Predominance of Nonatherosclerotic Internal Elastic Lamina Calcification in the Intracranial Internal Carotid Artery

Abstract

Background and Purpose-Calcification of the intracranial internal carotid artery (iICA) is an independent risk factor for stroke. These calcifications are generally seen as manifestation of atherosclerosis, but histological investigations are limited. The aim of this study is to determine whether calcifications in the iICA are present in atherosclerotic plaques, or in other parts of the arterial wall. Methods-Thirty-nine iICAs were histologically assessed, using digital microscopy to quantify the amount of calcification in the different layers of the arterial wall. Results-Calcifications were found in the intima, around the internal elastic lamina and in the medial layer of the arterial wall. In 71% of the arteries, internal elastic lamina calcification contributed most to the total calcified cross-sectional surface area. Internal elastic lamina calcification was unrelated to the occurrence of atherosclerotic intimal lesions. Intimal calcifications were most often associated with atherosclerotic lesions, but also many noncalcified atherosclerotic lesions were found. Conclusions-In

Computed Tomographic Distinction of Intimal and Medial Calcification in the Intracranial Internal Carotid Artery

“…[3] Three, medial calcification was found to comprise 71% of the dominant calcification burden and thereby it’s influence on physiopathology may be underestimated. [5] Four, clinically medial calcification is mostly thought to be a passive and chronic process, however, in a recent review it was shown that it is actually an active process resembling bone formation. [7] The limited knowledge on the clinical consequences and therapeutic options for medial calcification mainly comes from genetic syndromes and epidemiological studies outside the brain.…”

“…The arteries were divided in a proximal (C4 and C5 according to the classification system proposed by Bouthillier) and a distal (C6) segment (S1 Fig),[14] the intersection was perpendicular to the lumen Per segment, 2–3 histological slides, stained with hematoxylin and eosin and elastin van Giesson, were used to digitally analyse the total surface of calcifications in the intima, in the media and around the internal elastic lamina, as previously described. [5] Calcifications were characterized by quite sharp demarcated, acellular spots and areas, which were dark pink to purple colored on hematoxylin and eosin stained slides. For this study digital images of 142 slides were available.…”

“…[5] Because calcifications of the medial layer of the vascular wall and calcifications around the internal elastic lamina are thought to be related and are therefore from here on grouped as medial calcifications. [6]…”

The Use and Pitfalls of Intracranial Vessel Wall Imaging: How We Do It

“…DSA can depict stenotic lesions in large, as well as small arteries, including the A2 segment of the anterior cerebral artery, M2-M3 segments of the middle cerebral artery (MCA), P2 segment of the posterior cerebral artery, and even more peripheral segments of the intracranial arteries. With unenhanced CT, arterial VW calcifications can be detected that are associated with future stroke risk (10)(11)(12)(13). CT angiography is an easily accessible and fast procedure in patients with acute stroke and can depict stenotic lesions very accurately in the more proximal intracranial arteries and its branches (14).…”

Intracranial Carotid Artery Calcification Relates to Recanalization and Clinical Outcome After Mechanical Thrombectomy

“…Mechanisms underlying remain largely unknown, but it may be hypothesized that those patients with a higher burden of ICAC generally also have a worse condition of vessels more distal in the brain. 16,17 In addition, aside from intimal calcification, calcification of the internal elastic lamina 18 also occurs relatively commonly in the intracranial part of the internal carotid artery. This arterial stiffening may directly result in increased pulse pressure leading to damage in the microvasculature and surrounding tissue.…”