Immune activation in severe heart failure. Does etiology play a role?

Aim Immune activation in severe congestive heart failure (CHF) due to idiopathic conditions is a well-known phenomenon. The question remains: is it confined to a specific aetiology or is a disease-dependent derangement? We investigated immune alterations in ischaemic compared to idiopathic patients with CHF and healthy subjects. Methods and results We evaluated alterations of immune activation studying both in vivo and in vitro parameters. In both idiopathic and ischaemic CHF patients: (a) lymphocyte count was reduced (P < 0.01); (b) lymphocyte subsets were altered (CD4/CD8 ratio increased vs. controls: 2.53 ± 0.8 and 3.3 ± 2.1% in idiopathic and ischaemic patients, vs. 1.8 ± 0.6% in controls; P < 0.01); (c) lymphocytes from patients underwent a higher apoptosis (27.1 ± 4.3% in idiopathic CHF and 25.4 ± 3.5% in ischaemic CHF vs. 4.5 ± 1.4%; P < 0.0001); (d) TNF-a production from lymphocytes and monocytes of patients was higher than controls. A positive correlation was observed between TNF-a from monocytes of patients and the relevant serum levels (r = 0.58; P < 0.01); (e) conditioned media of lymphocytes and monocytes from patients significantly increased rate of endothelial apoptosis. Conclusions In severe CHF, irrespectively from aetiology, significant activation of immune system occurs: several pro-inflammatory cytokines and soluble factors are spontaneously released in serum, possibly contributing to disease progression, as they induce apoptosis.