Abstract
Platelets play a pivotal role in the development of arterial thrombus formation in both the setting of plaque rupture during ST elevation myocardial infarction (STEMI) and in routine PCI through disruption of previously stable coronary plaques. In the setting of acute coronary syndromes, there are critical changes that occur within platelets that promote clot formation. These changes include (1) platelet adhesion mediated by von Willebrand factor and other adhesive proteins; (2) platelet activation, mediated in part by thromboxane A2; and (3) platelet aggregation due to fibrinogen cross-linking of platelets (Fig. 11.1). Many commonly used oral antiplatelet agents discussed subsequently work through mechanisms that disrupt one or more of these pathways.
| Original language | English (US) |
|---|---|
| Title of host publication | Coresource 4 |
| Publisher | Springer London |
| Pages | 143-156 |
| Number of pages | 14 |
| ISBN (Electronic) | 9781447145288 |
| ISBN (Print) | 9781447145271 |
| DOIs | |
| Publication status | Published - 2014 |
| Externally published | Yes |
Keywords
- Acute Coronary Syndrome
- Major Bleeding
- Percutaneous Coronary Intervention
- Primary Percutaneous Coronary Intervention
- Unfractionated Heparin
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