In some patients with chronic fatigue syndrome, left ventricular function may be involved

April 09, 2003

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:

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-
The American Physiological Society (APS) is one of the world's most prestigious organizations for physiological scientists. These researchers specialize in understanding the processes and functions underlying human health and disease. Founded in 1887 the Bethesda, MD-based Society has more than 10,000 members and publishes 3,800 articles in its 14 peer-reviewed journals each year.

Contact: Donna Krupa @ 703-527-7357 (vm) Or 703-967-2751 (cell) or djkrupa1@aol.com Through April 10th, 2003.

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