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CFS may be an infectious cardiomyopothy of single or multiple viral etiology.
A fascinating presentation by A. Martin Lerner, M.D., at the University of Newcastle's CFS/Myalgic Encephalomyelitis Research conference 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 cardiomyopothy, a disease of the heart. Lerner stated that a recent, seperate study had replicated his results.
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.
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-disease specialist at Wayne State University, along with his colleagues in cardiology. The basic thesis of their well-documented research is that CFS is an infectious cardiomyopothy of single or multiple aitiology -- a cardiomyopothy 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. 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. Conversly, patients with prolonged illnesses of EBV mononucleosis consistently have abnormal 24-hour Holter monito 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 cardiomyopothy. Lerner's work cites studies showing that EBV and CMV are especially cardiotropic for 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 miochondria in cardiac tissue, findings indicitive of a cardiomyopothy. 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 monitor results should be included as part of the CDC case definition because it can distinguish CFS patients from those with fatigue of unexplained origin. This research holds the potential 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 up 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 the disease -- including flu symptoms, chills, fevers, weakness. Indeed, the cardiac connection is what is so ground breaking about this research.
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