Serum tumour necrosis factor-α, interleukin-2 and interleukin-10 activation in stable angina and acute coronary syndromes

Background Dynamic instability of coronary atherosclerotic plaque results in the development of both unstable angina and myocardial infarction. The aim of the study was to investigate the dynamics of serum concentrations of tumour necrosis factor (TNF)alpha, interleukin (IL)-10, and IL-2 in patients with myocardial infarction (MI) and unstable angina (UA) as compared to stable angina (SA) patients and healthy volunteers. Methods A total of 189 patients with coronary artery disease (CAD) were studied: 100 patients with SA (class II/III according to CCS), 57 patients with UA (Braunwald class IIIB; determinations at 6, 24, and 48 h after chest pain), and 32 patients with MI (determinations at admission, on the 7th and 30th days after MO. Twenty healthy volunteers acted as controls. Results Serum TNFalpha levels were elevated in all CAD groups (SA: 173 +/- 4; UA: 18.7 +/- 4; MI: 22.0 +/- 3 pg/ml; p < 0.001) in comparison to the controls (8.3 +/- 1.4 pg/ml). However, the highest values were characteristic of MI patients, especially values obtained at admission (P < 0.01 versus SA and UA Mean serum concentrations of IL-2 were significantly higher in patients with MI and ILIA (89.6 +/- 40; 870 +/- 24 pg/ml, respectively; p < 0.01) when compared to SA and the control group (58.3 +/- 49; and 51.5 +/- 39, respectively). Serum IL-10 levels were also higher in MI and UA patients. Levels of IL-2 and IL-10 measured following chest pain in unstable patients, as well as their consecutive determinations in MI patients did not show any change dynamics, that is, they were persistently elevated. Conclusions When compared to stable CAD and healthy subjects, acute coronary syndromes are associated with long-term increase of serum concentrations of pro- and anti-inflammatory cytokines. It seems likely that sudden CAD progression leading to acute coronary syndromes is triggered/accompanied by prolonged immune activation. (C) 2003 Lippincott Williams & Wilkins.