Soluble antiapoptotic molecules and immune activation in chronic heart failure and unstable angina pectoris

Programmed myocyte cell death and activation of the immune system have been shown to occur in patients with congestive heart failure. Besides, unstabl e angina episodes are likely to be associated with immune activation. Our a im was to evaluate the role of changes in circulating levels of soluble Fas (sFas), suggestive of an enhanced inhibitory response to ongoing apoptosis , and soluble 1L2 receptor (sIL2-R), indicative of T-lymphocyte activation, in chronic heart failure and unstable angina pectoris, Thirty patients aff ected by chronic heart failure (20 idiopathic and 10 ischemic cardiomyopath y) and 13 patients with unstable angina were evaluated. Twenty healthy indi viduals matched for age and gender were used as controls. A complete bioche mical determination of indexes of myocardial damage including cardiac tropo nin I (cTnI) and creatine kinase (MB/CK) was performed. The results demonst rated that mean levels of sFas and sIL2-R were significantly increased in p atients affected by chronic heart failure and unstable angina and were not associated with changes in renal function or with serum levels of cTnI. Hig hest values of sFas were found in NYHA class IV patients (IV NYHA class = 7 .39 +/- 0.52 vs. controls = 1.34 +/- 0.12 ng/ml; P < 0.01) and more elevate d in idiopathic than in ischemic cardiomyopathy (3.64 +/- 0.40 vs. 1.82 +/- 0.37 ng/ml; P < 0.01). Moreover, in chronic heart failure patients sFas an d ejection fraction were negatively correlated (P = 0.01), whereas sFas and sIL2-R were positively correlated (P < 0.01). In unstable angina patients too, sFas and sIL2-R appeared to be correlated (P = 0.03); whereas sFas (an gina group = 3.18 +/- 0.39 vs. controls = 1.34 +/- 0.12 ng/ml; P < 0.01) an d sIL2-R (angina group = 0.46 +/- 0.11 vs. controls = 0.00 Ul/ml; P < 0.01) were higher in angina group than in controls. In most of the cases, the in crease of sFas was associated with comparable changes in sIL2-R serum level s, indicating that the activation of Fas system is strictly associated with autoimmune-inflammatory reactions. This phenomenon, both in chronic heart failure and in unstable angina, occurs in the absence of biochemical eviden ces of myocardial damage and seems to parallel the activation of T cell. So luble Fas could have a role in sustaining inflammatory response and in prol onging the detrimental effects correlated with it in chronic heart failure and angina pectoris.