Cytomegalovirus

Cytomegalovirus (CMV) has long been known to be dangerous to the immunocompromised patient, to pregnant women, and to premature infants, but not, we thought, to cardiac surgical patients.

In 1960, Kreel et al described a febrile illness occurring after heart surgery that resembled infec­tious mononucleosis. This post-perfusion syndrome was subsequently shown to be caused by CMV transmitted in or reactivated by blood transfusions. This mild disease may cause diagnostic confusion after heart operations, but its self-limited nature has given it a clinical significance only slightly worse than the common cold. Now, with the report in this issue, (see page 18) Domart and colleagues have raised the specter that CMV infection after heart operations may be far more sinister.

They describe a series of 115 patients referred to them at the Hopital Bichat with bacterial mediastinitis after heart operations. Twenty five percent of these patients had CMV cultured from urine, blood or both. The presence of this virus (VE + ) correlated with increased morbidity from the infection, longer hospi­talization, increased failure rate of the primary treat­ment (systemic antibiotics plus mediastinal and sternal debridement with closure over drainage tubes), and a higher late mortality (after 15 days of hospitalization)— 55 percent in those shedding the virus (VE 4-) com­pared with 25 percent in those not shedding the virus (VE-).
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The authors did not demonstrate a correlation between those who were VE + and those with elevated IgG antibodies to CMV. However, their methodology could not have detected any correlation: viral cultures were obtained after the mediastinitis was manifest and at about the same time as the CMV antibody levels were drawn. The rise in CMV antibody after new infection or reactivation of the virus does not occur until about two to five months later. Only if the CMV antibody titers had been drawn serially over a longer period following the original operation could any meaningful correlation be made between virus shed­ding and antibody rise.