Key result
Microplate assay indices for the rate of clot formation and dissolution were independently associated with the use of aspirin versus warfarin in patients with cardiovascular disease.
Why the study?
Does a microplate assay better differentiate thrombogenesis and fibrinolysis indices compared to thromboelastography in patients with cardiovascular disease on aspirin or warfarin?
Cross-Sectional (n=181)
No
Does a microplate assay better differentiate thrombogenesis and fibrinolysis indices compared to thromboelastography in patients with cardiovascular disease on aspirin or warfarin?
Odds Ratio: 0.9 (95% CI 0.85–0.95)
p-value: p=<0.001
A novel microplate assay demonstrates superior ability compared to thromboelastography in differentiating thrombogenesis and fibrinolysis indices among cardiovascular patients on aspirin versus warfarin.
May support microplate assays for antithrombotic monitoring; leaves open prospective validation before clinical adoption.
As heart failure, coronary artery disease and atrial fibrillation all bring a risk of thrombosis, anti-thrombotic therapy is recommended. Despite such treatment, major cardiovascular events such as myocardial infarction and stroke still occur, implying inadequate suppression of thrombus formation. Accordingly, identification of patients whose haemostasis remains unimpaired by treatment is valuable. We compared indices for assessing thrombogenesis and fibrinolysis by two different techniques in patients on different anti-thrombotic agents, i.e. aspirin or warfarin. We determined fibrin clot formation and fibrinolysis by a microplate assay and thromboelastography, and platelet marker soluble P selectin in 181 patients with acute or chronic heart failure, coronary artery disease who were taking either aspirin or warfarin. Five thromboelastograph indices and four microplate assay indices were different on aspirin versus warfarin (p < 0.05). In multivariate regression analysis, only microplate assay indices rate of clot formation and rate of clot dissolution were independently related to aspirin or warfarin use (p ≤ 0.001). Five microplate assay indices, but no thrombelastograph index, were different (p < 0.001) in aspirin users. Three microplate assay indices were different (p ≤ 0.002) in warfarin users. The microplate assay indices of lag time and rate of clot formation were abnormal in chronic heart failure patients on aspirin, suggesting increased risk of thrombosis despite anti-platelet use. Soluble P selectin was lower in patients on aspirin (p = 0.0175) but failed to correlate with any other index of haemostasis. The microplate assay shows promise as a tool for dissecting thrombogenesis and fibrinolysis in cardiovascular disease, and the impact of antithrombotic therapy. Prospective studies are required to determine a role in predicting thrombotic risk.
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Lau et al. (2016) conducted a cross-sectional in Heart failure, coronary artery disease, and atrial fibrillation (n=181). Aspirin vs. Warfarin was evaluated on Microplate assay rate of clot formation (association with anti-thrombotic therapy) (OR 0.90, 95% CI 0.85-0.95, p=<0.001). Microplate assay indices for the rate of clot formation and dissolution were independently associated with the use of aspirin versus warfarin in patients with cardiovascular disease.
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