Pathomorphometry of ruptured intracranial vertebral arterial dissection: adventitial rupture, dilated lesion, intimal tear, and medial defect

Abstract

Object Subarachnoid hemorrhage (SAH) due to ruptured intracranial vertebral artery (VA) dissection is a life-threatening disease. Angiographic and symptomatic prognostic factors for rupture and rerupture have been investigated, but the pathological characteristics have not been fully investigated. The authors aimed to investigate these features by performing a pathomorphometic study of ruptured intracranial VA dissections. Methods This study included 50 administrative autopsy cases of fatal SAH due to ruptured intracranial VA dissection among 517 fatal nontraumatic cases of SAH occurring between March 2003 and May 2011. Pathomorphometry was performed using serial 5-μm histological cross-sections with elastica van Gieson staining from each 0.2-mm segment around the ruptured intracranial VA. The longitudinal lengths of 4 types of vascular lesions—adventitial ruptures, dilated lesions where the internal elastic lamina (IEL) was ruptured with adventitial extension, intimal tears where the IEL was ruptured, and medial defects—were calculated based on the numbers of the slides in which these lesions were continuously detected (minimum 2 adjoining slides). The distance from the vertebrobasilar junction to the center of adventitial rupture was also calculated in 37 cases. Results All cases showed one adventitial rupture with a mean length of about 1.9 ± 1.1 mm. The center of the adventitial rupture was located 5.0–26.8 mm (mean 14.6 ± 5.5 mm) from the intracranial VA bifurcation. Adventitial ruptures existed in the centers of dilated lesions, where the adventitia was highly extended. Other vascular lesions were serially observed surrounding the adventitial rupture. The mean lengths of dilated lesions, intimal tears, and medial defects were 9.4 ± 4.8 mm, 13.2 ± 6.3 mm, and 15.6 ± 7.2 mm, respectively. The lengths between proximal lesions and distal lesions from the center of the adventitial rupture for both medial defects and intimal tears were significantly longer at proximal lesions than at distal ones (chi-square test, p < 0.01). Conclusions Every ruptured intracranial VA dissection has a single point of adventitial rupture where the adventitia was maximally extended, so dilation appears to be a valuable predictive factor for hemorrhagic intracranial VA dissections. The adventitial ruptures were as small as 2 mm in length, and clinically detectable dilated lesions were about 9 mm in length. However, vascular vulnerability caused by IEL ruptures and medial defects existed more widely across a length of VA of 1.3–1.5 cm. Comparatively broader protection of the intracranial VA than the clinically detected area of dissection might be desirable to prevent rebleeding. Broader protection of proximal lesions than distal lesions might be effective from the viewpoint of site distribution of vascular lesions and blood flow alteration to the pseudolumen caused by the dissecting hematoma. Medial defects are the most widely seen lesions among the 4 types of vascular lesions studied. Medial degenerative disease, known as segmental arterial mediolysis, is suspected in the pathogenesis of intracranial VA dissections.

Pathomorphological Examination of Patients with the Simultaneous Rupture of Dissecting Intracranial Vertebral and Intraperitoneal Arteries: Involvement of Segmental Arterial Mediolysis in Intracranial Artery Dissection

“…We previously reported the presence of medial defect/ necrosis prior to IVA dissection. 1) In addition, in this study, in autopsy cases of the simultaneous onset of IVA dissection and intraperitoneal muscular artery dissection, we confirmed medial defect/necrosis of both arteries, suggesting the involvement of SAM in the pathogenesis of intracranial artery dissection. To clarify the pathogenesis, further detailed examination of intraperitoneal vascular lesions must be conducted in patients with intracranial artery dissection.…”

“…An animal experiment This was similar to the results of our previous study. 1) Adventitial rupture due to excessive extension by hematoma from arterial dissection may have led to fatal subarachnoid hemorrhage in a short period. In addition, we confirmed the repair response to the blood vessel at the site of rupture using anti-S100A4-antibody staining.…”

“…We previously investigated histopathological findings in 50 autopsy cases of the rupture of the dissecting intracranial vertebral artery (IVA), and reported that segmental arterial mediolysis (SAM) associated with extensive necrosis of the vascular media was observed at the site of IVA dissection. 1) SAM is an idiopathic arterial disease proposed by Slavin et al in 1976. 2) It is histopathologically characterized by segmental medial defect/ necrosis of muscular arteries as a result of mediolysis.…”

Plasma Soluble Human Elastin Fragments as an Intra‐Aneurysmal Localized Biomarker for Ruptured Intracranial Aneurysm

“…Fragmentation of the tunica media is a hallmark of aneurysm formation, progression, and rupture 1. Histological analyses in animals have characterized the wall of intracranial aneurysms, ultimately revealing a lack of an internal elastic lamina and fragmentation of the media.…”

Clinical Significance of Intraluminal Contrast Enhancement in Patients with Spontaneous Cervical Artery Dissection: A Black-Blood MRI Study

“…One theory presumes a spontaneous rupture of the vasa vasorum of the artery which leads to pseudoaneurysms or rupture if the defect is located between the adventitia and media of the arterial wall [5,6] or to stenosis or occlusion if located between the intima and media. Another theory suggests the creation of an intimal tear, which allows the entry of blood into the defect which then forms the vessel wall hematoma [7].…”