Contact: Donna Krupa
Phone 703.527.7357
Cell: 703.967.2751
djkrupa1@aol.com
April 9, 2003 (San Diego) – Chronic fatigue syndrome (CFS) is
a baffling disorder. Some 20 years ago, it was dubbed “the yuppie flu,” because
the complaints of a similar constellation of problems were reported primarily
by women in their 30s and 40s who were well educated and in upper-income
brackets. Since the 1980s, CFS has become better understood, which is good news
for the estimated 500,000 Americans of all ages, genders, ethnic origins, and
earning capacities who are believed to suffer from a CFS-like condition. Even
today, however, the causes of this illness remain a mystery.
Background
CFS is today a clinically defined
illness of still unknown origin. The minimum criteria for a CFS diagnosis are
unremitting, disabling fatigue, accompanied by several other
neuropsychological, rheumatological, and influenza-like symptoms. Patients
frequently report an infection as an antecedent event. Unfortunately, efforts
to find infectious or immunological causes have not been successful.
Growing evidence, however, points to
a possible problem with circulation. Previously reported findings include
autonomic dysfunction, lower plasma volume and/or red call mass, as well as
abnormalities in neurohormonal systems of circulatory control. Other studies
have found that CFS patients may have reduced blood flow in exercising muscles.
A New Study
The main symptom of the CFS
patient (i.e., chronic fatigue that is greatly exacerbated by even minor
effort) is similar to that of a patient with left ventricular dysfunction. A
team of researchers thus hypothesized that some patients with left ventricular
dysfunction who do not show overt signs of cardiac insufficiency may
nevertheless develop persistent, disabling fatigue and become diagnosed with
CFS. To explore this possibility, they conducted special tests on CFS patients
and healthy controls.
The authors of a new study,
“Left Ventricular Function in Chronic Fatigue Syndrome (CFS): Data From Nuclear
Ventriculography Studies of Response to Exercise and Postural Stress,” are
Arnold Peckerman, Rahul Chemitiganti, Caixia Zhao, Kristina Dahl, Benjamin H.
Natelson, Lionel Zuckier, Nasrin Ghesani, Samuel Wang, Karen Quigley and S.
Sultan Ahmed. All are affiliated with the Departments of Neurosciences and
Radiology, University of Medicine and Dentistry of New Jersey, Newark,
NJ, as well as with the War-Related Illnesses and Injuries Study Center, VA
Medical Center, East Orange, NJ. They will present their findings at the
American Physiological Society conference, Experimental Biology 2003, being
held April 11-15, 2003, at the San Diego Convention Center, San Diego, CA.
Methodology
Sixteen patients meeting case
definition for CFS established by the Centers for Disease Control and
Prevention (CDC) and 4 control subjects participated in the study. The control
subjects were sedentary individuals, gender and age-matched to the CFS group.
The researchers used the radioisotopic multiple gated acquisition (MUGA) blood
pool method of ventriculography to perform a series of dynamic studies of the
heart to assess for evidence of abnormalities with myocardial function.
MUGA ventriculography uses a
radionuclide tracer to label red blood cells, allowing visualization of cardiac
blood pools with a gamma camera. The emission counts are processed to estimate
volumes of blood in the left ventricle (the heart’s main chamber) at the end of
relaxation and at the end of contraction periods. Their ratio (called the
ejection fraction, or EF) is a measure of myocardial contractility, and is
considered to be the best non-invasive indicator of left ventricular function.
Protocol: MUGA studies were performed under 2
experimental conditions: (1) maximal exercise; (2) an active postural change.
Maximal exercise ventriculography is commonly used for evaluation of possible
heart disease. Postural testing was done in addition to exercise because many
CFS patients report worsening of symptoms during standing.
Exercise: Testing was performed lying down on a
cycle ergometer table. The initial workload was set at 200 kilopond meters
(kpm)/min (40 watts), and was increased by 200 kpm/min every 3 min until the
subject was no longer able to maintain the pedal speed due to fatigue, muscle
pain, or shortness of breath. Blood pressure, heart rate, and ratings of
perceived exertion were obtained at each stage. Failure to increase EF during
maximal exercise stage indicates possible abnormalities with left ventricular
function.
Postural Change: Measurements of cardiac functioning were
taken in the supine and standing positions. EF is expected to increase in the
standing position to counteract the effects of gravity on reduced blood flow to
the heart.
Results
Researchers observed the
following:
·
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.
-end-