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
In Vivo. 2004 Jul-Aug;18(4):417-24.
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. firstname.lastname@example.org
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
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.