Articles of increased importance are highlighted in green *O*

*O* Chronic Fatigue Syndrome May Be An Infectious Cardiomyopathy Of Single Or Multiple Viral Etiology by Maryann Spurgin, Ph.D.

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 cardiomyopathy of single or multiple viral etiology -- 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, EBV or 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.

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 decreasing 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.

RESEARCH BREAKTHROUGH: ME/CFS AN INFECTIOUS CARDIOMYOPATHY? by: Philipa D. Corning, Ph.D., B.Sc. (Reviewed and approved by Dr. A. Martin Lerner)

In this study, 100% of the ME/CFS participants showed abnormal oscillating T-waves at 24 hr. holter monitoring and 24% showed weakened function on the left side of the heart (abnormal cardiac dynamics). This is the side of the heart that pumps oxygenated blood to all of the body, except the lungs. Data, gathered from biopsies and a 24-hour electrocardiogram (EKG) Holter monitor, showed that patients exhibited evidence of cardiomyopathy or disease of muscle in the heart.

These researchers tracked EKGs over a 24-hour period with a Holter monitor device and documented abnormal T-waves. This wave measures electrical recovery after contraction of the left ventricle. A normal T-wave should be shaped like the rolling crest of a wave in water. In 100% of ME/CFS patients, Lerner and his associates documented T-wave Inversions and/or T-wave flattenings. This finding is so consistent, they suggest that the Holter results should be included as part of the CDC case definition; it distinguishes ME/CFS patients from those with fatigue or unexplained origin. This research holds the potential to distinguish ME/CFS patients from FM patients, from those with other pain syndromes who do not relapse with exertion, and from those with fatigue associated with depression, which is a group that also does not suffer relapse with exertion. This work offers hard evidence to back up ME/CFS patients' much disbelieved claim that exercise is harmful and causes disease progression in ME/CFS.

In Dr. Lerner's model, the weakened heart is aggravated by physical activity, accounting for the post-exertional sickness and accounting for the post-exertional sickness so common in this disease - including flu symptoms, chills, fevers and increasing weakness. Indeed, the cardiac connection is what is so ground-breaking about this research.

In experiments with mice, Dr. Lerner has shown that raised myocardial coxsackie viral titers accompany physical exertion in the mice. When the heart muscle tissue is infected, overactivity causes death of cardiac tissue and disease progression. This is in direct conflict with the U.S. government research conclusions that ME/CFS disease symptoms are caused by underactivity due to a sedentary lifestyle. Dr. Lerner advises resting the heart in order to "do no harm" and to prevent death of cardiac tissue.

Dr. Lerner and associates also have documented abnormal ejection fractions in ME/CFS. Normally, over half of the blood in the left ventricle is ejected when the left ventricle contracts (part of the heart that pumps oxygenated blood out to the body). In Dr. Lerner's ME/CFS subjects, the ejection fraction is sometimes decreased, an indication that not all the normally-expelled blood leaves the ventricle. 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, the ejection fraction will rise over 5% during exercise. Stationary or falling ejection fraction is abnormal in coronary artery disease or cardiac muscle disease. Declining ejection fractions are not seen in normal persons leading sedentary lives.

These cardiac abnormalities are hypothesized to be virally induced.

This model explains the John Hopkins' finding of Rowe et al in which ME/CFS patients exhibited abnormal response to upright tilt. Lerner argues that it is abnormal cardiac response of cardiomyopathy instead of abnormal neural response. Indeed, Dr. Lerner's thesis explains a myriad of phenomenon that other research has not. For example, it explains why patients relapse with exertion and why only physically active young persons may acquire the disease. It also explains why stress is a major aggravator in this disorder. Stress may aggravate both herpes viruses and heart conditions. It also explains the anti-viral lymphocyte enzyme system, the 2-5 A pathway, suggesting the presence of a chronic infection.

In short, Dr. Lerner's work explains why previously healthy, vigorous young adults fall ill with chronic cardiomyopathy due to viral infection and cannot exercise for fear of causing further heart damage. This is directly opposite to the work of Dr. Stephen Straus at National Institute of Health (NIH) whose theory states that ME/CFS is a psychiatric disorder. This new research of Dr. Lerner et al is both refreshing and insightful. Needless to say, it has also been long awaited.

Prevalence of abnormal cardiac wall motion in the cardiomyopathy associated with incomplete multiplication of Epstein-barr Virus and/or cytomegalovirus in patients with chronic fatigue syndrome. Lerner AM, Dworkin HJ, Sayyed T, Chang CH, Fitzgerald JT, Beqaj S, Deeter RG, Goldstein J, Gottipolu P, O'Neill W.
Department of Medicine, William Beaumont Hospital, Royal Oak, Michigan, USA. lerner@cdimed.com

We reported unique incomplete herpesvirus (Epstein-Barr Virus (EBV) and/or nonstructural (HCMV) cytomegalovirus) multiplication in 2 distinct subsets of CFS patients. The CFS subsets were identified by: a) presence of IgM serum antibodies to HCMV nonstructural gene products p52 and CM2 (UL44 and UL57), and/or b) IgM serum antibodies to Epstein-Barr virus viral capsid antigen (EBV, VCA IgM). Diagnostic IgM serum antibodies were found in two independent blinded studies involving 49 CFS patients, but the same antibodies were absent in 170 control patients (p<0.05). Abnormal 24 Hr-electrocardiographic monitoring, tachycardias at rest and, in severe chronic cases, abnormal cardiac wall motion (ACWM) were seen in these same CFS patients. We now report a prospective consecutive case control study from 1987--1999 of cardiac dynamics as measured by radionuclide ventriculography in 98 CFS patients from 1987--1999. Controls were patients with various malignancies who were evaluated in protocols requiring radionuclide ventriculography before initiation of cardiotoxic chemotherapeutic agents. The prevalence of abnormal cardiac wall motion (ACWM) at rest in CFS patients was 10 out of 87 patients (11.5%). With stress exercise, 21 patients (24.1%) demonstrated ACWM. Cardiac biopsies in 3 of these CFS patients with ACWM showed a cardiomyopathy. Among the controls, ACWM at rest was present in 4 out of 191 patients (2%) (p=0.0018). A progressive cardiomyopathy caused by incomplete virus multiplication of EBV and/or HCMV in CFS patients is present.

*O* CFS severity is related to reduced stroke volume and diminished blood pressure responses to mental stress Arnold Peckerman, John J. LaManca, Sharon L. Smith, and Benjamin H. Natelson; NJ CFS Research Center, University of Medicine and Dentistry of New Jersey Objective:

One plausible hypothesis of the pathophysiology of chronic fatigue syndrome (CFS) is a disorder of circulation. The present study examined whether cardiovascular homeostasis at rest and centrally-mediated hemodynamic responses to behavioral challenges are altered in CFS. Methods: Twenty-one patients fulfilling CDC criteria for CFS (18 women and 3 men) and 25 matched sedentary controls were evaluated in supine, standing, and sitting postures (resting homeostasis), and during the cold pressor test and simulated public speaking (stress responsivity). The measured responses, in addition to blood pressure and heart rate, included impedance cardiography-derived stroke volume and cardiac output. Patients with CFS were rated for illness severity on a 6-point scale using the New Jersey CFS diagnostic system. Results: As a group, patients with CFS displayed a similar cardiovascular functional status on most of the parameters. However, an observation was made that in patients with CFS, a lower stroke volume was highly predictive (r = -.72, p < .001) of illness severity. When divided into severe (N = 11) and less-than-severe (N = 10) groups, the severe CFS patients were found to have a lower stroke volume and cardiac output (p < .05) relative to a more moderate CFS group across three different postures. In response to the speech task, the less severe CFS group displayed attenuated blood pressure responses relative to a healthy control group (p < .05). A reduced blood pressure response to speech stressor in less severe CFS patients was attributable to a smaller increase in total peripheral resistance. In contrast, cardiovascular responses to the cold pressor test were not significantly different Conclusion: These findings suggest the possibility of a low flow circulatory state in the most severe cases of CFS. In patients with a less severe form of CFS, a diminished blood pressure response to a cognitive-behavioral (speech presentation), but not to an aversive-sensory (the cold pressor test) stressor may indicate a defect in the higher cortical modulation of cardiovascular autonomic control. In this latter group, situations may arise where a demand for blood flow to the brain may exceed the supply with a possibility of ischemia and a decrement of function.

[Note that the 'severe' patients in this study are in reality only mildly or moderately ill]

Response to Exercise	Healthy People	ME/CFS Patients
Sense of well-being	Invigorating, anti-depressant effect	Malaise, fatigue, worsening of symptoms.
Resting heart rate	Normal	Elevated
Heart rate at maximum workload	Elevated	Reduced heart rate
Maximum oxygen uptake	Elevated	Approximately ½ of sedentary controls
Age-predicted target heart rate	Can achieve it	Can NOT achieve it
Heart functioning	Increased	Sub-optimal
Cerebral blood flow	Increased	Decreased
Body temperature	Increased	Decreased
Respiration	Increased	Decreased
Cognitive processing	Normal, more alert	Impaired
Oxygen delivery to the muscles	Increased	Reduced
Gait Kinematics	Normal	Abnormalities
Recovery period	Short	Days or weeks

*O* ME/CFS Post-Exertional Malaise / Fatigue and Exercise by Marjorie van de Sande B.Ed, Grad. Dip. Ed.

An excerpt:

Even though post-exertional malaise is a hallmark feature of ME/CFS, exercise programs are often prescribed with little thought to the effect they may have on patients. The panel of experts for the ME/CFS clinical consensus document(1) stressed that a thorough evaluation of patients and their total illness burden, optimizing medical management, and a careful evaluation of pain generators and risk factors must be done before even considering an exercise program. As much care must be taken in prescribing appropriate exercise for ME/CFS patients as in prescribing pharmaceuticals.(5)

[Note that recovery may be incomplete in some patients even after 'days or weeks' as this chart states. Symptom execerbation or progression may in fact persist for many months or years following exertion, or may be irreversible. The use of the umbrella term 'ME/CFS' is also regrettable.]

The symptoms of Chronic Fatigue Syndrome are related to abnormal ion channel function Peter O. Behan*, Abhijit Chaudhuri*, Walter S. Watson**, John Pearn***
*University Department of Neurology, Institute of Neurological Sciences and **Department of Nuclear Medicine, Southern General Hospital, Glasgow (UK), ***Department of Child Health, University of Queensland, Brisbane (Australia).Presented at the American Association for Chronic Fatigue Syndrome Research Conference
October 10-11, 1998 -- Cambridge, Massachusetts

Objective: Many symptoms of chronic fatigue syndrome (CFS), including severity of fatigue, are periodic, fluctuant and are inducible by physical and mental activities. Chest pain is a common symptom of CFS, like patients with syndrome X, an ion channel disorder. Symptoms in CFS such as fatigue, myalgia and headache bear striking resemblance with neurological disorders that affect ion channel function, such as periodic paralysis and familial hemiplegic migraine. Maintenance of normal transmembrane ionic equilibrium is an active, energy-dependent process, and constitutes an important share of the resting energy expenditure (REE). We wanted to compare and contrast the clinical profile of CFS patients with other neurological disorders that are known to affect ion channel function, and estimate REE in CFS. We also studied the myocardial perfusion in CFS by thallium²⁰¹ SPECT scans to compare the results with Syndrome X. Methods: All patients who fulfilled the modified CDC criteria for CFS were included in our studies. For investigations that required the administration of radiopharmaceuticals (e.g. cardiac-thallium²⁰¹ SPECT scans), patients between the age of 18 - 65 years were recruited after informed consent. A comparable group of healthy, sedentary volunteers were tested as controls in the REE study. Results: Fatigue was fluctuant in most patients with CFS. This was induced or worsened by physical activities (exercise), mental stress and chemicals that affect ion channel function (e.g. alcohol, quinine and anaesthetics). Significant perfusion defects were observed in the cardiac-thallium²⁰¹ SPECT scans in 70% of CFS patients, similar to that described in patients with syndrome X. In a separate study, a significant number of CFS patients were found to have elevated REE as compared to the controls using total body potassium (TBK) as the refererence (REE _TBK).4 Conclusion: Abnormal thallium²⁰¹-cardiac SPECT scans in CFS similar to those described in syndrome X suggest a common mechanism for both these conditions. An abnormality of membrane ion channel function is considered the underlying mechanism in syndrome X. Increased REE_TBK; in a subgroup of CFS patients suggests that some CFS patients spend more energy in maintaining essential body function at the expense of the energy available for other physical activities. Since 30% of REE is expended to maintain physiological ion gradients in normal health, cell membranes that leak ions increase REE_TBK Elevated REE and abnormal cardiac perfusion scans in CFS provide the first objective and indirect support to our hypothesis that symptoms in CFS could be the result of an acquired abnormality of the voltage or ligand-gated ion channels. It is possible that such alteration of transmembrane ion traffic could affect normal receptor sensitivity to neurochemicals and neurohormones such as acetylcholine, serotonin or other monoamines, accounting for the neuroendocrine abnormalities previously documented in CFS.

*O* Information on the study "Left Ventricular Function in Chronic Fatigue Syndrome (CFS): Data From Nuclear Ventriculography Studies of Response to Exercise and Postural Stress," by Arnold Peckerman, Benjamin Natelson et al.

The two groups had similar resting ejection fraction (EF). During maximal exercise, EF increased in controls, but declined in CFS patients. The decreases in EF tended to be greater in patients with more severe symptoms. Using a decline in EF as a criterion, 13 CFS patients (81 percent) and 0 control subjects had positive tests. There were no group differences in levels of exertion, as indicated by similar cumulative work output, maximal heart rate, and increases in lactate levels. A similar patter of changes in EF (i.e., increases in controls and declines in CFS patients) was observed in response to postural stress. Conclusions This study provides a preliminary indication of reduced cardiac function in some patients with CFS. It raises the possibility that some CFS patients may have cardiac disorders that are subtle enough to escape the current net of clinical cardiological diagnoses, but may be significant enough in some patients -- perhaps in conjunction with other factors -- to lead to the clinical syndrome of CFS. The researchers note that their findings may also be explained by abnormalities other than those with the heart, including problems with the distribution of cardiac output, reduced blood volume, and neurogenic and endocrinologic abnormalities. Accordingly, further studies capable of defining more precisely the causes of altered cardiac stress responses are required.

Editorial Response: Microbial Persistence and Idiopathic Dilated Cardiomyopathy." Clinical Infectious Diseases (1999):29:526-7 PDF Format]

*O* Dr Paul Cheney on heart issues and ME/ICD-CFS 

"Now, do CFIDS patients prefer to stand up or lie down? Of course, they prefer to lie down. Do you know why? "Do you know what your cardiac output does when you stand up? It drops 30%. In all humans, without exception. So very critical to this technology is that it's the only one that could be done upright [again, four positions on the tilt table are best; standing up and laying down at a minimum]. And what they found is absolutely astonishing, truly astonishing. When [disabled CFIDS patients] stand up, [they're] on the edge of organ failure due to low cardiac output."

The Peckerman article Dr. Cheney refers to is available free online.

"Peckerman's research team at the VA Medical Center in East Orange, N.J., used a sophisticated test to measure how well the heart pumps blood. They gave the test to 16 chronic fatigue syndrome patients, both before and after they exercised. They also tested four non-athletic volunteers. All of the patients' and volunteers' hearts' pumped normally during rest. After exercise, however, 13 of the 16 chronic fatigue [syndrome] patients' hearts pumped less blood than they did at rest.

"Basically we are talking about heart failure," Peckerman tells WebMD. "But chronic fatigue syndrome is a progressive disease. If we were able to detect this in its early stages, it is quite possible there might be a way to treat it."

Peggy Munson’s book ‘Stricken: Voices from the Hidden Epidemic of CFIDS’ is available from this site which also features Peggy’s Awareness day letters from

2003. Dr. Paul Cheney explained how the bodies of CFIDS patients are choosing between lower energy and life, or higher energy and death. On a physiological level, CFIDS patients live in a near-death suspension, making patients feel much like they are dying, not tired.

Dr. David Bell has studied the near-death feeling as it relates to blood volume. "[T]he vast majority of Bell’s CFIDS patients had 'extraordinarily' low circulating blood volume (a combination of plasma and the red blood cells via which the plasma delivers oxygen throughout the body)," writes About.com columnist Joan Livingston. "While his average patients ran about 70 percent of normal, several patients with Chronic Fatigue Syndrome (PWCs) had only half the blood volume of a healthy person, an amount so low that it would ordinarily cause shock and prove fatal in a car accident."

*O* Circulating Blood Volume in Chronic Fatigue Syndrome David H. P. Streeten, MB, DPhil, FRCP, FACP David S. Be11, MD, FAAP

ABSTRACT. Chronic fatigue syndrome (CFS) is an illness associated with severe activity limitation and a characteristic pattern of symptoms despite a relatively normal physical examination and routine laboratory evaluation. The recent description of delayed orthostatic hypotension in patients with CFS, and previous findings of reduced red blood cell (RBC) mass in other patients with orthostatic hypotension not known to have CFS, led us to measure RBC mass and plasma volume in 19 individuals (15 female, four male) with well characterized, severe CFS. RBC mass was found to be significantly reduced (p < 0.001) below the published normal range in the 16 women, being subnormal in 15 (93.8%) of them as well as in two of the four men. Plasma volume was subnormal in 10 (52.6%) patients and total blood volume was below normal in 12 (63.2%). The high prevalence and frequent severity of the low RBC mass suggest that this abnormality might contribute to the symptoms of CFS by reducing the oxygen-carrying power of the blood reaching the brain in many of these patients.

Conclusion: Of the 19 patients reported here, abnormalities in blood volume were very common. The most common, found in 16 of 19 patients, was a reduction in red blood cell mass. Eleven subjects had low plasma volumes, and total circulating blood volume was subnormal in 12 of 19 subjects. In some individuals this abnormality was strikingly severe. Patient #15, for example, had an RBC mass of 12.9 mL/Kg, which is 46% of the expected normal, and a total blood volume of 35.8 mL/Kg, which represents 49.7% of the expected normal value (21). Her peripheral hematocrit was not impressively low at 33.8%, presumably because of the symmetrical reduction in both RBC mass and plasma volume. In other patients the plasma volume was normal or even elevated in the face of a low RBC mass, and in nqne of these patients was the RBC mass abnormality detected by conventional interpretation of the peripheral hematocrit.

All of the subjects in this study had symptoms of orthostatic intolerance which probably contributed to their activity restriction, but tilt table and autonomic nervous system testing was not carried out systematically in these individuals. Normal sitting blood pressures were recorded in all patients under office visit circumstances, except for relatively low values in three and a mildly elevated blood pressure in one. Some of these patients have been tested subsequently and found to have delayed orthostatic hypotension (12), which may be characteristic for CFS (11,12). In general, blood pressure measurements were not predictive of the results of circulating blood volume measurements.

Cardiac function at rest and with exercise in the chronic fatigue syndrome. Montague TJ, Marrie TJ, Klassen GA. Chest 1989; 95: 779-84.

Abstract: To evaluate a possible cardiac pathophysiology of the chronic fatigue syndrome, we compared the resting cardiac function and exercise performance of 41 patients to those of an age-matched and sex-matched normal control group. Persistent fatigue following an acute apparently viral illness was the major complaint of all patients; none had specific cardiac symptoms nor abnormal physical findings. Electrocardiographic spatial patterns were normal in the patients, and there were no differences in the body surface sum of positive T-wave integrals between the patients (240 microV.x 10(2) ± 107 microV.s x10(2)) and control (244 microV.x 10(2) ± 108 microV.s x 10(2) subjects. Twenty-four hour ambulatory ECGs revealed no differences in sinus rates and incidences of ventricular dysrhythmias in the two populations. Left ventricular dimensions and systolic fractional shortening values were also similar in both groups; moreover none of the patients had segmental wall motion abnormalities. On graded exercise testing, 20 of 32 normal subjects achieved target (85 percent of age-maximum) heart rates, compared to four of 31 patients (p less than 0.001). The duration of exercise averaged 12 ± 4 minutes for the normal subjects and 9± 4 minutes for the patients (p less than 0.01). The temporal profile of exercise heart rates was dissimilar in the two groups, with patients' rates consistently and progressively less than those of normal subjects. Peak heart rate averaged 152 ± 16 beats per minute for the normal group vs 124 ± 19 beats per minute for the patients (p less than 0.0001); in age-related terms, respectively, 82 ± 6 percent of the maximum heart rate vs 66 ± 10 percent (p less than 0.0001). Thus, patients with chronic fatigue syndrome have normal resting cardiac function but a markedly abbreviated exercise capacity characterized by slow acceleration of heart rate and fatigue of exercising muscles long before peak heart rate is achieved.

Exercise Capacity in Chronic Fatigue Syndrome.

RESULTS: The resting heart rate of the patient group was higher, but the maximal heart rate at exhaustion was lower, relative to the control subjects. The maximal workload and maximal oxygen uptake attained by the patients with CFS were almost half those achieved by the control subjects. Analyzing only those persons who performed a maximal exercise test, similar findings were observed.

CONCLUSIONS: When compared with healthy sedentary women, female patients with CFS show a significantly decreased exercise capacity. This could affect their physical abilities to a moderate or severe extent. Reaching the age-predicted target heart rate seemed to be a limiting factor of the patients with CFS in achieving maximal effort, which could be due to autonomic disturbances.

Physiological responses to incremental exercise in patients with chronic fatigue syndrome. Inbar O, Dlin R, Rotstein A, Whipp BJ.  Med Sci Sports Exerc 2001 Sep;33(9):1463-1470 Department of Life Sciences, Zinman College, Wingate Institute, ISRAEL; Links Clinic, Edmonton, CANADA; and Department of Physiology, St. George's Hospital Medical School, London, UNITED KINGDOM.

PURPOSE: The purpose of this investigation was to characterize the physiological response profiles of patients with chronic fatigue syndrome (CFS), to an incremental exercise test, performed to the limit of tolerance.

METHODS: Fifteen patients (12 women and three men) who fulfilled the case definition for chronic fatigue syndrome, and 15 healthy, sedentary, age- and sex-matched controls, performed an incremental progressive all-out treadmill test (cardiopulmonary exercise test).

RESULTS: As a group, the CFS patients demonstrated significantly lower cardiovascular as well as ventilatory values at peak exercise, compared with the control group. At similar relative submaximal exercise levels (% peak VO2), the CFS patients portrayed response patterns (trending phenomenon) characterized, in most parameters, by similar intercepts, but either lower (VCO2, HR, O2pulse, VE, VT, PETCO2) or higher (Bf, VE/VCO2) trending kinetics in the CFS compared with the control group. It was found that the primary exercise-related physiological difference between the CFS and the control group was their significantly lower heart rate at any equal relative and at maximal work level. Assuming maximal effort by all (indicated by RER, PETCO2, and subjective exhaustion), these results could indicate either cardiac or peripheral insufficiency embedded in the pathology of CFS patients.

CONCLUSION: We conclude that indexes from cardiopulmonary exercise testing may be used as objective discriminatory indicators for evaluation of patients complaining of chronic fatigue syndrome.

*O* Tricky Heart May Cause ME/CFS

Abnormal Heart Pumping After Exercise Linked to Chronic Fatigue Syndrome

Peckerman's research team at the VA Medical Center in East Orange, N.J., used a sophisticated test to measure how well the heart pumps blood. They gave the test to 16 chronic fatigue syndrome patients, both before and after they exercised. They also tested four non-athletic volunteers. All of the patients' and volunteers' hearts' pumped normally during rest. After exercise, however, 13 of the 16 chronic fatigue patients' hearts pumped less blood than they did at rest.

"Basically we are talking about heart failure," Peckerman tells WebMD. "But chronic fatigue syndrome is a progressive disease. If we were able to detect this in its early stages, it is quite possible there might be a way to treat it."

Emory University cardiologist Joseph I. Miller III, MD, says Peckerman's findings on a potential cause of chronic fatigue syndrome are very interesting. He agrees that these patients have serious heart problems. "Typically we see this in people with three-vessel heart disease," Miller tells WebMD. "A drop in [blood pumped by the heart] during exercise is not a typical response. It is actually a marker of significant coronary artery obstruction."

What's happening to the hearts of people with chronic fatigue syndrome? It's too soon to tell, but Peckerman has a theory. "There is some indication that chronic fatigue syndrome is precipitated by a viral infection," he says. "Some of the viruses that have been suspected have an affinity for the heart."

Page 2: Cardiac and Cardiovascular Research (continued)

Page 3: Cardiac and Cardiovascular Research (continued) and Relevant Books