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Atherosclerosis and Thrombus Formation
Pathology
 The
pathogenic process leading from the development of the cerebrovascular
or extracranial atherosclerosis of the occurrence of acute
ischemic stroke and consequent cell damage is complex, and
many of the intermediary damage is complex, and many of the
intermediary steps are not completely understood.
Ischemic stroke may arise from the atherosclerotic
large cerebral arteries (eg, carotid, middle cerebral, and
basilar arteries) or atherosclerotic small cerebral arteries
(eg, lenticulostriate, basilar penetrating, and medullary
arteries); ischemic stroke may also be cardioembolic in origin.
Most investigations of atherogenesis have focused on the coronary
arteries, but, with some possible exceptions, similar processes
occur in the cerebral circulation. In the brain, the
process is better characterized in the larger arteries than
in small arteries supplying deep cerebral white matter.
Some evidence suggests that the underlying pathogenetic process
in small arteries may differ from that described in larger
arteries [DeGraba TJ, et al. In: Barnett HJM, et al
(eds). Stroke. Pathophysiology, Diagnosis, and Management.
New York, Churchill Livingstone, 1992:29].
Atherogenesis is a decades-long process in which
the lumen of a blood vessel becomes narrowed by cellular and
extracellular substances to the point of obstruction [Breslow
JL. Science. 1996;272:685.] An autopsy study of coronary
arteries and aortas in 1,160 people who died between full-term
birth and age 29 years found that the earliest lesion of atherosclerosis
is the fatty streak [Stary HC. Atherosclerosis. 1989;9 (suppl
1): 119]. Approximately 65% of children between ages
12 and 14 years had such lesions. Fatty streaks, which
are grossly visible as areas of yellowish discoloration of
the surface of the intimal layer of the vessel wall, are widely
distributed throughout the coronary arterial vasculature.
On microscopy, the lesions primarily consist of lipid-filled
macrophages (foam cells).
The autopsy study revealed that an additional
8% of children in late childhood or early adolescence had
progressed beyond the fatty-streak stage and had developed
more advanced, focal lesions. These lesions, which occur
only in areas of eccentric thickening (ie, at branch points
of the arterial vessel), are characterized by the addition
of massive extra-cellular lipids that displaced normal cells
and matrix.
In the third decade of life, some atheromatous
lesions evolve into complicated fibrous plaques, consisting
of a central acellular area of lipid covered by a cap of smooth
muscle cells and collagen. Caps tend to form slowly
at first, but with deposition of platelets and fibrin on the
surface -- which appears to be the result of endothelial injury
-- the caps thicken quickly, possibly as a result of thrombosis-dependent
fibrotic organization.
The progression of early atherosclerotic lesions
to clinically relevant advanced atherosclerotic lesions occurs
with increased frequency in persons with risk factors for
atherosclerotic disease (eg, heypercholesterolemia, hypertension,
cigarette smoking) [Ip JH, et al, 1994].
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