Routine thienopyridine pretreatment for acute coronary syndrome without ST elevation

BMJ 2014; 349 doi: https://doi.org/10.1136/bmj.g6282 (Published 24 October 2014) Cite this as: BMJ 2014;349:g6282
  1. Jeffrey J Rade
  1. 1Division of Cardiology, University of Massachusetts Medical School, Worcester, MA 01655, USA
  1. jeffrey.rade{at}umassmed.edu

It’s time to rethink an ageing strategy

Acute coronary syndrome (ACS) results from thrombus formation at the site of ruptured or eroded atherosclerotic plaques, which restricts coronary blood flow resulting in myocardial ischemia and injury. Thrombosis is initiated by the exposure of tissue factor and collagen to the circulating blood, which leads simultaneously to local triggering of the coagulation cascade and activation and adhesion of platelets. Activated platelets release secondary agonists, including thromboxane and ADP, which recruit additional waves of platelet adhesion that facilitate thrombus growth. Given their central pathogenic importance, pharmacological inhibition of both platelet activation and thrombin generation have long been cornerstone treatments for the full spectrum of ACS.

Current European and North America guidelines provide a class I recommendation for the administration of dual antiplatelet therapy to patients presenting with non-ST elevation ACS consisting of aspirin to inhibit platelet thromboxane production and an ADP (P2Y12) receptor antagonist, such as the thienopyridine clopidogrel, to prevent secondary platelet activation.1 2 In the linked research article, Bellemain-Appaix and colleagues (doi:10.1136/bmj.g6269) explore …

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