The natural history of carotid artery disease.

ATHEROSCLEROSIS is a progressive disease which is usually silent clinically until late in its course. The reasons for the clinical silence are apparent upon study of the pathology of the disease. Early atherosclerosis is an inflammatory disease which destroys the normal anatomy of the arterial wall. The destruction of the elastin in the wall causes arterial dilation. Only late in its course does the thickening and scarring produced by atherosclerosis narrow and finally occlude the arterial lumen, although ulceration of an arteriosclerotic lesion may lead earlier in the course of the disease to thromboembolism, with end-organ damage. The first sign of advancing atherosclerotic stenosis is often an arterial bruit. This occurs when the arterial lumen is compromised to about 50% of its original lumen diameter, which is equivalent to 25% of the original cross-sectional area. Symptoms usually do not occur until vessel diameter is narrowed by 80% or so, i.e., until the diameter is 20% of its original value (and cross sectional area only 4% of that of the normal vessel!). In summary, early atherosclerosis is mural, not luminal. Stenosis is a late occurrence in the course of atherosclerosis, and its often apparently rapid progression is the end of a long pathologic process. Not surprisingly, neither noninvasive methods nor angiography are helpful in detecting early atherosclerosis. Furthermore, very little is known about the natural history of the disease — not only how long it takes for a lesion to progress from its earliest stages to a significant stenosis, but also the rate of progression from a 25% diameter stenosis to an 80% stenosis or a complete occlusion. Nowhere are these questions more pertinent than in the carotid circulation. The carotid bifurcation and the proximal internal carotid arteries are only a few centimeters from the skin surface. The latter vessels supply much of the blood to the brain; an exquisitely sensitive end-organ. Both scientifically and clinically, we would like to know the prevalence of carotid atherosclerosis, how often it progresses to throrhboembolism and occlusion, what influence risk factors like age, sex, blood pressure, cigarette smoking, blood lipids, and blood sugar have on the course of the disease, and what risks intervention with angiography and surgery entail. We need to