Key result
In unstable angina, cTnT ≥0.1 is linked to a ~168% higher rate of increased fibrin monomers.
Why the study?
The incidence of increased procoagulant activity in unstable angina patients and its relationship with cardiac troponin T and hemostatic activation markers was unclear.
Observational (n=44)
Absolute Event Rate: 72.2% vs 26.9%
p-value: p=0.003
In patients with unstable angina, elevated cardiac troponin T identifies those with increased procoagulant activity, suggesting a potential role in guiding the intensity of antithrombotic therapy.
Supports cTnT as marker of procoagulant activity in unstable angina; leaves open troponin-guided antithrombotic intensity in trials.
OBJECTIVE: The present study sought to determine the incidence of increased procoagulant activity in patients with unstable angina (UAP), and to evaluate the relationship between cardiac troponin T (cTnT) and molecular markers 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 acetylsalicylic acid. Quantitative levels of cTnT and plasma concentrations of fibrin monomers (FM), prothrombin fragments F1+2, thrombin antithrombin III complexes (TAT), plasminogen and alpha2-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 > or =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 microg/ml, p = 0.02). There was a close relationship between plasma levels of cTnT and FM (r = 0.74, p <0.004), prothrombin fragments 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 markers of the fibrinolytic system (plasminogen and alpha2-anti-plasmin). Plasma levels of cTnT > or =0.1 ng/ml identified a concomitant increase of hemostatic markers with a sensitivity, specificity and positive predictive value of 65, 79, and 72% for FM, 63, 76, and 67% for prothrombin fragments F1+2, and 58, 66, and 39% for TAT, respectively. CONCLUSIONS: In patients with UAP, cTnT identifies patients with increased procoagulant activity and is closely related to plasma levels of molecular markers of hemostatic activation. Therefore, cTnT alone or in combination with one of these markers may be helpful to identify patients requiring more potent antithrombin or antiplatelet therapy.
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A 2000 study conducted an observational in Unstable angina (n=44). Cardiac troponin T (cTnT) levels ≥0.1 ng/ml vs. cTnT <0.1 ng/ml was evaluated on Increased plasma concentrations of fibrin monomers (FM) (p=0.003). In patients with unstable angina, cTnT levels ≥0.1 ng/ml were associated with a significantly higher frequency of increased fibrin monomers compared to cTnT <0.1 ng/ml (72.2% vs 26.9%, p=0.003).
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