There now exists overwhelming evidence supporting the inflammatory hypothesis of atherosclerotic vascular disease. Cellular interactions between leukocytes, platelets and endothelial cells are critical in the initiation and progression of atherosclerotic disease. Acute coronary syndromes, namely unstable angina and acute myocardial infarction, and thromboembolic stroke represent acute unstable phases of atherosclerotic vascular disease that are associated with significant morbidity and mortality. Atherosclerotic plaque disruption, with consequent platelet aggregation and thrombosis, is the principal mechanism by which atherosclerosis leads to the acute ischaemic syndromes of acute myocardial infarction, stroke and sudden cardiac death. Pathophysiological studies have confirmed the importance of inflammation in the pathogenesis of these acute vascular events by demonstrating (i) acute inflammatory reaction in unstable atherosclerotic plaques, (ii) a systemically detectable acute inflammatory response, and (iii) elevated levels of circulating inflammatory markers. The clinical importance of inflammation in atherosclerotic cardiovascular disease can be seen in the development of novel screening programs for detecting asymptomatic disease and designing novel anti-inflammatory therapies for established disease.