Catheter thrombosis during primary percutaneous coronary intervention for acute ST elevation myocardial infarction despite subcutaneous low-molecular-weight heparin, acetylsalicylic acid, clopidogrel and abciximab pretreatment.

ABSTRACT

BACKGROUND: Subcutaneous enoxaparin is increasingly employed as the antithrombin of choice in non-ST elevation myocardial infarction and in conjunction with various fibrinolytic regimens in acute ST elevation myocardial infarction (STEMI). Few data exist describing the use of subcutaneous or intravenous enoxaparin as an anticoagulant in the highly thrombotic setting of primary percutaneous coronary intervention (PCI) for STEMI. METHODS: The Which Early ST Elevation Therapy (WEST) study compared fibrinolysis (with and without early cardiac catheterization) with primary PCI in a setting that expedited both strategies on first medical contact. Patients assigned primary PCI are administered acetylsalicylic acid 325 mg, clopidogrel 300 mg and subcutaneous enoxaparin 1 mg/kg before transport to a PCI centre. Of 36 initial patients treated with primary PCI, three patients had procedures that were complicated by extensive thrombosis within coronary catheters and on PCI equipment. RESULTS: Index cases were men aged 43 to 68 years who presented with confirmed STEMI and angiographically proven acute total or subtotal occlusion of a major epicardial coronary segment. During PCI, performed 76 min to 102 min following enoxaparin administration, a clot developed within the guide catheter or on the coronary guidewires and balloon catheter shafts, thus necessitating the replacement of all PCI equipment. In one case, there was evidence of continued intracoronary clot propagation and embolization. CONCLUSION: A single, conventional, weight-adjusted dose of subcutaneous enoxaparin before expedited primary PCI for STEMI may not provide a reliable antithrombotic effect. Supplementary intravenous enoxaparin is now strongly recommended within the WEST study, and a substudy evaluating pre- and postprocedural antifactor Xa activity has been initiated.