Related Experiment Videos
Temporal relation between ischemic episodes and activation of the coagulation system in unstable angina
L M Biasucci1, G Liuzzo, G Caligiuri
1Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy.
Insights
Patients with unstable angina experience frequent thrombin bursts, independent of ischemic episodes. Conversely, some ischemia events occur without clear signs of coagulation system activation, revealing a complex relationship.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Background:
- Coronary thrombosis is a key factor in unstable angina pathogenesis.
- Evidence suggests hemostatic system activation may extend beyond ischemic events in unstable angina.
Purpose of the Study:
- To investigate the temporal relationship between ischemic episodes and coagulation system activation in unstable angina patients.
Main Methods:
- Measured thrombin-antithrombin III (TAT) and prothrombin fragment 1 + 2 (F1 + 2) levels in patients during ischemic episodes (Protocol A).
- Assessed TAT and F1 + 2 levels over time in hospitalized unstable angina patients to correlate with ischemic events (Protocol B).
Main Results:
- In Protocol A, 77% of patients showed elevated TAT and F1 + 2 levels during ischemic episodes, with TAT peaking at 5 minutes.
- In Protocol B, coagulation activation was linked to ischemia in 30% of samples, but also occurred in 15% of samples not related to ischemia (P = .07).
Conclusions:
- Patients with active unstable angina exhibit frequent thrombin production bursts unrelated to ischemic episodes.
- Some ischemic episodes in unstable angina may not be associated with detectable thrombin activation.
Background:
Although a major role of coronary thrombosis in the pathogenesis of unstable angina has been demonstrated, the results of a series of studies have suggested that activation of the hemostatic system may not be confined to ischemic episodes. The purpose of this study was to investigate the temporal relation between ischemic episodes and activation of the coagulation system in unstable angina.
Methods And Results:
Thrombin-antithrombin III (TAT) and prothrombin fragment 1 + 2 (F1 + 2) levels were measured in 13 patients during spontaneous ischemic episodes (time 0, 5, and 15 minutes and 1 hour) to evaluate the time course of the activation of the coagulation system associated with the development of ischemia (protocol A). TAT and F1 + 2 levels were also measured in 28 patients with unstable angina on admission to hospital (every 6 hours for 24 hours and daily for 3 days) to assess their temporal relation with ischemic episodes (protocol B). In protocol A, TAT and F1 + 2 levels were elevated in 10 of 13 patients (77%) in at least 1 sample. The median value of TAT showed a peak at 5 minutes and returned to baseline within 15 minutes (P < .05), consistent with its plasma half-life of 5 minutes, whereas the median value of F1 + 2 showed no significant changes, possibly because of its longer half-life, which tends to dampen sudden bursts of thrombin production. In protocol B, activation of the clotting system was found in 10 of 33 samples (30%) temporally related to ischemia and also in 23 of 150 (15%, P = .07) of those not temporally related to ischemia.
Conclusions:
Our study demonstrates that patients with active unstable angina develop frequent bursts of thrombin production not necessarily associated with ischemic episodes and that, conversely, some ischemic episodes are not associated with evidence of thrombin activation.