Abstract
The incidence of carotid artery stenosis is debatable based upon the findings of the NASCET, ECST and ACAS reports. We generally determine the incidence of stenosis in patients through the limited directions by angiographic methods. However, there are likely some shortcomings of this evaluation procedure with the pathogenesis of carotid artery stenosis.
The importance of the carotid artery wall has recently been established. In general, these characteristics can be examined using ultrasound sonography. While the degree of ulceration, endothelial condition, lipid pool, thin cap and plaque intensity can ordinarily be examined, we are especially attempting to detect the existence of neovascularization in plaque. The importance of neovascularization in atherosclerosis has been recognized. Neovascularization is one of the pathological factors introducing plaque hemorrhage and rupture, which can result in carotid artery occlusion and artery-to-artery embolism.
Pulse inversion harmonic image (PIHI) using pulse inversion to eliminate and strengthen the harmonic frequency is more effective than conventional harmonic imaging. We can detect a tissue perfusion by contrast sonographic imaging with PIHI, and its clinical application has already been reported. Consequently, we use this method to test for cardiac infarction, liver tumor, brain tumor and cerebrovascular diseases.
We examined carotid artery wall perfusion (CAWP) and the rule of neovascularization within the plaque by this method.
The routes of vascular wall feeding are as follows:
1) Luminal diffusion feeds the vascular wall from the endothelium to the inner part of the medium and 2) the vasa vasorum feeds it from the adventitia to the outer part of the medium. Consequently, neovascularization does not occur at the former vascular wall region. However, some plaque is resistant to neovascularization.
As a result, we attempt to detect plaque using this method, and we have already described a classification of CAWP findings.
Type I exhibits no perfusion and lack of neovascularization.
Type II exhibits partial perfusion of CAWP that is indicative of mild neovascularization.
Type III exhibits multiple perfusion of CAWP that is indicative of moderate neovascularization.
Type IV exhibits general perfusion of CAWP that is indicative of neovascularization of the whole plaque. Type III and IV are usually observed in patients with intramural hemorrhage or artery-to-artery embolism.
We propose the following mechanism for plaque development.
The beginning of atherosclerosis→in some, neovascularization on the plaque development→The small neovasculature is vulnerable. Consequently, damage can occur by mechanical stimulation→then intramural hemorrhage can occur→resulting in the onset of ischemic symptoms as the development of stenosis or embolism.
We intend to examine the incidence of carotid artery stenosis with or without neovascularization and carefully observe such patients because of the rapid development of plaque, plaque rupture, occlusion of main extracranial arteries and artery-to-artery embolism.
