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This page is currently under construction. I did want to present to you this current important research at this time.

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CFS may be an infectious cardiomyopathy of single or multiple viral etiology!

A fascinating presentation by A. Martin Lerner, M.D., at the University of Newcastle's Chronic Fatigue Syndrome/Myalgic Encephalomyelitis ResearchConference in Sydney, Australia, has offered some hard data that continues to shatter the myth that Chronic Fatigue Syndrome is a form of depression,hysterical conversion, or deconditioning caused by patients' refusal to exercise.

Dr. Lerner and his colleagues at Wayne State University and the University of Michigan have found evidence that the disease may be caused by a persistent herpesvirus infection of the heart.

Lerner's study participants showed signs of weakened function on the left side of the heart. Biopsy data and 24-hour EKG Holter monitor results showed that patients exhibited evidence of cardiomyopathy, a disease of the heart.

Lerner stated that a recent, separate study had replicated his results. The following is a brief summary of Dr. Lerner's work by Maryann Spurgin,Ph.D., of Medical Professionals with CF(ID)S explaining Lerner's work in greater detail.

A. Martin Lerner can be reached for comment at his office at William Beaumont Hospital, 32804 Pierce Road, Beverly Hills, MI 48025; PHONE: (248) 540-9866; FAX: (248) 540-0139.

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CHRONIC FATIGUE SYNDROME : RESEARCH BREAKTHROUGH

CFS may be an infectious cardiomyopathy of single or multiple viral etiology by Maryann Spurgin, Ph.D.(318) 861- 4591

The most acutely perceptive and pioneering work on CFS these days is happening in a quiet corner of the country, out of the CFS limelight. The work is being conducted by A. Martin Lerner, M.D., an infectious-diseasespecialist at Wayne State University, along with his colleagues in cardiology. The basic thesis of their well-documented research is that CFS is an infectious cardiomyopathy of single or multiple viral aitiology -- a cardiomyopathy that in many cases is progressive and degenerative.

According to the theory, CFS results when an initial infection with a virus, or a reactivation of a latent virus -- for example, Epstein Barr Virus (EBV) or Cytomegalovirus (CMV) -- attacks cardiac tissue, producing exercise intolerance, the hallmark of CFS.

T The human cardiac myofiber becomes the site of persistent viral infection. The infection flares up when the infected person physically exerts him or herself.

This theory is especially noteworthy because it explains what has baffled researchers for years: why some EBV-infected are healthy while other EBV-infected are ill. In those EBV-infected who develop CFS,cardiac tissue is affected, while in those EBV-infected who do not develop CFS (they either recover from an acute infection or have latent subclinical infection), the heart was never involved (this holds for CMV as well).

According to this hypothesis, then, EBV or CMV seropositive non-CFS patients will not show EBV or CMV nucleic acids in cardiac myofibers, whereas these viral nucleic acids are theorized to be present in the cardiac myofibers of CFS patients.

Lerner and his associates have observed that patients with acute EBV mononucleosis who recover have normal 24-hour electrocardiogram Holter monitoring throughout their illness. Conversely, patients with prolonged illnesses of EBV mononucleosis consistently have abnormal 24-hour Holter monitor results. Lerner's work also accounts for why no single viral aitiology has been found for CFS, since a number of different viruses,among them coxsackie virus, can cause a cardiomyopathy.

Lerner's work cites studies showing that EBV and CMV are especially cardiotropic for the human myocyte. These researchers have backed up their theories with an impressive amount of data. Having performed biopsies on the cardiac tissue of CFS patients, they have documented myocardial fiber hypertrophy, myofiber disarray, interstitial fibrosis, fat infiltration, and increases in mitochondria in cardiac tissue, findings indicative of a cardiomyopathy.

They have also documented T-wave inversions and/or T-wave flattenings on 24-hour EKG Holter monitoring in 100% of CFS patients. Because of this consistent finding, they suggest that the Holter results should be included as part of the CDC case definition because it can distinguishCFS patients from those with fatigue of unexplained origin.

This research holds the potential to distinguish CFS patients from fibromyalgia patients and from those with other pain syndromes who do not relapse with exertion, as well as those with fatigue associated with depression, a group that also does not suffer relapse with exertion.

The work offers hard evidence to back CFS patients much-disbelieved claim that exercise is harmful and causes disease progression in CFS. On Lerner's model, a virus infecting the CFS patient's heart becomes more active following the patient's physical exertion, thus causing disease progression and accounting for the post-exertional sickness so common in this disease -- including flu symptoms, chills, fevers, weakness.

Indeed, the cardiac connection is what is so ground breaking about this research. With a mouse model, Lerner has shown that raised myocardial viral titers accompany physical exertion in the host. He shows that when an infectious cardiomyopathy is present, overactivity causes necrosis of cardiac tissue and disease progression. Government researchers, in contrast, routinely state that CFS is a disease of underactivity and that a couch-potato lifestyle is the cause of symptoms.

While government researchers advocate exercise, Lerner advises resting the heart in order to "do no harm" and to prevent necrosis of cardiac tissue.

Lerner and colleagues have also documented abnormal ejection fractions in CFS, another finding which backs up CFS patients' claim that disease progression occurs with exercise. An ejection fraction is the fraction of blood within the left ventricle that is ejected with the contraction -- when it goes down, the blood is not dispelling. Some patients had reduced ejection fractions at rest while others had an ejection fraction that decreased during exercise from 51% to 36 %. In a normal subject, an ejection fraction will rise during exercise. They note that a stationary or falling ejection fraction is abnormal.

Their work cites studies showing that declining ejection fractions are not seen in normal persons leading a sedentary life. Deconditioning and a sedentary lifestyle in normal subjects are not causes of decreased or falling left ventricular ejection fractions. On the contrary, these cardiac abnormalities are likely virally induced: in some of the CMV patients, ejection fractions reverted to normal after anti-viral therapy with ganciclovir.

Interestingly, these researchers offer an alternative theoretical framework to the important Johns Hopkins finding of Rowe et al. that CFS patients have an abnormal response to upright tilt. Lerner and colleagues deny that the basis of this abnormal response is an abnormal neural reflex(as Rowe argued), arguing instead that the abnormal cardiac response is induced by the cardiomyopathy itself.

When a theory comes along that explains more of the data than others have, I think the research community needs to take a serious look at that theory -- the thesis of Lerner and colleagues explains a myriad of phenomena that others, and other theories, have simply failed to explain.

For example, if CFS is indeed an infectious cardiomyopathy in which raised myocardial viral titers follow physical exertion, then we can understand more fully not only why patients relapse with exertion, but also why only physically active persons acquire the disease to begin with (and why bedridden patients in one hospital outbreak completely escaped contracting >>the disease). The thesis also explains why stress is a major aggravant in the disorder: Stress activates herpes viruses, and stress aggravates heart conditions.

If CFS is an EBV or CMV herpes infection of the heart, then obviously stress will be doubly harmful in the condition. As I mentioned above, the thesis also explains why some EBV or CMV seropositive individuals are healthy while others are sick. The infectious cardiomyopathy theory is also consistent with Robert Suhadolnik's recent finding that CFS entails an abnormality in an antiviral lymphocyte enzyme system, the 2-5A pathway, which suggests the presence of chronic viral infection.

Lerner's work stands in opposition to much of the writings on CFS by government researchers, especially to that of Stephen Straus of the National Institutes of Health (NIH).

Straus's work seeks to refute viral aitiology, whereas Lerner's work argues in favor of it. Straus's work argues for pre-morbid psychiatric disorder, whereas Lerner's published work argues that CFS strikes "previously healthy, vigorous young adults." In fact, Straus and colleagues argue that CFS itself is a psychiatrically mediated behavioral problem of patients who refuse to exercise -- that exercise avoidance in CFS is mediated by psychiatric disease. Lerner, in contrast, argues that exercise avoidance is mediated by a cardiomyopathy.

Straus proposes exercise as the treatment of choice (on analogy with depression). But Lerner's work demonstratesthat exercise causes myocardial viral titers to increase and left ventricular ejection fractions to decrease, and suggests resting the heart in order to "do no harm," the very opposite of what is recommended by government researchers.

The infectious cardiomyopathy thesis is a truly insightful thesis. From looking at his data, it would appear that Lerner's work has come closer to understanding this disorder than anything published to date.

BIBLIOGRAPHY Lerner, A Martin. Viral Myocarditis as an Incidental Discovery. Hospital Practice, October 15, 1990; pp. 81-90.

Lerner, A. Martin, Goldstein, J., Chang, C., et. al. Cardiac involvement in patients with chronic fatigue syndrome as documented with holter and biopsy data in Birmingham, Michigan, 1991-1993. Infectious Diseases in CLinical Practice, 1997; 6:327-333.

Lerner, A. Martin, Zervos, M., Dworkin, HJ. New cardiomyopathy: pilot study of intravenous ganciclovir in a subset of the chronic fatigue syndrome. Infectious Diseases in Clinical Practice, 1997; 6:110-117.

Lerner, A. Martin., Zervos, M., Dworkin, HJ. A unified theory of the cause of chronic fatigue syndrome. Infectious Diseases in Clinical Practice, 1997; 6:239-243.

Lerner, A. Martin, et. al. Repetatively negative changing t-waves at 24-h electrocardiographic moniters in patients with the chronic fatigue syndrome: left ventricular dysfunction in a cohort. Chest, 1993; 104:1417-1421.

Dworkin, Howard J., Lerner, A. Martin, et. al. Abnormal left ventricular myocardial dynamics in eleven patients with chronic fatigue syndrome. Clinical Nuclear Medicine, 1994; 19(8):675-677.

Suhadolnik, Robert J., Peterson, DL., O'Brien, K., et. al. Biochemical evidence for a novel low molecular weight 2-5A- dependent RNase L in chronic fatigue yndrome. Journal of Interferon and Cytokine Research, 1997; 17:377-385.

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Maryann Spurgin, Ph.D., formerly taught philosophy. She reviewed Hillary Johnson's "Osler's Web" for "The Nation." She recently wrote an article exposing logical flaws in Mark Demitrack's book, which can be accessed on the Web at http://pw1.netcom.com/~schweit2/Spurgin.html. Dr. Spurgin has also published on L.O. Simpson's research on red blood cell morphology.

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