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Ann Thorac Surg 2008;85:120-125. doi:10.1016/j.athoracsur.2007.08.035
© 2008 The Society of Thoracic Surgeons
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Original Articles: Cardiovascular

Endangered Cerebral Blood Supply After Closure of Left Subclavian Artery: Postmortem and Clinical Imaging Studies

Hannu Manninen, MD, PhDa,*, Harri Tulla, MD, PhDb, Ritva Vanninen, MD, PhDa, Antti Ronkainen, MD, PhDc

a Department of Radiology, Diagnostic Medical Imaging Centre, Kuopio University Hospital and Kuopio University, Kuopio, Finland
b Department of Thoracic and Cardiovascular Surgery, Kuopio University Hospital and Kuopio University, Kuopio, Finland
c Department of Neurosurgery, Kuopio University Hospital and Kuopio University, Kuopio, Finland

Accepted for publication August 14, 2007.

* Address correspondence to Dr Manninen, Kuopio University Hospital, Department of Radiology, PL 1777, Kuopio, FIN 70211, Finland (Email: hannu.manninen{at}kuh.fi).


   Abstract
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 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background: The aim of this study was to assess hemodynamic consequences of increasingly common coverage of the left subclavian artery (LSA) during endovascular stent-graft repair for thoracic aortic disease without surgical revascularization. We considered that critical arteries to examine are the right vertebral artery and posterior communicating arteries (PComA) because their simultaneous insufficiency would drastically endanger posterior cerebral circulation. The existence and the diameters of these arteries were studied in a postmortem anatomic study with review of clinical craniocervical computed tomographic (CT) and magnetic resonance (MR) angiographies.

Methods: The anatomic material was collected as a part of forensic medicine autopsies. The anatomy of the cerebral arteries of 92 deceased was assessed by angiography and permanent silicone casts.

Results: In five individuals (5.4%) the risk for acute neurological complication after "unprotected" closure of the LSA was estimated to be "substantial" because the diameter of the right vertebral artery above the posterior inferior cerebellar artery was less than 2 mm and was associated with incomplete PComA and in three additional cases (3.3%) with only hypoplastic right vertebral artery, as "possible." Review of a clinical teaching file of MR and CT angiographies with anatomic variations and abnormalities of the circle of Willis identified, also, other variants with increased risk.

Conclusions: When the LSA is closed, insufficient posterior cerebral circulation due to anatomic reasons occurs relatively infrequently, but in order to avoid the debilitating complications in these cases, careful imaging of the right vertebral artery up to the basilar artery is mandatory, and if proven hypoplastic, imaging of PComAs is necessary.


   Introduction
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 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
While endovascular stent-graft placement increasingly is replacing open surgical repair for disease of the descending thoracic aorta, the need to cover the left subclavian artery (LSA) origin by the graft is often mandatory to lengthen the fixation segment of the endograft. Especially in acute syndromes, the coverage of the LSA during endovascular stent-graft placement is tempting without surgical revascularization. In addition to the more benign upper limb ischemia, this procedure can cause serious acute neurological complications due to insufficient blood supply to posterior cerebral circulation, or vertebrobasilar insufficiency later on. Unilateral vertebral artery occlusion can be tolerated relatively well if the contralateral vertebral artery is not hypoplastic. If an acute vertebrobasilar territory infarction has developed it carries an extremely poor prognosis, with the mortality rate reaching over 20% of cases.

In situations when the left vertebral artery significantly participates in the supply of the superior portion of the anterior spinal artery, coverage of the LSA disrupts an important collateral pathway to the spinal cord and may cause an additional risk for paraplegia, especially in patients with a previous abdominal aortic prosthesis or who receive long stent grafts on the thoracic aorta. In addition to the more common atherosclerotic obstructions, these complications particularly threaten patients with various anatomic variations-anomalies of the vertebrobasilar circulation. The present study is based on the data received from postmortem permanent casts and angiography of the cerebral arteries, particularly focusing on the anatomy of vertebral and posterior communicating arteries (PComAs). Furthermore, illustrative cases of different types of anatomic variants in clinical magnetic resonance (MR) and computed tomography (CT) angiographies were reviewed to assess the potential hemodynamic consequences of LSA closure without surgical revascularization.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
The material was collected from autumn 1997 to the beginning of 1999 as a part of normal forensic medicine autopsies (ie, autopsies-dictated law such as in cases of accidental death, death during surgical intervention, or suspicion of crime). During this period 193 consecutive forensic medicine autopsies were carried out, of which 94 were excluded. The main reason for exclusion was destruction of the brain. Seven further cases were excluded because of poor quality silicon casting, leaving 92. This final sample included 62 (67%) men and 30 (33%) women. Their age ranged from 14 to 90 years with a mean age of 59 years. The basic reason for death was a disease in 50, accident in 26, and suicide in 16 subjects. Twelve individuals did not have any diagnosed comorbidities, while 42 had cardiovascular, 11 psychiatric, 3 malignant, and 1 neurological disease, and 23 were chronic alcoholics. By selecting forensic autopsy cases instead of sole medical autopsy cases, we were able to control the patient selection more easily to avoid subjects with known heavy general atherosclerosis that might cause difficulty in identifying anatomic variants. The anatomy of the cerebral arteries was assessed postmortem by angiography and permanent casts, which were made by experienced autopsy technicians. The study was approved by the ethical committee of our hospital but the ethics committee waivered the need for the consent from the patient‘s next of kin because autopsy was dictated by law.

Permanent Casts
The exact description of manufacturing and radiographic imaging of the casts is given elsewhere [1, 2]. Briefly, the permanent casts of cerebral arteries were performed before the autopsy and 210 g of lead oxide (Pb3O4) was used per 1 kg of liquid silicone rubber. The aortic arch of the deceased and the arteries branching from it (brachiocephalic trunk, left common carotid artery, and left subclavian artery), were exposed for a range of 3 cm. A plastic Y-shaped tube was connected so that one arm of the tube was fastened to the brachiocephalic trunk and the other to the left carotid artery. Then right and left subclavian arteries were exposed and clamped and the mixture was led into the cerebral arteries using a portable perfusion device with a physiological pressure of 110 to 140 mm Hg.

Angiography
Because lead oxide is used as the contrast medium, liquefied silicone rubber is radiopaque. After the solidification of the silicone rubber anterior and lateral X-rays were taken. This made the cervical and cerebral arteries visible. The brain was removed and placed on a plate with the base upward. Stereotopic images (at 5 degree projection difference) were taken at a frontal direction on high resolution film, facilitating spatial resolution up to 10 line pairs/mm.

Analysis of the Postmortem Casts and Angiographies
During interpretation, the radiographies were placed on the X-ray board next to each other and examined with specially designed binoculars that created a three-dimensional view of the cerebral arteries. The existence, visibility, and symmetry of the arteries were assessed by two experienced radiologists. Arterial diameters were measured with a high precision digimetric caliber device. A sample of 60 arteries from 10 individuals showed a close correlation (r = 0.911, p < 0.001) between the measurements made from the anatomic casts and those made from the cast angiographies. The vertebral artery (VA) was defined as dominant if its diameter at the cervical V2 segment assessed from the cervicocranial angiographies was at least twice as wide as the contralateral VA. The VA was classified hypoplastic if the diameter measured from the anatomic cast above the level of the posterior inferior cerebellar artery (PICA) was less than 2 mm. Criterion for hypoplastic PComA was a diameter less than 0.5 mm, correspondingly. The risk for neurological complication after "unprotected" closure of the LSA was estimated to be "substantial" if the diameter of the right vertebral artery (RVA) was less than 2 mm, associated with incomplete or hypoplastic PComA, or a persistent fetal type of posterior cerebral artery (PCA) supply associated with absent P1 segment. In case of only hypoplastic RVA, with normal PComAs the risk for neurological complication was estimated to be "possible."


   Results
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 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
Anatomic Study
When assessed from the V2 segment the left VA was dominant in eight cases (8.7%) and the right VA in 11 cases (12.0%). The right VA measured above the PICA was hypoplastic in eight (8.7%) cases and the left in seven (7.6%) cases. In three cases the right VA terminated to PICA but there were no cases where the left VA terminated to PICA. In 52 cases (56.5%) either left or right PComA was hypoplastic (or absent) and in seven cases (7.6%) both PComAs were absent.

In five individuals (5.4%) the risk for neurological complication after "unprotected" closure of the LSA was estimated to be "substantial" because the diameter of the RVA above the PICA was less than 2 mm, associated with incomplete posterior portion of the circle of Willis (for more details, see Table 1). In three additional cases (3.3%) with hypoplastic right VA the risk was estimated as "possible." Anatomic cast angiographies in Figures 1 and 2 illustrate cases where the RVA terminates to PICA or it is almost rudimentary above PICA, emphasizing the crucial role of preprocedural imaging of the distal portion of the vertebral arteries.


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  		Table 1 Anatomic Variants Among 92 Cerebral Artery Casts With Estimated "Substantial" Risk for Acute Neurological Complication After "Unprotected" Closure of LSA
 

Figure 1
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  		Fig 1. Cast angiography; "substantial" risk for acute complication after closure of LSA. (A) Cervicocranial angiography demonstrates almost symmetrical cervical portions of vertebral arteries. (B) Cerebral cast angiography at axial view depicts missing right VA above PICA, hypoplastic right PComA, and persistent fetal left PCA. (PCA = posterior cerebral artery; PComA = posterior communicating artery; VA = vertebral artery.)

 
Clinical MR and CT Angiographies
Clinical MR angiography, CT angiography, and digital subtraction angiography studies demonstrating different types of anatomic variations and anomalies of the cervicocranial arteries have been prospectively collected into a teaching file in our hospital. Evaluation of these cases revealed several additional types of vascular variations or anomalies, predisposing the patient to a risk for neurological complication in case of "unprotected" closure of the LSA. Three illustrative cases are shown in Figures 3 to 5. Go Go Figure 3 shows that, in the case of a dominant right VA, it can be risky to occlude the left LSA because the left VA may be ending to PICA, predisposing the patient to hypoperfusion in the territory of the left PICA with no collateral reserves. Magnetic resonance angiography in Figure 4 presents an anatomic variant in which it is difficult to predict hemodynamic consequences of LSA closure, even after full visualization of intracranial circulation. Figure 5 illustrates an anatomic variation where LSA closure might theoretically predispose the patient not only to posterior circulation problems but also to middle cerebral artery (MCA) territory hypoperfusion. These examples show the wide variability of vascular anatomy of the posterior circulation and advocate these noninvasive imaging modalities with a capability to demonstrate even complicated arterial communications and collateral pathways in this anatomic area.


Figure 3
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  		Fig 3. Clinical computed tomographic angiography of a 55-year old male demonstrates left VA ending to PICA creating an obvious risk for neurological complication in case of closure of LSA. (A) Mirrored posterior view in the three dimensional reconstruction image, arrows indicating the aplastic left VA above PICA. (B) Axial slice at V2 segment with dominating VA on the right. (C) Absent intradural portion of left VA. (BA = basilar artery; PICA = posterior inferior cerebellar artery; VA = vertebral artery.)

 

Figure 4
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  		Fig 4. Magnetic resonance angiography of a 44-year old male shows hypoplastic proximal basilar artery and the right VA is ending to PICA (A). Persistent trigeminal artery (arrow in B) connecting the right internal carotid artery to basilar artery supplies right PCA, and there is persistent fetal PCA supply on the left. After closure of LSA there arises concern whether blood supply to left PICA retrogradely through the rudimental proximal basilar artery is sufficient, especially because the left upper extremity now steals blood from the left VA. (BA = basilar artery; ICA = internal carotid artery; PCA = posterior cerebral artery; PICA = posterior inferior cerebellar artery; VA = vertebral artery.)

 

Figure 5
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  		Fig 5. Magnetic resonance angiography of a 40-year old female shows missing A1 segment of the left anterior cerebral artery (arrow in A) and severe hypoplasia of the left ICA. Blood supply to left MCA is mainly dependent on the retrograde flow through the hyperplastic posterior communicating artery (arrow in B). After closure of the left subclavian artery there arises concern whether the right vertebral artery can supply enough blood to the whole posterior circulation and left MCA territory. (BA = basilar artery; ICA = internal carotid artery; MCA = middle cerebral artery; PCA = posterior cerebral artery.)

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
A large portion of patients (25% to 43% in recent studies) [3, 4] undergoing thoracic endovascular stent-graft placement have lesions adjacent to or involving the origin of the LSA. While some recommend extraanatomic revascularization with subclavian-carotid transposition or bypass [5, 6], others advocate "unprotected" deploying the covered portion of the stent-graft over the LSA origin [7, 8]. Although several authors mention hypoplasia of the RVA as a contraindication for covering the LSA surface with the stent-graft, the definition of hypoplasia is not mentioned [3, 4]. Various criteria have been used for defining hypoplastic vertebral artery. Diameters of less than 2 to 3 mm (measured mainly from the V2 segment) have been used in ultrasound imaging studies [9–11]. The frequency of vertebral artery hypoplasia in these studies has been 1.9% to 11.6%, and it is two to three times more frequent on the right VA than on the left VA. A recent ultrasound imaging study on stroke patients defined hypoplasia in the V2 segment by a diameter of the artery equal to or less than 2.5 mm or a difference to the contralateral side of more than 1:1.7, a significant decrease in velocities as compared with the contralateral side, and an increased ipsilateral flow resistance (resistance index [RI] ≥ 0.85) [12]. Hypoplasia was predominant on the right side (70%) and was diagnosed in 13% (32 of 247) of all posterior circulation strokes. We used a VA diameter less than 2 mm measured from the anatomic cast above the level of PICA as a criterion for hypoplasia, and found a frequency of 8.7% for RVA hypoplasia in our material.

In cases of a complete circle of Willis the functional PComAs can supply sufficient blood flow to posterior circulation even in cases of totally occluded dominant VA. Therefore we also analyzed the status of PComAs in order to accurately estimate the risk for neurological complications after closure of the LSA. Macchi and colleagues [13] demonstrated, by MR angiography, that circle of Willis has a complete configuration in only 47% of subjects. A complete configuration of its posterior part was present in 48.5%. In healthy volunteers studied by MR angiography, Krabbe-Hartkamp and colleagues [14] reported entirely complete circle of Willis in 42%; complete posterior circulation was seen in 52% of cases. According to another study [15], the PComA may be hypoplastic or absent on one or both sides of the brain in about 25% to 30% of patients referred to carotid endarterectomy. Although a diameter of 1 mm has been used in anatomic studies as a criterion for hypoplasia for the collaterals in the circle of Willis [16, 17], more recent studies imply that the lowest limit for functional PComA is as low as 0.4 to 0.6 mm. A transcranial Doppler US revealed that the cross flow through the posterior circulation was insufficient in 45% of individuals in an atherosclerotic population [18]. We chose to use the 0.5 mm cutoff value. By this criterion, insufficient posterior portion of circle of Willis was identified in 56.5% of the individuals, a result that is well in line with that observed by others. In our criteria, we included additional hypoplasia in PComAs and(or) fetal type PCAs when estimating the risk for acute neurological sequels to be "substantial." With these strict criteria 5.4% percent of the individuals would have encountered acute neurological complication after "unprotected" closure of the LSA. By including the three further individuals with hypoplastic right VA, up to 8.7% of cases would have been in danger for acute neurological complication. The relatively small sample size makes our estimate of anomalies subject to large variation, however. It is to be noted also that in an elderly population undergoing thoracic aorta interventions the percentage of risk patients is probably higher due to adjunctive atherosclerotic obstructions.

While some authors have not encountered any neurological complications with overstenting of the LSA [19, 20], a recent study [3] reported neurological complication in five out of eight patients who had the nontransposed subclavian origin covered at the time of endograft deployment. Four patients experienced stroke, of which three were at the posterior circulation territory. In two of these patients the right vertebral artery was absent, showing the clinical importance of the anomalies. One patient suffered infarct at the middle cerebral distribution (probably from atheroembolization from the aortic arch), and one patient developed subclavian-vertebral steal shortly after the operation. No neurological complications were encountered among the 23 patients undergoing revascularization before or at the time of stent-graft placement. In another recently published study [4] cerebrovascular accidents were observed in 11% (3 of 28) of patients with the LSA partially or totally covered without revascularization.

Our study shows that "unprotected" LSA occlusion necessitates careful imaging of the cervicocranial vessels to avoid unnecessary complications due to anatomic variations. It is important to note that recognition of these abnormalities requires diagnostic imaging not only in the posterior circulation to the level of basilar artery but also intracranial anterior circulation to visualize functional PComAs. A patient example from the clinical MR angiographies (Fig 5) demonstrates that, even in case of well-developed vertebral arteries, this does not necessarily exclude neurological complication because blood supply to anterior circulation may be largely dependent on the vertebrobasilar-to-carotid communications. It is evident that unselective angiography with aortic arch injection is not sufficient and subclavian artery injections, at minimum, are mandatory to evaluate vertebrobasilar arteries. Our MR and CT angiography study examples, as well as our clinical experience of imaging candidates for thoracic aorta endografting, show that these noninvasive imaging modalities are capable of demonstrating even complicated arterial communications and collateral pathways in this anatomic area. Especially with modern multiple row detector equipment, CT angiography is possible even for patients with acute aortic syndromes in conjunction with primary diagnostic CT of the aorta, requiring only a few minutes extra time.


Figure 2
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  		Fig 2. Cerebral cast angiography. "Substantial" risk for acute complication after closure of LSA because of hypoplastic right VA, missing left PComA, and hypoplastic right PComA. (PComA = posterior communicating artery; LSA = left subclavian artery; VA = vertebral artery.)

 

   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
  1. Merkkola P, Tulla H, Ronkainen A, et al. Incomplete circle of Willis and right axillary artery perfusion Ann Thorac Surg 2006;82:74-79.[Abstract/Free Full Text]
  2. Weman SM, Salminen US, Penttilä A, Männikkö A, Karhunen PJ. Post-mortem cast angiography in the diagnostics of graft complications in patients with fatal outcome following coronary artery bypass grafting (CABG) Int J Legal Med 1999;112:107-114.[Medline]
  3. Peterson BG, Eskandari MK, Gleason TG, Morasch, MD. Utility of left subclavian artery revascularization in association with endoluminal repair of acute and chronic thoracic aortic pathology J Vasc Surg 2006;43:433-439.[Medline]
  4. Riesenman PJ, Farber MA, Mendes RR, Marston WA, Fulton JJ, Keagy BA. Coverage of the left subclavian artery during thoracic endovascular aortic repair J Vasc Surg 2007;45:90-95.[Medline]
  5. Czerny M, Zimpfer D, Fleck T, et al. Initial results after combined repair of aortic arch aneurysms by sequential transposition of the supra-aortic branches and consecutive endovascular stent-graft placement Ann Thorac Surg 2004;78:1256-1260.[Abstract/Free Full Text]
  6. Grabenwoger M, Hutschala D, Ehrlich MP, et al. Thoracic aortic aneurysms: treatment with endovascular self-expandable stent grafts Ann Thorac Surg 2000;69:441-445.[Abstract/Free Full Text]
  7. Gorich J, Asquan Y, Seifarth H, et al. Initial experience with intentional stent-graft coverage of the subclavian artery during endovascular thoracic aortic repairs J Endovasc Ther 2002;9(suppl 2):II39-II43.[Medline]
  8. Tiesenhausen K, Hausegger KA, Oberwalder P, et al. Left subclavian artery management in endovascular repair of thoracic aortic aneurysms and aortic dissections J Card Surg 2003;18:429-435.[Medline]
  9. Delcker A, Diener HC. Various ultrasound methods for studying the vertebral artery–a comparative evaluation[in German] Ultraschall Med 1992;13:213-220.[Medline]
  10. Jeng JS, Yip PK. Evaluation of vertebral artery hypoplasia and asymmetry by color-coded duplex ultrasonography Ultrasound Med Biol 2004;30:605-609.[Medline]
  11. Touboul PJ, Bousser MG, LaPlane D, Castaigne P. Duplex scanning of normal vertebral arteries Stroke 1986;17:921-923.[Abstract/Free Full Text]
  12. Perren F, Poglia D, Landis T, Sztajzel R. Vertebral artery hypoplasia: a predisposing factor for posterior circulation stroke? Neurology 2007;68:65-67.[Abstract/Free Full Text]
  13. Macchi C, Catini C, Federico C, et al. Magnetic resonance angiographic evaluation of circulus arteriosus cerebri (circle of Willis): a morphologic study in 100 human healthy subjects Ital J Anat Embryol 1996;101:115-123.[Medline]
  14. Krabbe-Hartkamp MJ, van der Grond J, de Leeuw FE, et al. Circle of Willis: morphologic variation on three-dimensional time-of-flight MR angiograms Radiology 1998;207:103-111.[Abstract/Free Full Text]
  15. Kim GE, Cho YP, Lim SM. The anatomy of the circle of Willis as a predictive factor for intra-operative cerebral ischemia (shunt need) during carotid endarterectomy Neurol Res 2002;24:237-240.[Medline]
  16. Alpers BJ, Berry RG, Paddison RM. Anatomical studies of the circle of Willis in normal brain AMA Arch Neurol Psychiatry 1959;81:409-418.[Medline]
  17. Battacharji SK, Hutchinson EC, McCall AJ. The circle of Willis–the incidence of developmental abnormalities in normal and infarcted brains Brain 1967;90:747-758.[Free Full Text]
  18. Hoksbergen AW, Legemate DA, Ubbink DT, Jacobs MJ. Collateral variations in circle of Willis in atherosclerotic population assessed by means of transcranial color-coded duplex ultrasonography Stroke 2000;31:1656-1660.[Abstract/Free Full Text]
  19. Lambrechts D, Casselman F, Schroeyers P, De Geest R, D’Haenens P, Degrieck I. Endovascular treatment of the descending thoracic aorta Eur J Vasc Endovasc Surg 2003;26:437-444.[Medline]
  20. Scharrer-Pamler R, Kotsis T, Kapfer X, Gorich J, Orend KH, Sunder-Plassmann L. Complications after endovascular treatment of thoracic aortic aneurysms J Endovasc Ther 2003;10:711-718.[Medline]

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