(Circulation. 2001;103:1718.)
© 2001 American Heart Association, Inc.
Editorial |
Inflammation and Thrombosis
The Clot Thickens
From the Brigham and Women’s Hospital, Boston, Mass.
Correspondence to Peter Libby, MD, Brigham and Women’s Hospital, 221 Longwood Ave, LMRC 307, Boston, MA 02115. E-mail plibby@rics.bwh.harvard.edu
Key Words: Editorials • growth substances • thrombosis • platelets • atherosclerosis • inflammation
Textbooks often portray thrombosis as a bland protective mechanism critical for stanching blood loss after injury: the prick of a lancet, the wound of a scalpel, or the predator’s fangs neatly trigger a proteolytic cascade culminating in fibrin formation and cross-linking. However, in diseases such as atherosclerosis, the picture differs substantially from this simplistic model. In the natural history of atherosclerosis, thrombosis involves an inciting injury more subtle than a wound. In such pathological states, the importance of an intricate interface between inflammation and thrombosis becomes apparent.
Septic Shock: An Extreme Example of Inflammatory Activation of the Endothelium
Consider the case of septic shock, a dramatic example of the link between inflammation and thrombosis. When Gram-negative bacteria release their endotoxin into the bloodstream, the lipopolysaccharide can change endothelial lining of blood vessels from an anticoagulant, profibrinolytic surface into one that promotes thrombosis. Bacterial endotoxin potently stimulates expression of the gene encoding tissue factor, a procoagulant molecule that multiplies manyfold the activity of coagulation factors VIIa and Xa. Endotoxin also can augment endothelial cell production of fibrinolytic inhibitor plasminogen activator inhibitor-1 (PAI-1). These alterations in endothelial function lead to the frequent clinical scenario of disseminated intravascular coagulation, a common concomitant of Gram-negative sepsis.
Less-global endothelial activation may contribute to
thrombosis in situ in more-chronic diseases such as atherosclerosis.
Many inflammatory mediators found in human atherosclerotic plaques can
augment tissue factor gene expression by endothelial cells. For
example, interleukin-1 (IL-1) or tumor necrosis factor not only augment
tissue factor gene expression but also PAI-1 production by human
endothelial cells. Bacterial endotoxins within atheroma
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