Carotid atherosclerosis is a chronic disease of the carotid arteries, with potentially-life threatening acute complications, particularly stroke. Atheromata can become clinically-evident either by the growth of the lesion within the vascular wall, until blood flow through the lumen is obstructed, and/or by provoking thrombo-emboli, with or without blood flow obstruction, by exposing the bloodstream to throm-bogenic substances within the lesion.
In response to injury, inflammation may moderate the healing of the vessel wall, as in other tissues. In atherogenesis, the vascular healing process goes awry. Atheromata are made by insudates of inflammatory cells and inflammants, particularly lipids, and, in advanced lesions, by the hyperplasia of vascular tissue. Inflammatory cells and molecules are drawn into atherosclerotic lesions both through the intima and outer layers of the vessel wall. The internal microenvironment of the atheroma is a haywire network of cell signaling and a poisoned atmosphere, with oxidants which derange inflammatory and endothelial cells. Vascular inflammation can perpetuate itself, by stimulating the (mal)formation of new, incompetent vasa vasorum which spill inflammatory cells and substances into the lesion. If the vessel wall fails to heal, after decades, then the endothelium loses its capacity for further self-repair; such endothelial senescence opens the intimal door to tissue inflammants.
Yet not all carotid atheromata become clot-provoking lesions. Some resolve into silent fibrotic or calcific scars. The incidence and fate of nascent atheromata are determined at all levels, even beyond the plaque itself, reflecting a profile of the whole patient, from genetics, cellular events, and blood biochemistry , to patient diet and behavior. For example, the 'vulnerable patient' and the patient who is less or not vulnerable to a stroke may, theoretically, have identical plaques, but one patient is 'vulnerable' because his or her blood has a composition with a greater predisposition to clotting, when exposed thrombogenic factors within the plaque. As such, other non-imaging clinical tests, particularly serum analyses, will play a great role, in risk-stratifying patients with carotid atherosclerosis.
The character of the plaque is a key to distinguishing the vulnerable patient, as carotid symptoms and events are associated with specific plaque characteristics. The concentration of inflammation in the cap and rupture of malformed vessels frequently mark the 'vulnerable plaque'. Noninvasive imaging has begun to provide physicians with the ability to detect and measure the plaque features which precipitate carotid stroke, on anatomical and biochemical levels, as subsequent chapters will discuss.
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