Tissue factor and homocysteine levels in ischemic heart disease are associated with angiographically documented clinical recurrences after coronary angioplasty

Background In ischemic heart disease (IHD) patients high plasma levels of T issue Factor (TF), the trigger of coagulation cascade, are present. Homocys teine (Hcy) is a risk factor for coronary artery disease, and several diffe rent pathophysiological mechanisms by which Hey may play a role in thrombus formation have been postulated in "in vitro" studies. We investigated the "in vivo" role of Hey in affecting plasma levels of TF, its inhibitor Tissu e Factor Pathway Inhibitor (TFPI) and hypercoagulability. Methods and Resul ts. We investigated 119 IHD patients who underwent PTCA and compared them w ith 103 healthy subjects. TF, TFPI, Thrombin-Antithrombin complexes (TAT) a nd Hey levels were significantly higher in the patients than in the control s. A positive correlation was found between Hey and TF (r = 0.54; p < 0.000 1), Hey and TFPI (r = 0.26; p < 0.05) as well as Hey and TAT (r = 0.33; p < 0.0001) levels. An inverse correlation existed between folate intake and H ey levels (r = -0.28; p = 0.001). Hey levels within the first quartile and in the highest quartile were associated with a lower (p < 0.001) and higher (p < 0.0001) rate of clinical recurrences, respective ly. Patients with TF values in the first quartile had a lower rate of angiographically document ed clinical recurrences as compared to those in the fourth quartile (p < 0. 01); those in the highest quartile of TF showed a higher rate of recurrence s (p = 0.001). Multivariate analysis confirmed these results (first quartil e of Hey: OR 0.02, Cl 0.002-0.27; fourth quartile of Hey: OR 36.5, Cl 3.6-3 65/first quartile of TF: OR 0.006, Cl 0.001-0.44; fourth quartile of TF: OR 16.4, Cl 3.0 - 90.0), also after adjustment for risk factors and Hey and T F respectively. Conclusions. In this study we show that TF, TFPI and TAT le vels are correlated with Hey plasma levels in IHD patients, providing evide nce of an "in vivo" pathophysiological mechanism of hyperhomocysteinemia. T he observed association between angiographically documented clinical recurr ences and TF and Hey values awaits confirmation in studies designated to ev aluate this issue on a larger number of patients.