrical signals or impulses going to the heart through the nervous system, from the brain stem. Whilst palpitations can be serious, in most cases they are relatively harmless. However their manifestation can cause considerable anxiety and stress in some patients, and can interrupt regular sleeping patterns etc. if experienced whilst lying down. Palpitations are therefore a pattern of irregular electrical signals to the heart. To alleviate the palpitations (in the short term) and return the beating pattern and electrical signalling from the brainstem to normal, a variety of methods can be employed.

Chest Pains:

Chest pains are somewhat different to palpatations and are usually indicative of a slightly different type of problem, more localised in the cardiac muscle, typically in the right atrium in Diastolic Cardiomyopathy. Sometimes they are indistinguishable from palpatations and may occur at the same time and share some similar causes. Often palpitations can lead to chest pains as the heart is beating harder and using up more energy, and may become strained in mitochondrial terms (hence the pain). The methods for alleviating chest pain are similar to those for alleviating palpitations, but with the emphasis more on supporting the heart muscle and mitochondrial function in general. These are listed below. These may also help with palpitations. Some examples that help both chest pains and palptations are listed above and marked with a '*'.

Articles about reducing hypertension (high blood pressure) naturally can be found below.


back to top

back to home