To the Editor:
Recently, Ommen et al1 published in Circulation a very important observation: that relative lymphocyte concentration could be a prognostic marker in patients with symptomatic heart failure. I would like to add something about the importance of the cellular immune system in cardiovascular disease. I have shown that in acute myocardial infarction (AMI), a low CD4/CD8 ratio and low CD4 cell count on the first day of AMI strongly correlated with low ejection fraction and high myocardial mass destruction, as reflected by high creatine kinase levels.2 Patients with the lowest CD4 counts on admission and those whose CD4 counts did not rise had a reinfarction or death.2 Another study3 demonstrated that patients with AMI had significantly diminished delayed-type hypersensitivity and reduced numbers of T lymphocytes.
One possible explanation for the “lymphopenia” phenomenon is the increase in cortisol during a stress response, which causes a decrease in the relative concentration of lymphocytes.1 Another possible explanation is that T lymphocytes modulate smooth muscle proliferation during vascular repair. Rats that lacked T lymphocytes had larger myocardial lesions than normal rats.4 It is assumed that T lymphocytes produce interferon-γ, which inhibits smooth muscle cell proliferation.5 Thus, it might be that the relative depletion in T lymphocytes is not just a marker but also a causative factor in the deterioration of myocardial function in AMI and heart failure.
- Copyright © 1998 by American Heart Association
Ommen SR, Hodge DO, Rodeheffer RJ, McGregor CGA, Thomson SP, Gibbons RJ. Predictive power of the relative lymphocyte concentration in patients with advanced heart failure. Circulation. 1998;97:19–22.
Hansson GK, Holm J, Holm S, Fotev Z, Hedrich HJ, Fingerle J. T-lymphocytes inhibit the vascular response to injury. Proc Natl Acad Sci USA. 1991;88:10530–10534.
Hansson GK, Holm J. Interferon-γ inhibits arterial stenosis after injury. Circulation. 1991;84:1266–1272.
We appreciate Dr Blum’s interest in our article. He raises the intriguing hypothesis that the relative lymphocytopenia observed in acute myocardial infarction (AMI) and in chronic congestive heart failure (CHF) may be a cause rather than an effect.
We have documented decreases in the total and relative number of circulating lymphocytes during AMIR1 and advanced CHF.R2 However, the kinetics of these changes may be different. In AMI, most patients have a rise in endogenous cortisol with associated lymphocytopenia and granulocytosis.R3 R4 In our experience, these changes in the peripheral blood rapidly returned to normal if the patient had an uncomplicated AMI (unpublished observations). In contrast, only a minority of patients with CHF have lymphocytopenia. We do not have any information about its duration.
Additional studies are necessary to determine if the relative lymphocytopenia is an effect of the stress response, as we have suggested, or a cause of myocardial dysfunction, as Dr Blum suggests.