Objective. The present study sought to determine the incidence of increased
procoagulant activity in patients with unstable angina (UAP), and to evalu
ate the relationship between cardiac troponin T (cTnT) and molecular marker
s of hemostatic activation. Method. We studied 44 patients with UAP further
classified by plasma cTnT levels. All patients received an antithrombotic
therapy consisting of therapeutic doses of unfractionated heparin and acety
lsalicylic acid. Quantitative levels of cTnT and plasma concentrations of f
ibrin monomers (FM), prothrombin fragments F1+2, thrombin antithrombin III
complexes (TAT). plasminogen and alpha(2)-antiplasmin were sampled serially
within the first 48 h. Results. Increased plasma concentrations of FM were
detected in 45.5% of patients and were more frequently present among those
with cTnT concentrations greater than or equal to 0.1 ng/ml (13 of 18 vs 7
of 26 patients, p = 0.003). In these patients, mean plasma concentrations
of FM were significantly higher than in patients with cTnT <0.1 ng/ml (7.93
+/- 2.3 vs 3.12 +/- 0.6 mu g/ml, p = 0.02). There was a close relationship
between plasma Levels of cTnT and FM (r = 0.74, p <0.004), prothrombin fra
gments F1+2 (r = 0.71, p = 0.046) and a trend to significance was noted for
TAT (r = 0.42, p = 0.055). No significant correlation was observed with ma
rkers of the fibrinolytic system (plasminogen and alpha(2)-antiplasmin). Pl
asma levels of cTnT greater than or equal to 0.1 ng/ml identified a concomi
tant increase of hemostatic markers with a sensitivity. specificity and pos
itive predictive value of 65, 79, and 72% for FM, 63, 76, and 67% for proth
rombin fragments F1+2. and 58, 66, and 39% for TAT, respectively. Conclusio
ns. In patients with UAP, cTnT identifies patients with increased procoagul
ant activity and is closely related to plasma levels of molecular markers o
f hemostatic activation. Therefore, cTnT alone or in combination with one o
f these markers may be helpful to identify patients requiring more potent a
ntithrombin or antiplatelet therapy.