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Myocardial damage, coagulation activity and the response to thrombin inhibition in unstable coronary artery disease
Jonas Oldgren1, Agneta Siegbahn, Lars Grip
1Department of Medical Sciences, Cardiology, Uppsala University Hospital, Uppsala, Sweden. Jonas.Oldgren@medsci.uu.se
Insights
Elevated troponin T in unstable coronary artery disease signals higher risk and coagulation activity. However, some troponin-negative patients show poor response to thrombin inhibitors, increasing ischemic event risk post-treatment.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Background:
- Unstable coronary artery disease (CAD) often involves plaque rupture, coagulation activation, and thrombus formation, leading to myocardial damage.
- Assessing the relationship between cardiac biomarkers, coagulation markers, and ischemic events is crucial for risk stratification in unstable CAD.
Purpose of the Study:
- To evaluate the association between troponin T levels, markers of coagulation activity (prothrombin fragment 1+2, thrombin-antithrombin complex, soluble fibrin, D-dimer), and ischemic events in unstable CAD patients.
- To compare the clinical outcomes of patients treated with inogatran versus unfractionated heparin.
Main Methods:
- A randomized trial involving 320 unstable CAD patients assigned to 72-hour infusions of inogatran or unfractionated heparin.
- Measurement of troponin T and coagulation markers (prothrombin fragment 1+2, thrombin-antithrombin complex, soluble fibrin, D-dimer) at baseline, during treatment, and 24 hours post-treatment.
Main Results:
- Troponin-positive patients exhibited higher baseline and on-treatment levels of coagulation markers and tended towards worse short-term outcomes.
- In troponin-negative patients, persistently high or increasing prothrombin fragment 1+2 or thrombin-antithrombin complex during treatment correlated with a higher 30-day ischemic event rate (19% and 15%, respectively).
- Conversely, a decrease in these markers in troponin-negative patients was associated with a significantly lower event rate (5.7% and 4.5%, respectively).
Conclusions:
- Troponin T elevation in unstable CAD indicates increased risk and heightened coagulation activity.
- Among troponin-negative patients, persistent thrombin generation during treatment suggests a poor response to thrombin inhibitors and an elevated risk of early ischemic events after treatment cessation.
Abstract:
Unstable coronary artery disease is in most cases associated with plaque rupture, activation of the coagulation system and subsequent intracoronary thrombus formation which may cause myocardial cell damage. The aim of the present analysis was to assess the relation between troponin T, markers of coagulation activity, i.e. prothrombin fragment 1+2, thrombin-antithrombin complex, soluble fibrin and D-dimer, and ischemic events, i.e. death, myocardial (re-)infarction or refractory angina. 320 patients with unstable coronary artery disease were randomized to 72 hours infusion with inogatran, a low molecular weight direct thrombin inhibitor, or unfractionated heparin. Patients with elevated troponin levels had higher levels of prothrombin fragment 1+2, soluble fibrin and D-dimer before, during, and at 24 hours after cessation of anticoagulant treatment. These troponin-positive patients tended to have worse short-term clinical outcome, without relation to markers of coagulation activity. Troponin-negative patients with unchanged or early increased thrombin generation during treatment had a cluster of ischemic events within 24 hours after cessation of the study drug. The 30-day ischemic event rate was 19 % in troponin-negative patients with unchanged or early increased prothrombin fragment 1+2, and 5.7 % in patients with decreased prothrombin fragment 1+2, p=0.006, and similarly 15 % in troponin-negative patients with unchanged or early increased thrombin-antithrombin complex and 4.5 % in patients with decreased thrombin-antithrombin complex, p=0.02. In conclusion, in unstable coronary artery disease a troponin elevation indicates higher risk and higher coagulation activity. However, among the troponin negative patients, with a lower risk and lower coagulation activity, a part of the patients seem to be non-responders to treatment with a thrombin inhibitor expressed as unchanged or raised coagulation activity and a raised risk of ischemic events early after cessation of treatment.
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