The role of cytokines in unstable angina.

A growing body of evidence suggests that inflammation plays a major role in the pathogenesis of unstable angina; this evidence is mainly derived from the prognostic role of the acute phase reaction proteins, such as C-reactive protein (CRP) and fibrinogen. Since the production of acute phase protein is under the control of the pro-inflammatory cytokines, it is probable that citokines, such as tumour-necrosis factor (TNF)-alpha, interleukin (IL)-1 and IL-6 are involved in the same process. Indeed, elevated levels of IL-1 and IL-6 have been found by our group and by others, in patients with acute coronary syndromes. Cytokines may have procoagulant effects, directly or via endothelial dysfunction, and may induce plaque vulnerability or rupture. They may also be responsible for the activation of other cells, as neutrophils or mast-cells. Although it is conceivable that activated lymphocytes, via interferon-gamma production, are responsible for macrophage activation and cytokine production in unstable angina, the trigger and the precise mechanism of this event are still unknown. The multiple roles of cytokines in unstable angina suggest that a targeted anti-inflammatory therapy might be a novel approach in the future for the treatment of this syndrome.