Editorial

Thrombotic and Fibrinolytic Factors in Acute Coronary Syndrome

Authors: Sarabjeet Singh, MD, Mukesh Singh, MD, MRCP, Sandeep Khosla, MD, FACC

Abstract

It is now generally accepted that intracoronary thrombosis after plaque disruption is a major cause of the acute coronary syndromes (ACS) of unstable angina, myocardial infarction, and sudden cardiac death. Thrombus arises from procoagulant changes in complex plaques, which trigger both platelet activation and coagulation pathways.1 The magnitude of the local thrombogenic response also contributes to occlusive complications after percutaneous coronary intervention (PCI), either via thrombus formation or by other mechanisms.2,3 High levels of the biochemical markers of the activation of the hemostatic mechanism have been found in patients with ongoing intracoronary thrombosis and may therefore be helpful in identifying patients who are at the greatest risk of an unfavorable outcome.

This content is limited to qualifying members.

Existing members, please login first

If you have an existing account please login now to access this article or view purchase options.

Purchase only this article ($25)

Create a free account, then purchase this article to download or access it online for 24 hours.

Purchase an SMJ online subscription ($75)

Create a free account, then purchase a subscription to get complete access to all articles for a full year.

Purchase a membership plan (fees vary)

Premium members can access all articles plus recieve many more benefits. View all membership plans and benefit packages.

References

1. Selwyn AP. Prothrombotic and antithrombotic pathways in acute coronary syndromes. Am J Cardiol 2003;91(suppl 1):3H–11H.
 
2. Edelman ER, Rogers C. Pathobiologic responses to stenting. Am J Cardiol 1998;81(7A):4E–6E.
 
3. Orford JL, Selwyn AP, Ganz P, et al. The comparative pathobiology of atherosclerosis and restenosis. Am J Cardiol 2000;86(4B):6H–11H.
 
4. Turker Y, Dogan A, Ozaydin M, et al. Association of thrombotic and fibrinolytic factors with severity of culprit lesion in patients with acute coronary syndromes without ST elevation. South Med J 2010;103:289–294.
 
5. Maresca G, Di Blasio A, Marchioli R, et al. Measuring plasma fibrinogen to predict stroke and myocardial infarction: an update. Arterioscler Thromb Vasc Biol 1999;19:1368–1377.
 
6. Danesh J, Collins R, Appleby P, et al. Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease: meta-analyses of prospective studies. JAMA 1998;279:1477–1482.
 
7. Blombäck B, Blombäck M, Edman P, et al. Human fibrinopeptides: isolation, characterization and structure. Biochim Biophys Acta 1966;115:371–396.