Heparin, a glycosaminoglycan of varying polysaccharide units and molecular
weights, has been shown to reduce ischemic events beyond that of aspirin alone
in the setting of an acute coronary syndrome (ACS).1 This
benefit translated into a class I indication for unfractionated heparin in
the 2000 American College of Cardiology/American Heart Association (ACC/AHA)
treatment guidelines for non–ST-segment elevation ACS.2 Unfractionated
heparin has several known limitations, however, including a narrow therapeutic
window, poorly predictable kinetics, platelet activation, and inability to
inhibit clot-bound thrombin.
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