Circulation. 1998;98:287-289
(Circulation. 1998;98:287-289.)
© 1998 American Heart Association, Inc.
Low-Molecular-Weight Heparins
An Intriguing New Twist With Profound Implications
Elliott M. Antman, MD;
; Robert Handin, MD
From the Cardiovascular Division (E.M.A.) and Department of Medicine
(R.H.), Brigham and Women's Hospital, Boston, Mass.
Correspondence to Elliott M. Antman, MD, Director, Samuel A. Levine Cardiac Unit, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail eantman@bustoff.bwh.harvard.edu
Key Words: Editorials • heparin • thrombin
Modern
antithrombotic therapy for acute coronary syndromes rests on a
growing body of basic and clinical evidence that rupture or erosion of
the surface of a vulnerable plaque sets in motion a sequence of events
culminating in thrombus formation in the culprit
vessel.1 When the contents of a vulnerable plaque
are exposed to the bloodstream, platelets adhere to the
subendothelial matrix, release ADP and
thromboxane A2, and amplify the
generation of thrombin.2 As a result, a
platelet aggregate begins to develop. In addition, the coagulation
cascade is activated and fibrin strands are formed.
Importance of Thrombin
Thrombin (factor IIa) plays a pivotal role in the processes
described above because of its extensive procoagulant and prothrombotic
actions.3 In addition to catalyzing the
transformation of soluble fibrinogen into fibrin monomers and
activating factor XIII to produce cross-linked fibrin, thrombin
promotes clot formation by activating factors V and VIII. It is also
one of the most potent agents responsible for platelet adhesion,
activation, and aggregation. In vessels with a diseased
endothelium, thrombin promotes the release of the
vasoconstrictor endothelin 1. Importantly, thrombin also potentiates
the proliferative effects of multiple growth factors and is a key
mediator of early smooth muscle cell proliferation after
arterial injury.
There is now abundant evidence that thrombus formation can be
prevented by direct or indirect inactivation of thrombin or by
inhibition of thrombin production via the intrinsic or
extrinsic limbs of the coagulation pathway.3
Unfractionated heparin, the standard antithrombotic agent in clinical
practice, is a glycosaminoglycan, consisting of
chains of . . . [Full Text of this Article]
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