ABSTRACT
Introduction 17 Histologic appearance of the atherosclerotic artery 17 Endothelial dysfunction and lesion initiation 21 Accumulation of cholesterol, and its metabolism
within the arterial wall 22 Inflammation – role of the macrophage 24
Healing – role of the vascular smooth muscle cell 25 Plaque disruption and thrombosis 27 Atherosclerosis in women 29 Summary 30 Acknowledgment 30 References 31
Atherosclerosis is as an abnormal thickening of the vessel wall comprising lipids, inflammatory cells, and fibrous tissue. Pathologic studies have shown that atherosclerotic lesions appear in infancy,1 but by adulthood the extent to which the vascular tree is afflicted, the rate of lesion progression, and the microscopic composition of the lesions varies tremendously between individuals. Despite its presence in all adult humans, in the majority, atherosclerosis remains asymptomatic throughout life. In others, complications develop, characteristically from late middle age onwards. Complications such as angina and intermittent claudication are caused by transient episodes of ischemia, as a result of atherosclerotic narrowing of the arterial lumen. Typically, symptoms occur when oxygen demand in the tissue supplied by the obstructed artery is high. Angina brought on by exercise is a typical example. Life-threatening complications such as myocardial infarction (MI) and cerebral infarction are usually a result of sudden severe ischemia caused by thrombotic arterial occlusion.
