Coronary artery disease (CAD) is caused by atherosclerosis, a disease of the large arteries. Blockage of the coronary circulation can result in ischaemia and eventual myocardial infarction. Patients with CAD may be classified into two groups: stable CAD where patients are asymptomatic or have stable effort angina, and unstable CAD manifesting as acute coronary syndrome. The latter is further divided into patients with unstable angina and patients with myocardial infarction (MI). Stable angina is characterised by a relatively stable stenosis in one or more coronary arteries. Unstable CAD is characterised by an unstable atherosclerotic plaque with either rupture or erosion of the fibrous cap exposing the pro-thrombogenic core. This may lead to downstream vessel occlusion. The challenge is to identify those individuals who will progress from stable to unstable disease. This is likely to involve an ongoing inflammatory response, which is the basis for the disease. Leukocytes play a key role in this process. We conclude that the state of coronary artery disease-associated inflammation can be monitored by: (1) quantifying the expression of protein markers (cluster of differentiation or CD antigens) on the surface of peripheral blood mononuclear cells isolated from both stable and unstable angina patients; and (2) qualitative analysis of cellular fragments (microparticles) released into the plasma as a result of inflammation-induced apoptosis.