DIFFERENTIAL EXPRESSION OF TISSUE FACTOR PROTEIN IN DIRECTIONAL ATHERECTOMY SPECIMENS FROM PATIENTS WITH STABLE AND UNSTABLE CORONARY SYNDROMES

Tissue factor (TF) is a cell membrane-associated protein that catalyze s the rate-limiting step of the extrinsic coagulation pathway, which i s the major source of thrombin production in vivo. To explore the pote ntial role that TF may play in ischemic coronary syndromes, directiona l coronary atherectomy specimens were tested for the presence of TF pr otein using immunohistochemical techniques. Methods and Results Frozen sections from atherectomy specimens in 61 patients were examined for TF expression using an IgG murine monoclonal antibody against human TF . Patients were classified according to their admission diagnosis as h aving either an unstable or a stable coronary syndrome. An unstable co ronary syndrome was defined as either angina pectoris occurring at res t or post-myocardial infarction (<1 week) angina. Stable coronary synd romes included patients with stable, progressive, and new-onset (<6 we eks) angina without rest pain. TF was detected in 15 (43%) of 35 patie nts with unstable coronary syndromes versus only 3 (12%) of 26 patient s with stable coronary syndromes (odds ratio, 5.7; 95% confidence inte rval, 1.3 to 24.3; P=.018). Within the subgroup of patients with unsta ble coronary syndromes, TF was detected in 14 (60%) of 25 patients wit h de novo lesions versus only 1 (10%) of 10 patients with a restenosis lesion (P<.02). An additional 8 patients with stable coronary syndrom es due to a restenosis lesion were also negative for TF. Therefore, th e overall incidence of TF expression was only 6% (1 of 18) in restenos is lesions compared with 33% (14 of 43) in de novo lesions (P<.03). Co nclusions This study provides the first description of TF protein expr ession in human coronary artery lesions in vivo. Tissue factor was rea dily detected in de novo lesions in patients with unstable coronary sy ndromes, suggesting a role for TF in the pathogenesis of this disease process. Conversely, TF was rarely detected in patients with restenosi s lesions even if the resulting clinical presentation was an unstable coronary syndrome. These results may have implications for the managem ent of patients with unstable angina from de novo lesions and patients with ischemic symptoms from a restenosis lesion.