Thrombus formation in a coronary artery with obstruction of coronary blood flow and reduction in oxygen SUPPLy to the myocardium produces the acute coronary syndromes (ACS). These thrombotic episodes largely occur in response to atherosclerotic lesions that have progressed to a high-risk inflammatory/prothrombotic stage. Although apparently distinct, the atherosclerotic and thrombotic processes appear to be closely interrelated as the causal presentation of ACS through a complex multifactorial process called atherothrombosis. The composition of the plaque, rather than the stenosis, appears to be the main determinant of risk of plaque rupture and the ensuing thrombotic episode. High-risk rupture-prone lesions usually have a large lipid core, a thin fibrous cap, and high density of inflammatory cells. Platelets have been shown to play a key pathogenic role in atherothrombosis, although platelet aggregation and activation of the coagulation cascade are complementary processes. In fact, thrombosis may also be triggered by a hyperthrombogenicity due to systemic factors. Finally, platelets have also been shown to contribute to the complex cell-vessel wall interactions that underlie the atherothrombotic process by mediating the inflammatory response and participating in progenitor cell recruitment.
|Title of host publication||Therapeutic Advances in Thrombosis, Second Edition|
|Publisher||Blackwell Publishing Ltd.|
|Number of pages||11|
|State||Published - 3 Oct 2012|
- Blood flow
- Platelet receptors
- Vessel wall