Imaging diagnosis
Case 182
【Progress】
He was prescribed antiplatelet agent to prevent from secondary thrombus formation at the atheromatous lesion of right internal carotid artery.
【Discussion】
There are two types of carotid artery stenosis: web and atheroma plaque. Both stenosis can have lipid accumulation in the vessel wall. Carotid artery web arises from fibromuscular dysplasia (1, 2), and atheroma plaque arises from minute intimal injury due to hypertension or diabetes mellitus.
As typical diseases of atheroma plaque, two occlusive diseases are listed; carotid artery stenosis and coronary artery stenosis. There exists basically common mechanism in both lumen stenosis but includes the different aspect (3). Both occlusion initiates from a minor injury of intima because of the stress to intima such as hypertension or diabetes. Lipid usually attaches to lipoprotein. Cholesterol attaches to lipoprotein; Low density lipoprotein (LDL) carries cholesterol to the vessel: High density lipoprotein carries cholesterol from vessel to liver. LDL cholesterol accumulation to the injury site induces macrophage accumulate and phagocyte LDL cholesterol granules, becoming foamy cells. Foamy cells are also phagocyted by other macrophages, inducing giant cells. When foamy cells die and other macrophages cannot dispose them, LDL cholesterol accumulation initiate in the vessel wall (3).
Histologic examination of the atheroma plaque reveals cholesterol crystals, lipid-rich necrotic core, fibrous cap, smooth muscle layer and endothelium in both stenosis of coronary artery and carotid artery. Vulnerable and unstable plaque includes the larger size of plaque, the presence of hemorrhage and lipid component and the thinner fibrous cap than stable plaque. Stable plaque is known to have thick fibrous cap and coarse calcification (4).
The difference aspect is that neovascularization from vaso vasorum to the atheroma in carotid artery stenosis was evident but not in coronary artery stenosis (4-6). When cholesterol crystals thicken and accumulate, their edges become more sharp, inducing to injure the neovessel and the fibrous cap. It brings about hemorrhage in atheroma plaque and ulceration of plaque surface, respectively. Hemorrhage causes expansion of plaque and narrowing of lumen. Further, it brings about the rupture of fibrous cap, inducing peripheral embolization of the atheroma component. Hence, the presence or absence of hemorrhage in atheroma plaque is an imperative factor to predict the future symptomatic brain stroke (5, 6).
There are several non-contrast blood black imaging MRI methods (7, 8). We performed time of flight, MRA and blood black imaging using 3D fat suppression spin-echo with various flip angles. It showed high signal intensity in atheroma plaque of right internal carotid artery corresponded to the stenotic lesion depicted on MRA and time of flight, indicative of hemorrhagic plaque. Because our patient is not symptomatic, he was under watchful observation, being prescribed anti-platelet medicine.
【Summary】
We present an eighty tow-year-old male presented in our hospital for tachycardia emerged during cataract surgery in a local clinic. Neck echogram showed stenosis of right internal carotid artery. Blood black imaging using 3D fat suppression spin-echo showed high signal intensity at the stenotic lesion of the right internal carotid artery, indicative of hemorrhagic atheroma. It is borne in mind that although the atheroma mechanism in carotid artery is similar as in coronary artery such as that they have the common components such as cholesterol crystals, lipid-rich necrotic core, fibrous cap, smooth muscle layer and endothelium, the difference aspect is that neovascular vessels develop to the atheroma in carotid artery but not that in coronary artery. When cholesterol crystal with sharp edge injures neo-vessels, inducing hemorrhage, making the lumen narrower and rupture thin fibrous cap, leading brain embolism. Blood black imaging plays an important role of whether the atheroma is stable or unstable and vulnerable.
【References】
1.Choi PM, et al. Carotid Webs and Recurrent Ischemic Strokes in the Era of CT Angiography. (2015) AJNR. American journal of neuroradiology. 36 (11): 2134-9.
2.Jonathan M, et al. Mandell. Carotid artery web and ischemic stroke. (2017) Neurology. 88 (1): 65.
3.Sigala F, et al. Coronary versus carotid artery plaques. Similarities and differences regarding biomarkers morphology and prognosis. Curr Opin Pharmacol. 2018;39:9-18.
4.Butcovan, D, et al. Assessment of vulnerable and unstable carotid atherosclerotic plaques on endarterectomy specimens. Exp Ther Med. 2016 May; 11(5): 2028–2032.
5.Horie N, et al. Communication of inwardly projecting neovessels with the lumen contributes to symptomatic intraplaque hemorrhage in carotid artery stenosis. J Neurosurg. 2015;123(5):1125-32.
6.Sedding DG, et al. Vasa Vasorum Angiogenesis: Key Player in the Initiation and Progression of Atherosclerosis and Potential Target for the Treatment of Cardiovascular Disease. Front Immunol. 2018 Apr 17;9:706
7.Edjlali M, et al. 3D fast spin-echo T1 black-blood imaging for the diagnosis of cervical artery dissection. AJNR Am J Neuroradiol. 2013 Sep;34(9):E103-6.
8.Monica Sigovan, M, et al. 3D black blood MR Angiography of the Carotid Arteries. A simple sequence for plaque hemorrhage and stenosis evaluation. Magn Reson Imaging. 2017 Oct; 42: 95–100.
2020.3.4