Trial reportJournal of thrombosis and thrombolysis2012
Anticoagulation after subcutaneous enoxaparin is time sensitive in STEMI patients treated with tenecteplase.
Trial report in Journal of thrombosis and thrombolysis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adequacy of anticoagulation with enoxaparin as an adjuvant to fibrinolytic therapy for STEMI is unclear and has implications for both efficacy and safety; especially in patients undergoing a pharmacoinvasive reperfusion strategy. A subset of fibrinolytic-treated patients in the WEST study was enrolled in a systematic anti-Xa substudy. All received ASA and subcutaneous (SQ) enoxaparin 1 mg/kg followed by TNK-tPA. Incremental IV dosing of enoxaparin (0.3-0.5 mg/kg) was allowed prior to percutaneous coronary intervention (PCI). Anti-Xa blood samples were drawn prior and after angiography. Data are presented as percentages, medians and IQRs. Forty-five patients underwent angiography 2.8 h (2.5-14.6) after fibrinolytic. The pre-angiography median anti-Xa acquired 179 min (153-875) after SQ enoxaparin was 0.48 U/ml (0.42-0.65); a relationship between anti-Xa activity and time from administration was evident (r = 0.418, p < 0.007). Without supplemental IV enoxaparin the 2nd anti-Xa acquired 218 min (195-930) after SQ enoxaparin was 0.48 U/ml (0.41-0.80, n = 29). After supplemental IV enoxaparin, the 2nd anti-Xa was 0.92 U/ml (0.72-1.10, n = 16). An incremental IV enoxaparin dose and anti-Xa relationship was demonstrated (r = 0.59, p = 0.001) i.e. no IV 0.48 U/ml (0.41-0.80, n = 29), 0.3 mg/kg IV 0.81 U/ml (0.63-1.00, n = 12), and 0.5 mg/kg IV 1.34 U/ml (1.16-1.54, n = 4). Most fibrinolytic treated STEMI patients receiving weight-adjusted SQ enoxaparin (1 mg/kg) had subtherapeutic anti-Xa levels (<0.5 U/ml) after ~3 h. A strategy of supplemental 0.3 mg/kg IV enoxaparin at time of PCI reliably achieved anti-Xa ≥ 0.5 U/ml. Our findings provide a rational novel strategy for anti-thrombotic management in STEMI patients undergoing a pharmacoinvasive reperfusion strategy.
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