Nuclear factor-kappaB immunoreactivity is present in human coronary plaque and enhanced in patients with unstable angina pectoris.

BACKGROUND

Nuclear factor-kappaB (NF-kappaB) is a transcription factor which plays a coordinating role in inflammation and cellular proliferation and is thought to be involved in the pathogenesis of atherosclerosis. Its role in unstable coronary plaque in humans is unknown.

METHODS AND

RESULTS

Coronary atherectomy plaque was obtained via directional coronary atherectomy from 32 patients [16 with unstable angina pectoris (UAP) and 16 with stable angina pectoris (SAP)]. The predominant pathology in UAP consisted of richly cellular areas with atheromatous gruel or loose intimal proliferative tissue within a myxoid matrix (P<0.05 compared with SAP). By contrast, SAP plaques showed more dense fibrosis (P<0.01 compared with UAP). Sections were then stained with a monoclonal antibody to the activated p65 subunit of NF-kappaB and this staining was present in 31/32 specimens, localized to smooth muscle cells, macrophages and foam cells. Staining was then graded semiquantitatively by three independent observers. Immunostaining grades for activated NF-kappaB were significantly higher in UAP compared with SAP (2.60+/-0.1 vs. 1.98+/-0.18; P<0.01).

CONCLUSIONS

NF-kappaB immunoreactivity is present in coronary atherosclerotic plaque and is increased among patients with unstable coronary syndromes. These data support a role for NF-kappaB in the pathogenesis of acute coronary syndromes in humans.