Relationship of cardiac troponin T and procoagulant activity in unstable angina.
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.
Giannitsis
E
E
Medizinische Klinik II der Medizinischen Universität zu Lübeck, Germany.
Bardorff
M M
MM
Schweikart
S
S
Wiegand
U
U
Kampmann
M
M
Katus
H A
HA
D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000453:epidemiology; D000789:Angina, Unstable / Q000097:blood* / Q000453:epidemiology; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000187:drug effects; D015331:Cohort Studies; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000187:drug effects / Q000378:metabolism; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D015994:Incidence; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000453:epidemiology; D009206:Myocardium / Q000737:chemistry*; D010446:Peptide Fragments / Q000378:metabolism; D010958:Plasminogen / Q000378:metabolism; D011516:Prothrombin / Q000378:metabolism; D020107:Troponin T / Q000097:blood / Q000494:pharmacology* / Q000502:physiology; D000979:alpha-2-Antiplasmin / Q000378:metabolism
D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D010446:Peptide Fragments; D020107:Troponin T; D000979:alpha-2-Antiplasmin; C011468:fibrinmonomer; C045879:prothrombin fragment 1.2; D011516:Prothrombin; D010958:Plasminogen