More intensive CMV-infection in chronic heart failure patients contributes to higher T-lymphocyte differentiation degree.

Immunosenescence in chronic heart failure (CHF) is characterized by a high frequency of differentiated T-lymphocytes, contributing to an inflammatory status and a deficient ability to generate immunocompetent responses. CMV is the best known inducer of T-lymphocyte differentiation, and is associated with the phenomenon of immunosenescence. In this study, we included 58 elderly chronic heart failure patients (ECHF), 60 healthy elderly controls (HEC), 40 young chronic heart failure patients (YCHF) and 40 healthy young controls (HYC). High differentiation of CD8+ T-lymphocytes was found in CMV-seropositive patients; however, the differentiation of CD4+ T-lymphocytes was increased in CMV-seropositive but also in CHF patients. Anti-CMV antibody titers showed positive correlation with more differentiated CD4+ and CD8+ subsets and inverse correlation with CD4/CD8 ratio. Immunosenescence found in CHF patients is mainly due to the dynamics of CMV-infection, since the differentiation of T-lymphocyte subsets is related not only to CMV-infection, but also to anti-CMV antibody titers.

Disease complexity in acute coronary syndrome is related to the patient's immunological status.

BACKGROUND: Our aim was to investigate whether patients with acute coronary syndrome (ACS) display an overall T cell immunosenescence that could be contributing to worsening the stage of the disease. METHODS AND RESULTS: We compared the immunological status of 52 ACS patients, 21 controls with absence of coronary artery disease (CAD) (C1), and 50 healthy individuals (C2). We characterized leukocyte and T lymphocyte subpopulations by flow cytometry. CAD was classified according to SYNTAX score, number of diseased coronary vessels, previous episodes of ACS and left ventricular ejection fraction (LVEF). ACS patients showed an increased number of total leukocytes, neutrophils and monocytes (p < 0.001), but a decreased number of lymphocytes (p < 0.05). ACS patients had significantly higher levels of NK cells and CD8+ T-cells (p < 0.05). ACS was associated with high differentiation in CD4+ and CD8+ T-lymphocytes. Frequencies of naïve, naïve CD31+, EM1, and pE1 subsets were significantly reduced in ACS patients (p < 0.05), while EM3, EM4 (in CD4+), and E (in CD8+) subsets were increased (p < 0.05). Aging of T-lymphocyte subpopulations was associated with a worse SYNTAX score (p < 0.05), and aging of CD4+ T-lymphocytes with a larger number of affected vessels, larger number of previous ACS episodes and lower LVEF, in ACS patients (p > 0.05). Furthermore, the proliferation ability of CD4+ and CD8+ T-lymphocytes was significantly impaired in ACS patients (p < 0.05), although they had increased activation (p < 0.05). CONCLUSIONS: We conclude that ACS patients show a higher degree of T-lymphocyte immunosenescence than healthy controls, which could contribute to disease impairment through a compromised adaptive immune response.