A novel enoxaparin regime for ST elevation myocardial infarction patients undergoing primary percutaneous coronary intervention: a WEST sub-study.
ABSTRACT To evaluate the anticoagulation effect of subcutaneous (SQ) and intravenous (IV) enoxaparin through systematic anti-Xa sampling during primary PCI for acute STEMI.
Although appropriate anticoagulation is essential to maximize the efficacy and safety of primary PCI, the optimal dosing of enoxaparin in this setting is unclear.
STEMI patients randomized to primary PCI received ASA, clopidogrel 300 mg and enoxaparin 1 mg/kg SQ at earliest point of care, including prehospital. Plasma anti-Xa determination occurred just prior to and after primary PCI. Supplemental IV enoxaparin (0.3-0.5 mg/kg) and abciximab was encouraged prior to PCI.
The 1st anti-Xa level 56 min (median, IQR 47-77) post SQ enoxaparin was 0.28 U/ml (0.23-0.41); 85% of patients (28/33) were <0.5 U/ml (the recommended therapeutic level). Following PCI, 126 min (118-185) after SQ enoxaparin in those without IV dosing (8/33) the 2nd anti-Xa level was 0.44 U/ml (0.29-0.53); 6 of 8 patients remained <0.5 U/ml. With IV enoxaparin (25/33) the 2nd anti-Xa was 0.96 U/ml (0.82-1.16) 97 min (82-109) after SQ enoxaparin: all were >or=0.5 U/ml and 2 had levels 1.5 U/ml.
A single SQ enoxaparin dose fails to achieve anti-Xa levels >or=0.5 U/ml in the majority of STEMI patients. When combined with a strategy of supplemental IV enoxaparin, adequate anti-Xa levels were achieved in all patients with few having levels >1.5 U/ml. This regime of SQ injection with additional IV enoxaparin provides an attractive strategy enhancing effective early anti-thrombotic therapy at first medical contact prior to primary PCI.
- SourceAvailable from: Kurt Huber
Article: Low-Molecular-Weight Heparins[Show abstract] [Hide abstract]
ABSTRACT: The clinical spectrum of acute coronary syndromes (ACS) encompasses unstable angina, non-ST-elevation, and ST-elevation myocardial infarction (STEMI). Within an atherosclerotic plaque, disruption of the endothelium can lead to exposure of tissue factor, with platelet adhesion, activation and aggregation, along with activation of the coagulation cascade, culminating in thrombin formation and the development of a cross-linked fibrin clot at the site of injury. Therapy aimed at blocking thrombin formation is now an integral part of the current cardiovascular guidelines in the treatment of ACS. Although unfractionated heparin (UFH) has been the mainstay of antithrombin therapy in the past, it has numerous clinical and biochemical limitations, including substantial protein binding (leading to inconsistent bioavailability), a need for frequent monitoring and adjustment, unreliable and variable degrees of anticoagulation, significant platelet activation, risk of heparin-induced thrombocytopenia, and the inability to block clot bound thrombin. With all of these limitations of UFH, low-molecular-weight heparins (LMWHs) have emerged as attractive alternatives. This review discusses the mechanism of action of LMWHs, and summarizes available literature concerning the use of LMWHs in a variety of clinical settings. Included in this review is an analysis of both current and prior data showing LMWH is as effective as UFH in the conservative and invasive management of patients with ACS. As well, very recent data are evaluated showing the safety and efficacy of LMWHs used in patients transitioning to the cardiac catheterization laboratory, and in those patients undergoing elective or urgent percutaneous coronary intervention (PCI). We also appraise the literature, along with the very recent studies investigating the use of LMWHs as adjunctive therapy to fibrinolytics in patients with STEMI. Finally, we set forth real-world conclusions concerning the use of LMWHs in contemporary interventional practice, including elective PCI and the treatment of ischemic coronary artery disease in the context of rapid invasive management of ACS.American Journal of Cardiovascular Drugs 8(1). · 2.20 Impact Factor
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ABSTRACT: Risk, the possibility of loss or injury, is indeed a fixture in all aspects of our lives, from investing in the stock market to crossing the street. This concept that we now take for granted is in fact relatively novel. Some have argued that the ability to describe, estimate and control risk is a key distinction between past and modern times.1 In early civilization, the future of human beings was largely thought to be at the whim of the gods. The turning point came during the Renaissance when Chevalier de Méré, a French nobleman with an affinity for gambling and mathematics, challenged the famed French mathematician Blaise Pascal to solve an infamous puzzle: How to divide the stakes of an unfinished game of chance between two players when one of them is ahead.1,2 Collaboration between Pascal and Pierre de Fermat, a lawyer and a talented mathematician, resulted in a solution and consequently, the theory of probability was born. And it is this concept that is at the heart of modern cardiovascular medicine and research.Nephron Clinical Practice - NEPHRON CLIN PRACT. 01/2007;