Fatty deposits formed on arterial walls lead to atherosclerosis but it is the interplay between these deposits and the vessel walls which governs the growth of plaque formation. Cells in the vessel walls trigger the body's defenses and through a series of mechanisms lead to the promotion of plaque growth. Crucially however the vast majority of acute coronary syndromes such as, myocardial infarction, and sudden ischaemic cardiac death is caused by atherosclerotic plaque rupture and not from a stenosis growing and blocking the blood flow. Although the stress caused by the blood flow does play a role in plaque rupture, it has been found that the degree of stenosis is a relatively minor factor in predicting which plaques are most prone to rupture. In fact, atherosclerotic plaques expand into the vessel wall during much of their existence and this can make their detection problematic.