Inflammatory and thrombotic mechanisms in coronary atherosclerosis
- 1Cardiology Unit, Athens University Medical School, Athens, Greece
- 2Cardiology Unit, Hammersmith Hospital, Du Cane Road, London, UK
- 3Cardiology Unit, Saint Vincent’s Hospital Medical Center, New York, USA
- Correspondence to:
Dr Dimitris Tousoulis, Cardiology Unit, Athens University Medical School, S Karagiorga 69, 16675, Athens, Greece;
drtousoulis{at}hotmail.com
- Accepted 7 April 2003
Abstract
Many molecular and cellular mechanisms link inflammation and haemostatic mechanisms. Inflammation, and perhaps chronic infection, may play important roles in the initiation and progression of atherosclerosis. Atherosclerotic lesions are heavily infiltrated by cellular components associated with inflammation (macrophages and T lymphocytes), and acute plaque rupture is also associated with inflammatory components. Several markers of systemic inflammation may predict future cardiovascular events in apparently healthy subjects as well as in patients with chronic and acute syndromes. There may thus be therapeutic potential in modifying the atherosclerotic, vasomotor, and thrombotic components of ischaemic heart disease.
- CRP, C reactive protein
- ICAM, intercellular adhesion molecule
- IL, interleukin
- LDL, low density lipoprotein
- Lp(a), lipoprotein(a)
- MCP, monocyte chemoattractant protein
- NF-κB, nuclear transcription factor κB
- PAI, plasminogen activator inhibitor
- TGF, transforming growth factor
- TNF, tumour necrosis factor
- VCAM, vascular cell adhesion molecule
- VLA, very late activation antigen
