Levels of serum IL-1β, IL-2, IL-8 and tumor necrosis factor-α in patients with unstable angina pectoris

Abstract

Objectives: Inflammation is the most important mechanism of plaque disruption playing an essential role in acute coronary syndromes. It is controversial whether the inflammatory mediators are the cause or the result in the development of plaque rupture. Stimulation of interleukins increases adhesion molecules, fibrinogen and plasminogen activator inhibitors, which cause the activation of inflammation and thrombosis. However, the importance of interleukins in acute coronary syndromes has not been clearly defined. We did not find any article concerning relations between the levels of serum interleukin (IL)-1β, IL-2, IL -8 and tumor necrosis factor (TNF)-α in patients with unstable angina pectoris (UAP). So the aim of this study was to determine the levels of serum IL-1β, IL-2, IL-8 and TNF-α during the early stage of UAP. Methods and results: Thirty-seven patients with UAP (12 females and 25 males; mean age, 57.5 ± 9.7 years) within 6 h of admission and 20 healthy volunteers (eight females and 12 males; mean age, 51.3 ± 6.3 years) were included in the study. IL-1β, IL-2, IL-8 and TNF-α levels were measured using the enzyme-linked immunosorbent assay method. Patients with acute or chronic inflammation, renal failure or chronic heart failure were excluded from the study. The age, gender and risk factors of the study and control groups were similar. The levels of IL-1β, IL-8 and TNF-α were significantly increased (p < 0.0001, p < 0.001 and p < 0.016, respectively) in patients with UAP. There was no difference of IL-2 levels between the UAP group and controls. Conclusion: We detected high levels of IL-1β, IL-8 and TNF-α in patients with UAP during early phase. We suggest that proinflammatory cytokines (e.g. IL-1β, IL-8, TNF-α) may play an important role in the development of atherosclerosis and its complications.