Antiplatelet therapy in cardiovascular disease
- 1Division of Cardiovascular Medicine, University Hospital, Nottingham, UK
- 2Cardiovascular Research Group, Northern General Hospital, Sheffield, UK
- Correspondence to: Dr M W H Behan Clinical Research Fellow, Division of Cardiovascular Medicine, University Hospital, Derby Road, Nottingham NG7 2UH, UK; miles.behannottingham.ac.uk
- Received 27 February 2003
- Accepted 8 June 2003
Abstract
Platelet activation and aggregation are considered to be central to arterial thrombus formation. Antiplatelet therapy is therefore important for both the treatment and prevention of cardiovascular disease. Aspirin, the most widely used antiplatelet agent, inhibits platelet cyclo-oxygenase and the conversion of arachidonic acid to the potent platelet agonist thromboxane A2 but does not prevent platelet activation occurring via various signalling pathways that are independent of thromboxane A2 release. Therefore a number of other compounds have been developed to complement aspirin’s beneficial effect. These include the thienopyridines (clopidogrel and ticlopidine), dipyridamole, and the αIIbβ3 (glycoprotein IIb/IIIa) receptor inhibitors.
- platelets
- aspirin
- clopidogrel
- dipyridamole
- αIIbβ3 (GPIIb/IIIa) receptor antagonists
- cardiovascular disease
- antiplatelet therapy
- ADP, adenosine diphosphate
- cAMP, cyclic adenosine monophosphate
- cATP, cyclic adenosine triphosphate
- cGMP, cyclic guanine monophosphate
- PCI, percutaneous coronary intervention
- PTCA, percutaneous transluminal coronary angioplasty







