By Piriya Mahendra
An early invasive strategy following thrombolysis for ST-segment-elevation myocardial infarction (STEMI) is associated with significant changes in the levels of inflammatory and thrombotic biomarkers, a substudy of the Norwegian study on district treatment of STEMI (NORDISTEMI) shows.
Sigrun Halvorsen (Oslo University Hospital, Norway) and team explain that elevations of proinflammatory biomarkers such as C-reactive protein and interleukin-6, and coagulation markers have been associated with adverse clinical outcomes, whereas elevations of antiinflammatory biomarkers such as interleukin (IL)-10 have been linked to a more favorable prognosis.
Pharmacologic and invasive treatment might influence these inflammatory and prothrombotic responses, they add, but it is not clear how.
They therefore investigated whether circulating levels of inflammatory and thrombotic biomarkers differed among 246 STEMI patients treated with thrombolysis who were randomly assigned to receive early invasive (immediate revascularization) or standard therapy (in-hospital treatment with ischemia-guided referral for invasive evaluation).
Enzyme-linked immunosorbent assay analysis revealed that at 3 days after randomization, the levels of prothrombin fragment 1+2 and D-dimer were higher in the early invasive compared with the standard therapy group, at 240 versus 175 pmol/L and 800 vs 750 ng/mL, respectively (p<0.001 for both).
By contrast, levels of soluble CD40 ligand were lower in the early invasive group compared with the standard treatment group at day 3 (p=0.009).
There were no significant differences between the treatment groups in any of the other measured markers: C-reactive protein (CRP), interleukins, tumor necrosis factor-α, monocyte chemoattractant protein-1, or soluble tissue factor.
Significant, albeit weak, individual correlations were found between levels of CRP, IL-6, prothrombin fragment 1+2 and D-dimer, and infarct size assessed by single photon emission computed tomography at 3 months.
"The higher D-dimer and F1+F2 levels in the early invasive group might be explained by early discontinuation of anticoagulation treatment," the authors suggest.
"Further studies are needed to establish the relation between these changes in markers and clinical outcome," they conclude in Thrombosis Research.
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