Abstract
Objective
Acute hemorrhagic cerebral artery dissection may show a subtle stenosis and bulge on an angiogram, for which diagnosis and treatment are difficult. This report describes seven cases of acute hemorrhagic cerebral artery dissection treated by endovascular techniques.
Patients and methods
From January 2018 to April 2019, seven patients (22–76 years old) were diagnosed with subarachnoid hemorrhage caused by cerebral artery dissection. Six patients were treated by low-profile visualized intraluminal support stent-assisted coiling and there was a sacrifice of the posterior cerebral artery in one patient. Cerebral angiography results were obtained immediately after intervention and at follow-up. Clinical outcome was evaluated by a modified Rankin Scale score.
Results
Four dissections were angiographic changes of subtle stenosis and small bulges; three were apparent angiographic changes of stenosis or fusiform morphologies. All seven aneurysms were completely obliterated, a low-profile visualized intraluminal support stent was used in six patients and coil occlusion of the parent artery in one patient. Complications occurred in two cases of proximal posterior cerebral artery dissection. One bleeding complication was observed intra-procedure and one ischemic complication was observed after stent-assisted coiling. The angiographic and clinical follow-up was obtained at 3–8 months in five patients. Good recovery was achieved for six patients (modified Rankin Score 0); one patient who presented Weber syndrome caused by ischemic complication had a modified Rankin Score of two at 8 months follow-up.
Conclusion
Hemorrhagic cerebral artery dissection may show subtle stenosis, small bulges or fusiform morphologies on angiograms. Treatment of proximal posterior cerebral artery dissection is challenging. Endovascular reconstruction with a low-profile visualized intraluminal support stent was effective depending on the angiographic morphology.
Keywords: Cerebral artery, dissection, acute hemorrhage, treatment
Introduction
Acute hemorrhagic cerebral artery dissection (CAD) is a not uncommon, fatal disease with a high risk of rebleeding and consequent unfavorable outcomes.1–4 The high rate of rebleeding and consequent mortality among patients treated conservatively suggests treatment in the acute phase.5 However, the published series on this pathology remains short, and there is still no consensus on the management of this group of patients. Treatment options include endovascular or surgical trapping of the dissection and proximal occlusion and embolization of the parent artery at the site of the dissection.6 Endovascular treatment has been reported to be safe and effective in small series or case reports with or without stent placement, and initial complete occlusion was a favorable factor for stable follow-up and improved outcomes.7–10 This report presented seven CADs, for which diagnosis and treatment are difficult, as source of subarachnoid hemorrhage (SAH).
Material and methods
From January 2018 to April 2019, seven patients (five men and two women, age 22–76 years) were diagnosed with SAH caused by CAD. Seven dissections underwent endovascular treatment within 3 days of hemorrhage (Table 1). All patients were a Hunt-Hess grade I. The diagnosis was carried out by computed tomography (CT) and cerebral angiography in all cases: angiography showed focal stenosis and dilatation of the artery at the site of the dissection. The following arteries were affected: the supraclinoid segment of the internal carotid artery (ICA) (two patients), vertebral artery (VA)-posterior inferior cerebellar artery (three patients) and P1 segment of the posterior cerebral artery (PCA) (two patients). All patients were treated under general anesthesia by endovascular embolization: low-profile visualized intraluminal support (LVIS) stent-assisted coiling in six and sacrifice of PCA in one. In five patients, preloading aspirin 300 mg and clopidogrel 300 mg were administered orally 3 hours before treatment. In the other two stenting patients, preloading antiplatelet medications were not given before general anesthesia and tirofiban (preloading 0.005 mg/kg injected through guiding catheter after stent placement, 0.003 mg/kg/hour intravenously for 24 hours) was administered during and after the treatment. The dual antiplatelet medication (aspirin 100 mg/day and clopidogrel 75 mg/day) beginning the next day was continued to 2 months and aspirin 100 mg/day to 6 months. Cerebral angiography results obtained immediately after intervention and at follow-up. Clinical outcome was evaluated by a modified Rankin Scale score.
Table 1.
Seven cases of acute hemorrhagic CAD.
| Case number | Age | Sex | Location | Demonstration on angiograms | Stent | Complications | Results | Follow-up | Outcome (mRS) |
|---|---|---|---|---|---|---|---|---|---|
| 1 | 37 | F | Supraclinoid ICA | Small bulge | LVIS 3.5 × 20 | No | Com | 1 month | 0 |
| 2 | 40 | M | P1-2 | Small fusiform | No | Bleeding | Com | 2 months | 0 |
| 3 | 52 | F | VA-PICA | Stenosis and bulge | LVIS 4.5 × 30 | No | Com | 3 months | 0 |
| 4 | 22 | M | VA-PICA | Fusiform | LVIS 3.5 × 20 | No | Com | 7 months | 0 |
| 5 | 62 | M | P1-2 | Small fusiform | LVIS 3.5 × 15 | Web syndrome | Com | 8 months | 2 |
| 6 | 76 | M | Supraclinoid ICA | Stenosis and small bugle | LVIS 3.5 × 20 | No | Com | 3 months | 0 |
| 7 | 37 | M | VA-PICA | Fusiform | LVIS 3.5 × 15 | No | Com | 6 months | 0 |
CAD: cerebral artery dissection; F: female; ICA: internal carotid artery; LVIS: low-profile visualized intraluminal support; M: male; VA-PICA: vertebral artery-posterior inferior cerebellar artery; mRS: modified Rankin Score scale; Com: complete occlusion.
Results
Four dissections were angiographic changes of subtle stenosis and small bulges; three were apparent angiographic changes of stenosis or fusiform morphologies. All seven acute bleeding CADs were completely obliterated endovascularly (Figures 1 and 2). Two treatment-related complications developed. One bleeding complication was caused by micro-guidewire perforation during the attempt to pass a stent catheter through the proximal PCA dissection. The proximal PCA and dissection was occluded immediately without any neurological sequelae (Figure 2). One patient developed Weber syndrome because of a P1 segment occlusion after stent-assisted coiling of a proximal PCA dissection. Follow-up angiography over 3 months in five patients showed no recurrence and the other two patients did not undergo imaging follow-up. Good recovery was achieved by six patients (modified Rankin Score 0); one patient who presented Weber syndrome caused by ischemic complication had a modified Rankin Score of two at 8 months follow-up.
Figure 1.
A 76-year-old female of acute internal carotid artery (ICA) dissection caused acute subarachnoid hemorrhage (SAH). (a) Left ICA angiogram, oblique review, showing a subtle stenosis and small bulge of the supraclinoid segment of ICA (arrow). (c) Left ICA angiogram post-treatment, lateral review, showing the stenosis has disappeared and the small bulge was coiled after a 3.5 mm × 20 mm low-profile visualized intraluminal support (LVIS) stent placement.
Figure 2.
A 40-year-old male of right proximal posterior cerebral artery (PCA) (P1-2) dissection caused by acute subarachnoid hemorrhage (SAH). (a) Left vertebral artery (VA) angiogram, frontal view, showing a subtle dilation of the right proximal PCA (arrow) with no stenosis. Passing a stent catheter through the dissection was initially attempted but failed and a vessel perforation was observed. The proximal PCA and the dissection was occluded immediately. (b) Left VA angiogram, working angle, showing occlusion of the proximal PCA without contrast leakage. (c) Right internal carotid artery (ICA) angiogram, lateral view of late arterial phase, showing the contrast still filling the aneurysm. (d) Right ICA angiogram, lateral view, showing the residual aneurysm was occluded through the right posterior communicating artery. (e) Right ICA angiogram, lateral view of venous phase, showing the retrograde filling of the right PCA via the cortical vessels after PCA occlusion (arrow). (f) Computed tomography (CT) scanning post-treatment showing the increased blood.
Discussion
Patients with CAD developing SAH have been observed to have poor outcomes.5 In Western countries dissecting aneurysms is an occasional source of SAH.2,3,5,11 Our data suggest that SAH caused by CAD may be subtle angiographic morphological changes. This is not uncommon and may be mistakenly viewed as negative on an angiogram. Some cases show more apparent changes. Most of the reported autopsied cases showed disruption of the entire wall. Pathological studies of CADs with SAH showed the plane of dissection is between the media and adventitia, with a rupture site in the adventitia.11 Previously we thought most of the dissections involved intracranial portions of the VA. The supraclinoid ICA is also a common location of dissection. To our knowledge, such an association has never been reported in the literature. The major changes in the vessel wall structure of ICA and VA vessels as it pierces the dura to enter the cranium, especially a thinning of the adventitia and media, must play an important role of the dissection formation.
Treatment in the acute phase is considered essential because of the high risk of rebleeding and the consequent unfavorable outcome.3,5 However, the location, potential for involvement of eloquent vessels and the histopathological characteristics of the vessel wall make treatment demanding from both a technical and anatomical point of view.11–15 Clipping or circumferential wrapping are used as surgical methods.6 However, complication rates and higher failure rates were revealed according to previous studies.6 Endovascular stent-based methods can achieve stabilization of the dissected artery without sacrificing the artery.7,16–18 Maintaining arterial patency is aimed for in our patients. We prefer to treat our patients using a combination of an LVIS stent and coils.
The radiological evidence of CAD including the following features: intramural hematoma, intimal flap (or double-lumen sign), pearl-and-string sign, localized dilation with proximal or distal stenosis, or contrast media stasis found by digital subtraction angiography (DSA), magnetic resonance angiography, or CT angiography.5 However, in some dissections stenosis and dilation is too subtle to be diagnosed as CAD. If the dissection is neglected, the patient may die of rebleeding. This has been encountered by some physicians. In our case, initial CT scan helped detect the acute SAH. For diagnosis of CAD, DSA showed subtle dilation and proximal stenosis clearly. DSA not only confirmed diagnosis but helped endovascular treatment planning. Magnetic resonance imaging and magnetic resonance angiography are not performed for acute bleeding in our patients.
Endovascular therapy, which is relatively less invasive, is used widely at present. These procedures can be classified as artery sacrificing or artery preserving.7,10,12,14 Artery sacrificing would occlude the involved parent arteries to lower the rebleeding risk by relieving the flow pressure on the aneurysm wall. It is very interesting that we present here a VA dissection, which was treated 20 years ago by VA occlusion using detachable balloons and the lesion has shown no progression over the 20 years (Figure 3). Stenting and coiling as an artery-preserving method for CAD can lower the impact of flow on dissection and preserves the parent artery flow.
Figure 3.
A 43-year-old female with a hemorrhagic right vertebral artery (VA) dissection treated by VA occlusion using two detachable balloons 20 years ago. (a) Right VA angiogram, frontal view, showing the VA-posterior inferior cerebellar artery (VA-PICA) dissection (arrow). (b) The fluoroscopic image, later view, showing the VA was occluded using two detachable balloons (arrows) without coiling the dissection. (c) Control angiogram of the left VA 20 years later, frontal view, showing the distal of right VA becomes small, dilation has not progressed and the PICA is patent.
In the cases reported here, the LVIS stent is chosen for the following reasons. An LVIS stent promotes aneurysm thrombosis, restoration of vessel lumen and facilitates endothelialization.19,20 The disruptive inflow caused by the redirection of blood flow in stents promotes thrombosis. Additional coil embolization lowers the impact of flow significantly and leads to decreased rebleeding risk. The low-profile device prevents the migration of small coil loops from aneurysms. The stent redirects blood flow that ensures the diameter of the true lumen. The reduced wall stress of the pseudoaneurysm contributes to the prevention of recurrent bleeding. The self-expanding stent we used may offer safer procedures for low pressure during deployment. The stent provides a matrix for the formation of the neointima layer. Remodeling of the endothelial growth on the surface of the stent may protect the dissection from rupture. Stent placement accompanied by an initial complete occlusion was a favorable factor for long-term outcomes in a previous study.19,20 However, stents are intravascular, implanted metallic devices that may provoke a thrombogenic response when blood comes into contact with the foreign material. Stents, to preserve the artery caliber, may contrarily end in vessel stenosis. Antiplatelet agents must be used for prophylaxis before or during the procedure and within 6 months of stent intervention.
Conclusion
Hemorrhagic CAD may be a subtle stenosis, small bulge or fusiform morphology on angiograms. Treatment of proximal PCA dissection is challenging. Endovascular reconstruction with an LVIS stent was effective depending on the angiographic morphologies.
Declaration of conflicting interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by Beijing Municiple Administration of Hospitals Incubating Program PX2020039, Beijing, China.
ORCID iD
Xianli Lv https://orcid.org/0000-0001-8270-8464
References
- 1.Fukuma K, Ihara M, Tanaka T, et al. Intracranial cerebral artery dissection of anterior circulation as a cause of convexity subarachnoid hemorrhage. Cerebrovasc Dis 2015; 40: 45–51. [DOI] [PubMed] [Google Scholar]
- 2.Nakahara T, Satoh H, Mizoue T, et al. Dissecting aneurysm of basilar artery presenting with recurrent subarachnoid hemorrhage. Neurosurg Rev 1999; 22: 155–158. [DOI] [PubMed] [Google Scholar]
- 3.Nakajima H, Ishiguro T, Komiyama M. Basilar artery dissection presenting with subarachnoid hemorrhage: Report of two cases. NMC Case Rep J 2015; 2: 97–100. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Zhao WY, Krings T, Alvarez H, et al. Management of spontaneous haemorrhagic intracranial vertebrobasilar dissection: review of 21 consecutive cases. Acta Neurochir (Wien) 2007; 149: 585–596. [DOI] [PubMed] [Google Scholar]
- 5.Lee CJ, Lee KW, Chen WL, et al. Images diagnosis and emergent endovascular treatment of acute hemorrhagic basilar artery dissection: A case report. Acta Neurol Taiwan 2016; 25: 45–50. [PubMed] [Google Scholar]
- 6.Uhl E, Schmid-Elsaesser R, Steiger HJ. Ruptured intracranial dissecting aneurysms: Management considerations with a focus on surgical and endovascular techniques to preserve arterial continuity. Acta Neurochir (Wien) 2003; 145: 1073–1084. [DOI] [PubMed] [Google Scholar]
- 7.Dion-Cloutier P, Tampieri D. Endovascular management of cranial artery dissection with stent placement and stent-assisted coiling. Can Assoc Radiol J 2011; 62: 203–208. [DOI] [PubMed] [Google Scholar]
- 8.Li L, Li T, Xue J, et al. Stent treatment for basilar artery dissection: A single-center experience of 21 patients. Interv Neuroradiol 2016; 22: 260–265. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Lv X, Ge H, Jin H, et al. Endovascular treatment of unruptured posterior circulation intracranial aneurysms. Ann Indian Acad Neurol 2016; 19: 302–306. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Lv X, Lv M, Li Y, et al. Endovascular treatment of ruptured and unruptured vertebral artery aneurysms. Neuroradiol J 2011; 1: 797–806. [DOI] [PubMed] [Google Scholar]
- 11.Sedat J, Chau Y, Mahagne MH, et al. Dissection of the posteroinferior cerebellar artery: Clinical characteristics and long-term follow-up in five cases. Cerebrovasc Dis 2007; 24: 183–190. [DOI] [PubMed] [Google Scholar]
- 12.Lv M, Lv X, Li Y, et al. Dissecting aneurysm at proximal anterior cerebral artery treated by parent artery occlusion. Interv Neuroradiol 2009; 15: 123–126. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Lv M, Lv X, Li Y, et al. Vertebral dissecting aneurysm treated with the Wingspan stent deployment and detachable coils: Technical note. Interv Neuroradiol 2009; 15: 113–116. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Lv X, Li Y, Jiang C, et al. Endovascular management for P2 aneurysms of the posterior cerebral artery: Experience on proximal occlusion of P2 segment. Interv Neuroradiol 2009; 15: 341–348. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Wu Z, Lv X, Yang X, et al. Ruptured vertebro-inferoposterior cerebellar artery dissecting aneurysm treated with the Neuroform stent deployment and vertebral artery occlusion. Eur J Radiol Extra 2009; 70: e100–e103. [Google Scholar]
- 16.Jiang C, Li Q, Liu JM, et al. Endovascular treatment for the basilar artery dissection. Cardiovasc Intervent Radiol 2014; 37: 646–656. [DOI] [PubMed] [Google Scholar]
- 17.Lv X, Li Y, Jiang C, et al. Endovascular treatment using stents for vertebral artery fusiform aneurysms. Neurol Res 2010; 32: 792–795. [DOI] [PubMed] [Google Scholar]
- 18.Lv X, Li Y, Xinjian Y, et al. Results of endovascular treatment for intracranial wide-necked saccular and dissecting aneurysms using the Enterprise stent: A single center experience. Eur J Radiol 2012; 81: 1179–1183. [DOI] [PubMed] [Google Scholar]
- 19.Ge H, Lv X, Yang X, et al. LVIS stent versus enterprise stent for the treatment of unruptured intracranial aneurysms. World Neurosurg 2016; 91: 365–370. [DOI] [PubMed] [Google Scholar]
- 20.Zhu D, Fang Y, Yang P, et al. Overlapped stenting combined with coiling for blood blister-like aneurysms: Comparison of low-profile visualized intraluminal support (LVIS) stent and non-LVIS stent. World Neurosurg 2017; 104: 729–735. [DOI] [PubMed] [Google Scholar]