Atherosclerotic Infarction

Atherosclerotic Infarction

Atherosclerotic plaque at a bifurcation or curve in one of the larger vessels leads to progressive stenosis with the final large artery occlusion due to thrombosis of the narrowed lumen. Arteriosclerotic plaques may develop at any point along the carotid artery and the vertebral-basilar system, either extracranial or intracranial. The most common sites are the bifurcation of the common carotid artery into the external and internal carotid arteries, the origins of the middle and anterior cerebral arteries, and the origins of the vertebral from the subclavian arteries. The site of infarction depends on the collateral flow, but is usually in the distal fields or border zones. Specifying the degree of stenosis that will lead to perfusion difficulty is dependent on multiple factors and is often not easily defined. Classification schemes have relied on stenoses greater than 70 to 80% as more predictive of impending hemodynamic compromise.

Infarcts are also produced by emboli arising from the proximally-situated atheromatous lesions to otherwise healthy branches located more distal in the arterial tree. This mechanism of infarction has earned its own category, tandem arterial pathology. Embolic fragments may arise from extracranial arteries affected by stenosis or ulcer; stenosis of any major cerebral artery stem; the stump of the occluded internal carotid artery; and even from intracranial tail of the anterograde thrombus atop an occluded carotid. Making the diagnosis of an antherosclerotic infarction depends upon finding a stenosis or occlusion on carotid/vertebral Duplex Doppler, transcranial Doppler, magnetic resonance angiography, or even conventional cerebral angiography.

Cardiac Embolism

The most common sources of cardiac embolism include: atrial fibrillation, valvular heart disease (mitral stenosis, mitral regurgitation, rheumatic heart disease); intracardiac thrombus particularly along the left ventricular wall (mural thrombus) after anterior myocardial infarction or in the left atrial appendage in patients with atrial fibrillation; ventricular or septal aneurysm; and cardiomyopathies leading to stagnation of blood flow and an increased propensity for the formation of intracardiac thrombus.

Embolism is inferred when the brain image demonstrates an infarction confined to the cerebral surface territory of a single branch, combinations of infarcts involving branches of different divisions of major cerebral arteries, or hemorrhagic infarction. The difficult problem in arriving at a diagnosis of embolism is the identification of the occluding particle and the source. Mural thrombi and platelet aggregates are remarkably evanescent, as has been inferred by findings on angiography. Embolic fragments are found in over 75% of cases angiogramed within 48 hours of onset of the stroke, and are then gone when angiogram is repeated later. Embolic obstruction of an arterial lumen is cleared most commonly by recanalization and fibrinolysis. The evanescent quality of emboli may explain the wide variation in the frequency with which this subtype is diagnosed in retrospective or prospective studies of stroke.
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One Response to Atherosclerotic Infarction

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