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Re: Vertebral artery hypoplasia: A predisposing factor for posterior circulation stroke?

We read the article by Perren et al concerning the possible role of vertebral artery hypoplasia (VAH) as a predisposing factor for posterior circulation stroke with great interest. [1] In this study, 725 sequentially admitted first-ever stroke patients were evaluated using color-coded duplex flow imaging.

The authors reported that VAH was more frequent in posterior circulation than other territories infarction. There were no differences in age and other risk factors between the two groups. The authors concluded that VAH may be a risk factor for stroke in the posterior circulation. However, the mean age of the patients with VAH and posterior circulation stroke was not mentioned in the manuscript.

Interestingly, we followed three cases of young adults (one female 40 years old and two males 38 and 37 years old) with lateral medullary ischemic events associated with VAH ipsilaterally to the clinical ischemic event. [2] The diagnosis of VAH was confirmed in all three cases with two imaging methods. All patients had two additional atherosclerotic or non atherosclerotic risk factors for stroke. [2] None of our patients in a three year follow-up period had recurrent TIA or stroke with the secondary stroke prevention treatment. In addition, none of them had other ischemic lesions in other vascular territories except those that correspond to the posterior inferior cerebellar artery (lateral medulla). These observations supported the hypothesis that their strokes were related to the hypoplastic vertebral artery.

The two VAs are of similar size in 25%, while the left is the dominant artery in 50% of the population. The absence of vertebrobasilar insufficiency symptoms in all these cases suggested that even a pronounced VA asymmetry could be regarded as normal variant. [3,4] However, the study by Perren et al. [1] and others [5] indicate that VAH may be a risk factor for posterior circulation stroke. In addition, our three cases in young adults implied that a hypoplastic VA in association with other risk factors may contribute to an ischemic brainstem event even in young population. [2]

Although the clinical significance of VAH is still unclear, there is a possibility that it contributes to posterior circulation stroke in some patients. Larger detailed studies are needed to characterize the role of VAH in posterior circulation stroke and more importantly in young adults.

References

1. Perren F, Poglia D, Landis T, Sztajzel R. Vertebral artery hypoplasia: a predisposing factor for posterior circulation stroke? Neurology. 2007;68:65-67.

2. Giannopoulos S, Markoula S, Kosmidou M, Pelidou SH, Kyritsis AP. Lateral medullary ischemic events in young adults with hypoplastic vertebral artery. J Neurol Neurosurg Psych (In press).

3. loud GC, Markus HS. Diagnosis and management of vertebral artery stenosis. Q J Med 2003;96:27-34.

4. ratting S, Hubsch P, Polzeitner D. Color-coded Doppler imaging of normal vertebral arteries. Stroke 1990;21:1222-1225.

5. Chuang YM, Huang YC, Hu HH, Yang CY. Toward a further elucidation: Role of vertebral artery hypoplasia in acute ischemic stoke. Eur Neurol 2006;55:193-197.

Send Correspondence to journal:
Re: Vertebral artery hypoplasia: A predisposing factor for posterior circulation stroke?

Perren et al noted in a 725-patient study that vertebral artery hypoplasia was more frequent in posterior circulation territory infarction (13%) than in strokes in other territories (4.6%), p<0.001. [1] We congratulate the authors for reporting this thoughtful study on vertebral artery hypoplasia.

Eighteen out of 32 patients with posterior circulation stroke and vertebral hypoplasia were thought to be related to embolism. This contradicts earlier reports that vertebral hypoplasia was associated with large artery atherosclerosis subtype of ipsilateral posterior circulation infarction. [5,6] It would be interesting if Perren et al could look into the analysis of the prevalence of posterior circulation stroke subtypes with or without vertebral artery hypoplasia in different stroke subtypes including large artery atherosclerosis, cardioembolism, small vessel occlusion, stroke of other determined or undetermined etiologies to further elaborate on their findings. [7] The association can be explained alternatively by reduced compensatory circulation reserve of the posterior circulation. [3]

References

1.Perren F, Poglia D, Landis T, Sztajzel R. Vertebral artery hypoplasia: A predisposing factor for posterior circulation stroke. Neurology 2007;68:65-67.

2.Chaturvedi S, Lukovits TG, Chen W, Gorelick PB. Ischemia in the territory of a hypoplastic vertebrobasilar system. Neurology 1999;52:980- 983.

3.Chuang YM, Huang YC, Hu HH, Yang CY. Toward a further elucidation: Role of vertebral artery hypoplasia in acute ischemic stroke. Eur Neurol 2006;55:193-197.

4.Adams HP, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh EE, TOAST Investigators. Classification of subtype of acute ischemic stroke. Stroke 1993;24:35-41.

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Re: Reply from the Author

Dr Giannopoulos et al mention their report of three interesting case reports of young adults (37, 38, and 40 years old) with posterior circulation strokes and vertebral artery hypoplasia (VAH). [2] As mentioned in our article [1], we did not find statistical differences in age between patients with strokes in the posterior or anterior circulation, with or without VAH. Our data thus cannot confirm the assumption that strokes in the posterior circulation in relation to VAH might affect especially young individuals.

We also thank Drs. Wong and Poon for their thoughtful comments. They raise the question whether vertebral artery hypoplasia (VAH) is associated with large artery atherosclerosis rather than with embolism as postulated in two reports. [5,6] There are a number of methodological and selection differences between these studies and ours [1] which might explain the relatively high proportion (56%) of embolic origin. The most important is that we included only patients with first ever stroke and excluded patients with occlusions, stenosis or atheromatosis of the vertebral arteries.

Chaturvedi et al [6] report on 8 selected patients out of some 4000 strokes or TIA’s of whom all had also basilar artery hypoplasia and 5 bilateral VAH (none in our series). Chuang et al [5] analyzed 191 patients with acute ischemic stroke. Their only exclusion criteria were “traumatic cervical vascular dissection or cervical rotatory -injury-related cerebral infarctions”. Our goal was to assess the role of “pure” congenital VAH as a potential risk factor for posterior circulation stroke and not that of reduced vertebral artery diameter of various origins including “post stenotic or atherosclerotic” VAH. These selection differences might also be one of the reasons for the very striking difference (72%; recalculated 54% for [5]; and 13% for [6] of the frequency of VAH in posterior circulation stroke between the two studies.