The role of C-reactive protein activation of nuclear factor kappa-B in the pathogenesis of unstable angina.

摘要

Inflammation is pivotal in all phases of atherosclerosis, from the nascent lesion to the culmination in acute coronary syndromes (ACS) (1). Nuclear factor kappa-B (NF-kB) is a master switch in the inflammatory cascade and indeed has been documented in human atheroma (2). C-reactive protein (CRP), the prototypic marker of inflammation, has been advanced as a risk marker for heart disease, and indeed in patients with unstable angina higher levels augur a poorer prognosis (3). Whether CRP definitely participates in this process remains to be proven. In this issue of the Journal, Liuzzo et al. (4) carefully document that patients with unstable angina with elevated levels of CRP (>3 mg/1) have increased monocytic NF-kB activity and increased release of proinflammatory cytokines, interleukin (IL)-6, and tumor necrosis factor (TNF) from lipopolysaccharide (LPS)-stimulated monocytes. Furthermore, they show, in an albeit limited sample size, that the patients with unstable angina with elevated CRP and increasedNF-kB activity have the worst outcomes based on recurrence of acute coronary events. Therefore, they argue that CRP might indeed be a participant in the genesis and clinical sequelae of ACS.