Tissue-factor antigen and activity in human coronary atherosclerotic plaques

Background Coronary atherosclerotic-plaque thrombosis is a key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque rupture or fissuring frequently occurs in atherosclerosis, only a small proportion of ruptured plaques develop thromboses. Methods Tissue-factor antigen and activity were measured in atherectomy samples from 50 consecutive patients with coronary artery disease (stable angina n=19, unstable angina n=24, and myocardial infarction n=7). Findings Median tissue-factor antigen and activity concentrations were significantly higher in plaques from patients with unstable angina and myocardial infarction than in those from patients with stable angina (antigen: 66·1 pg/mg [interquartile range 43·8–82] vs 32·4 pg/mg [9·8–43·4], p=0·0001; activity: 0·22 mU/mg [0·17–0·41] vs 0·13 mU/mg [0·05–0·16], p=0·0004). Interpretation Tissue-factor, an initiator of the coagulation cascade, may account for the different thrombotic responses to the rupture of human coronary atherosclerotic plaques.