BACKGROUND: Unstable coronary syndromes are currently believed to be caused by rupture of an atherosclerotic plaque due to local events, which may be of general inflammatory etiology. There is increasing evidence that nuclear factor-kappaB (NF-kappaB) is a key transcription factor in controlling gene expression concerning inflammatory response, and that plasma concentrations of C-reactive protein (CRP) is a sensitive marker of inflammation in unstable coronary syndromes. However, whether NF-kappaB activation is associated with coronary heart disease (CHD) activity as well as plasma CRP level has been less well investigated. The aim of this study was to explore whether NF-kappaB activation was associated with CHD activity and plasma CRP elevation in patients with unstable angina (UA). METHODS: NF-kappaB activity derived from white blood cells circulating in 33 patients with CHD was determined by electrophoretic mobility shift assay. Of these, 16 had UA and were within 24h of the last episode of chest pain. The remaining 17 were being evaluated for stable angina (SA). The CRP was also evaluated in both groups using a high-sensitivity ELISA. RESULTS: There was marked NF-kappaB activation and elevated levels of CRP in UA group compared with SA group (4.02+/-0.71 AU versus 1.24+/-0.23 AU and 5.0+/-0.7mg/l versus 1.4+/-0.4mg/l, respectively, P<0.01), no NF-kappaB signal was observed in normal subjects (n=10). The NF-kappaB activation had a positive correlation with levels of CRP in patients with UA (n=11, gamma=0.771, P<0.01), but had no relationship between other clinical characteristics and the status of NF-kappaB activation. CONCLUSIONS: Our data suggest that inflammation is an important feature of unstable coronary artery disease, and both NF-kappaB and CRP are useful markers for the detection of UA or vulnerable plaques.
BACKGROUND: Unstable coronary syndromes are currently believed to be caused by rupture of an atherosclerotic plaque due to local events, which may be of general inflammatory etiology. There is increasing evidence that nuclear factor-kappaB (NF-kappaB) is a key transcription factor in controlling gene expression concerning inflammatory response, and that plasma concentrations of C-reactive protein (CRP) is a sensitive marker of inflammation in unstable coronary syndromes. However, whether NF-kappaB activation is associated with coronary heart disease (CHD) activity as well as plasma CRP level has been less well investigated. The aim of this study was to explore whether NF-kappaB activation was associated with CHD activity and plasma CRP elevation in patients with unstable angina (UA). METHODS: NF-kappaB activity derived from white blood cells circulating in 33 patients with CHD was determined by electrophoretic mobility shift assay. Of these, 16 had UA and were within 24h of the last episode of chest pain. The remaining 17 were being evaluated for stable angina (SA). The CRP was also evaluated in both groups using a high-sensitivity ELISA. RESULTS: There was marked NF-kappaB activation and elevated levels of CRP in UA group compared with SA group (4.02+/-0.71 AU versus 1.24+/-0.23 AU and 5.0+/-0.7mg/l versus 1.4+/-0.4mg/l, respectively, P<0.01), no NF-kappaB signal was observed in normal subjects (n=10). The NF-kappaB activation had a positive correlation with levels of CRP in patients with UA (n=11, gamma=0.771, P<0.01), but had no relationship between other clinical characteristics and the status of NF-kappaB activation. CONCLUSIONS: Our data suggest that inflammation is an important feature of unstable coronary artery disease, and both NF-kappaB and CRP are useful markers for the detection of UA or vulnerable plaques.