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LETTER TO EDITOR
Year : 2013  |  Volume : 61  |  Issue : 3  |  Page : 312-314

Temporal evolution of hypertrophied vasa vasorum of common carotid artery triggered by cerebral ischemia: A serial angiographic investigation


1 Department of Imaging Sciences and Interventional Radiology, Sree Chitra Institute of Medical Sciences and Technology, Trivandrum, Kerala, India
2 Department of Neurology, Sree Chitra Institute of Medical Sciences and Technology, Trivandrum, Kerala, India

Date of Submission16-Apr-2013
Date of Decision17-Apr-2013
Date of Acceptance30-May-2013
Date of Web Publication16-Jul-2013

Correspondence Address:
K Santhosh
Department of Imaging Sciences and Interventional Radiology, Sree Chitra Institute of Medical Sciences and Technology, Trivandrum, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.115079

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How to cite this article:
Santhosh K, Jaydadevan E R, Kapilamoorthy T R, Sylaja P N. Temporal evolution of hypertrophied vasa vasorum of common carotid artery triggered by cerebral ischemia: A serial angiographic investigation. Neurol India 2013;61:312-4

How to cite this URL:
Santhosh K, Jaydadevan E R, Kapilamoorthy T R, Sylaja P N. Temporal evolution of hypertrophied vasa vasorum of common carotid artery triggered by cerebral ischemia: A serial angiographic investigation. Neurol India [serial online] 2013 [cited 2019 Aug 19];61:312-4. Available from: http://www.neurologyindia.com/text.asp?2013/61/3/312/115079


Sir,

Recanalization of occluded internal carotid artery (ICA) via hypertrophied vasa vasorum is a rare well-recognized phenomenon, described in atherosclerotic arterial occlusions. [1] The development and maturation of hypertrophied vasa vasorum is unclear, thought to be augmented by the ischemia of the arterial wall and the downstream arterial territory as well as by the inflammatory reactions induced by atherosclerotic plaque formation. [1],[2],[3] The time course of this development is uncertain, believed to occur within a year of ongoing cerebral ischemia. In this report, we demonstrate with the help of serial angiograms, the development of hypertrophied vasa vasorum within the occluded common carotid artery (CCA) as a response to progressive cerebral ischemia. The development of hypertrophied vasa vasorum could occur early, probably within months of inciting triggers. Probably this is the first such documentation in aortoarteritis.

A 22-year-female presented with a sudden onset weakness of left upper and lower limb and facial deviation in October 2011. Clinical examination revealed absence of both radial pulses as well as bruit over bilateral carotid arteries. Computed tomography brain showed infarct in the posterior limb of the right internal capsule and subcortical white matter hypodensities in the right middle cerebral artery (MCA) territory. Digital subtraction angiography performed in February 2012 demonstrated 70% narrowing of right brachiocephalic artery, occlusion of right CCA from its origin, occlusion of second part of right subclavian artery beyond vertebral artery and mild narrowing of vertebral artery ostium. Left CCA showed mild proximal narrowing and left vertebral ostium that was <50%. She underwent brachiocephalic angioplasty to improve the cerebral circulation with 5 mm × 40 mm angioplasty balloon under Spider FX filter protection resulting in significant improvement of stenosis. Though her symptoms significantly improved, she developed recurring episodes of graying of vision and black outs 4 months later and she underwent repeat angiographic study in October 2012. Angiogram showed progression of the disease with alteration of cerebral perfusion dynamics [Figure 1]. Between the two angiograms, there was progressive decline in perfusion of right MCA territory from posterior cerebral pial arteries, with increasing contribution from anterior cerebral artery pial arteries via anterior communicating artery. Flow reversal was observed in right ICA with the development of tortuous hypertrophied vasa vasorum of CCA that antegradely supplied cervical ICA and external carotid artery (ECA) branches. She was managed conservatively and was kept on close clinical surveillance.
Figure 1: Initial angiogram obtained in February 2012 (a-d) demonstrated right middle cerebral artery (MCA) territory being perfused via anterior cerebral artery (ACA) pial collaterals predominantly; posterior cerebral artery (PCA) collateral perfusion was limited to posterior temporal region. Note the retrograde opacification of right internal carotid artery (ICA) and external carotid artery (ECA) (dashed arrows) via persistent trigeminal artery (dotted arrows) in c and d. Follow-up angiogram (e-h) in October 2012 demonstrated decline of perfusion of right MCA territory from ACA collaterals and increased contribution from pial collaterals of PCA (white arrows). The initial brachiocephalic stenosis (i) was angioplastied with Spider FX emboli protection device (j) and post-procedure angiogram showed good opening of the segment and antegrade flow (k) Follow-up angiogram depicted progression of the arteritis with occlusion of right vertebral artery and increased severity of left common carotid artery stenosis (l) Well-developed vasa vasorum (m and n) that antegradely perfuse cervical ICA and ECA (white arrows) were noted

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Recanalization of occluded ICA via hypertrophied vasa vasorum are described in diverse pathologies such as dissection, atherosclerosis or in therapeutic surgical or endovascular ICA occlusion. [3],[4],[5] These channels are often thin and tortuous and are located outside the expected lumen, which helps in differentiating it from the recanalized or residual arterial lumen. [4] Single-photon emission computed tomography studies demonstrated that the cerebral hypoperfusion of affected arterial territory might be a triggering factor for the development of vasa vasorum. [3] In the case demonstrated, there was progressive occlusion of right vertebral artery resulting in the reduction of pial and Willisian collateral blood flow to the right cerebral hemisphere. Angiographic studies separated by 6 months demonstrated the changing blood flow pattern and prolongation of circulation time of affected hemisphere indicating cerebral hypoperfusion. [3] This increasing metabolic demand, clinically manifested as new ischemic symptoms may have potentially triggered the development and hypertrophy of the vasa vasorum. This vasa vasorum could have arisen from the ICA or ECA or from the brachiocephalic and perfused retrograde or antegrade depending on its origin. [6],[7] The appearance of this angiographic finding suggests ongoing ischemic insult and patient should be optimized for anti-inflammatory agents and be put on strict clinical surveillance.

 
  References Top

1.Langheinrich AC, Kampschulte M, Buch T, Bohle RM. Vasa vasorum and atherosclerosis-Quid novi? Thromb Haemost 2007;97:873-9.  Back to cited text no. 1
[PUBMED]    
2.Ritman EL, Lerman A. The dynamic vasa vasorum. Cardiovasc Res 2007;75:649-58.  Back to cited text no. 2
[PUBMED]    
3.Cho HJ, Roh HG, Chun YI, Moon CT, Chung HW, Kim HY. Hypertrophy of the vasa vasorum: Vascular response to the hungry brain. Neurologist 2012;18:133-5.  Back to cited text no. 3
[PUBMED]    
4.Martin MA, Marotta TR. Vasa vasorum: Another cause of the carotid string sign. AJNR Am J Neuroradiol 1999;20:259-62.  Back to cited text no. 4
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5.Colon GP, Deveikis JP, Dickinson LD. Revascularization of occluded internal carotid arteries by hypertrophied vasa vasorum: Report of four cases. Neurosurgery 1999;45:634-7.  Back to cited text no. 5
[PUBMED]    
6.Mulligan-Kehoe MJ. The vasa vasorum in diseased and nondiseased arteries. Am J Physiol Heart Circ Physiol 2010;298:H295-305.  Back to cited text no. 6
[PUBMED]    
7.Bo WJ, McKinney WM, Bowden RL. The origin and distribution of vasa vasorum at the bifurcation of the common carotid artery with atherosclerosis. Stroke 1989;20:1484-7.  Back to cited text no. 7
[PUBMED]    


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