|Year : 2021 | Volume
| Issue : 1 | Page : 9-13
Is foetal variant of posterior cerebral artery a risk factor for ischemic stroke?
Karthik Thamarai Kannan, Madhavi Karri, Balakrishnan Ramasamy, Aleesha Ummer
Department of Neurology, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India
|Date of Submission||22-Mar-2021|
|Date of Decision||14-Jun-2021|
|Date of Acceptance||18-Jul-2021|
|Date of Web Publication||27-Aug-2021|
Dr. Karthik Thamarai Kannan
Department of Neurology, PSG Institute of Medical Sciences and Research, Coimbatore - 641 004, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Context: Posterior cerebral artery (PCA) derives its blood supply from the vertebrobasilar system. However, in 10% of the population, they get blood supply from the internal carotid artery via a posterior communicating artery. This variant is called as fetal type of PCA (fPCA). Whether fPCA is an anatomical variant or a predisposing factor for a cerebrovascular event remains an enigma.
Aims: The aim is to assess if fPCA is associated with increased risk of ischaemic stroke or other vascular anomalies.
Settings and Design: It is a retrospective cross-sectional observational study.
Subjects and Methods: Patients who underwent MR or CT angiography, over 5 years for various neurological illnesses were screened for fPCA. Those patients were assessed for vascular anomalies and ischaemic stroke.
Statistical Analysis Used: Chi-square in the Statistical Package for the Social Sciences v23.
Results: On analysis of 250 patients, five had aneurysms; three had AV malformation, one with Fenestration and one with vascular loop. And 51% were found to have an ischaemic stroke, in which 34% had large vessel disease, 41% had lacunar infarct, 7% had a cardioembolic stroke and 18% had an embolic stroke of unknown source with predominantly middle cerebral artery territory infarct (55%). Among 127 patients with ischaemic stroke, 45% had infarcts ipsilateral to fPCA vs 28% on the opposite side of fPCA.
Conclusions: We conclude that patients with fPCA had increased risk of MCA infarct probably due to poor collaterals from posterior circulation and fPCA is not associated with increased risk of aneurysms or AV malformations.
Keywords: Foetal posterior cerebral artery, hypoplastic vertebral artery, stroke, trial of ORG 10,172 in acute stroke treatment classification
|How to cite this article:|
Kannan KT, Karri M, Ramasamy B, Ummer A. Is foetal variant of posterior cerebral artery a risk factor for ischemic stroke?. J Cerebrovasc Sci 2021;9:9-13
|How to cite this URL:|
Kannan KT, Karri M, Ramasamy B, Ummer A. Is foetal variant of posterior cerebral artery a risk factor for ischemic stroke?. J Cerebrovasc Sci [serial online] 2021 [cited 2022 May 16];9:9-13. Available from: http://www.jcvs.com/text.asp?2021/9/1/9/324820
| Introduction|| |
The posterior cerebral artery (PCA) usually derives its blood supply from the vertebrobasilar system. However, in 10% of the population, they get blood supply from the internal carotid artery (ICA) through the posterior communicating artery. This variant is called as foetal PCA (fPCA). Prevalence of fPCA varies from 4% to 26% unilaterally and 2%–4% bilaterally. In patients with fPCA, ICA thrombosis can cause a massive infarct involving the occipital lobe, along with anterior cerebral artery (ACA) and middle cerebral artery (MCA) territories. More wide usage of computerized tomography angiography (CTA) and magnetic resonance angiography (MRA) has made increased the detection of fPCA. CTA and MRA are less invasive compared to conventional digital subtraction angiography. Whether fPCA is an anatomical variant or a predisposing factor for a cerebrovascular event remains an enigma.
Aims and objectives
To analyse whether fPCA predisposes to stroke or other vascular anomalies such as aneurysms, white matter small vessel ischaemic changes, AV malformations, fenestrations, or vascular loop, and whether a hypoplastic vertebral artery is associated with risk of stroke of a specific type or in a specific territory.
| Subjects and Methods|| |
It is a retrospective observational study. Patients who underwent MRA or CTA over 5 years, between January 2014 and December 2019, were taken for this study. The institutional ethics committee has approved the study.
Patients with fPCA were assessed for their demographic details such as age and sex. proforma was divided into four subdivisions:
- Unilateral or bilateral fPCA
- Unilateral or bilateral hypoplastic vertebral artery
- Presence of ischaemic stroke, type and territory of stroke
- Presence of vascular malformations such as aneurysm, ACA A1 segment hypoplasia, vertebral artery hypoplasia, white matter small vessel ischaemic changes, arteriovenous malformation, aneurysm, fenestrations and vascular loop.
Vertebral hypoplasia was defined as the size of the vertebral artery <2 mm or >50% difference when compared to the opposite side.
Type of ischaemic stroke was divided based on Trial of ORG 10172 in acute stroke treatment (TOAST) classification into large vessel disease, small vessel disease, cardioembolism and embolic stroke of unknown source.
Sources for cardioembolism include atrial fibrillation, Mitral stenosis, cardiac thrombus and severe left ventricular systolic dysfunction. Patients were classified into embolic stroke of unknown source (ESUS) after ruling out other causes of emboli using a transthoracic echocardiogram and 72 h Holter monitor.
CTA was performed using a 128-slice spiral multidetector computerized tomography (Siemens) with nonionic contrast. Magnetic resonance imaging (MRI) and MRA was done using a 1.5 Tesla system (Siemens). MRI had the following sequences– Fluid attenuated inversion recovery, diffusion-weighted imaging and apparent diffusion coefficient. The radiologist, with more than 10 years of experience, reported the imaging.
Data were entered in excel and mean was calculated. The analysis was performed for correlation of fPCA with type of stroke and territory of the infarct. Similarly, the correlation between vertebral artery hypoplasia and TOAST classification and territory of infarct was also calculated. The analysis was performed using Chi-square in Statistical Package for the Social Sciences v23 (IBM Corp, Armonk, NY). A P < 0.05 was considered significant.
| Results|| |
In this study, we have analysed 250 patients with fPCA who underwent neuroimaging for various clinical presentations, over 5 years.
In our study, we have found that the mean age of patients was 62.3 years. Predominant of the patient population was more than 60 years (57%), followed by 40–60 years (39%), 20–40 years (4%) and <20 years (<1%). On sex ratio, 61% of the study population were male, and 39% were female.
Patients with ischaemic stroke were classified based on TOAST classification, 43 (34%) had large vessel disease, 43 (41%) had lacunar infarct, 9 (7%) had a cardioembolic stroke and 23 (18%) had an embolic stroke of unknown source. Among stroke patients, 7 (6%) had involvement of ACA territory, 70 (55%) had MCA territory, 16 (13%) had PCA territory, 20 (16%) had basilar– vertebral artery territory and 14 (11%) had infarcts involving multiple vascular territories.
Foetal posterior cerebral artery and vascular anomalies
Among the fPCA, 39% were right-sided, 34% were left-sided and 27% were bilateral. Hypoplastic A1 segment of the ACA was noticed in 57 (23%) patients. Subcortical white matter small vessel ischaemic changes were noticed in 56% of patients. Among 250 patients with fPCA five had aneurysms, three had AV malformation, one with fenestration in the superior cerebellar artery and one with the vascular loop in the superior cerebellar loop. In those five patients with aneurysms, four were in the intracranial segment of ICA and one in the basilar artery.
Foetal posterior cerebral artery and stroke
Among 250 patients, 127 (51%) were found to have an ischaemic stroke. On analysis of those 127 patients, 58 (45%) had infarcts ipsilateral to fPCA, 35 (28%) had infarcts contralateral to fPCA and 34 (27%) had bilateral fPCA or infarcts in the bilateral hemisphere [Table 1]. We analysed, comparing fPCA with the type of ischaemic stroke and territory of infarct [Figure 1] and [Figure 2]. There was no difference between unilateral vs bilateral fPCA on the incidence of stroke. Patients with left fPCA had more incidence of PCA stroke as compared to the right and bilateral fPCA (11% vs. 5% and 2%). We observed, patients with bilateral fPCA had increased risk of MCA infarct (35% vs. 25%), but the result is not statistically significant.
|Figure 1: Territory of infarct in patients with fetal Posterior cerebral artery|
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|Figure 2: Type of stroke in patients with fetal Posterior cerebral artery|
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Hypoplastic vertebral artery and stroke
In 250 patients with fPCA, 120 had hypoplastic vertebral artery, 69 (57%) had right side hypoplastic, 36 (30%) had left side hypoplastic and 15 (13%) had bilateral hypoplastic. In our study, 50% (64/127) patients with ischaemic stroke and fPCA had hypoplastic vertebral artery [Table 2]. The hypoplastic vertebral artery is present in 33 patients (42%) with anterior circulation strokes and 22 patients (63%) with posterior circulation strokes. Analysis was performed, comparing the hypoplastic vertebral artery with the type of ischaemic stroke and territory of infarct [Figure 3] and [Figure 4]. Patients with bilateral hypoplastic vertebral arteries have more incidence of stroke as compared to the normal vertebral artery. Patients with bilateral hypoplastic vertebral artery are more prone to embolic stroke of unknown source (20% vs. 11%), though not statistically significant.
|Figure 3: Territory of infarct in patients with hypoplastic vertebral artery|
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| Discussion|| |
In this study, the mean age of the study population, in which fPCA has been detected was 62.3 years, compared to a mean age of 51.8 years in a study conducted by Arjal et al. and 54.9 years by Indiran and Maduraimuthu., This could be due to the demographics of the patient population visiting our centre. The study has a predominantly male population of 61% which is similar to a study conducted by Indiran and Maduraimuthu, were they noticed 57% were male. Among fPCA, 39% were right-sided, 34% were left-sided and 27% were bilateral, whereas Indiran and Maduraimuthu noticed 50% was right-sided, 28% was left-sided and 22% bilateral, which shows approximately one-fourth had bilateral fPCA in both the studies. In this study, we noticed only five patients with aneurysms (four in the ICA and one in the basilar artery) which is discordant to the findings made by Thiarawat et al., where he noticed 45% of patients with posterior communicating artery aneurysm and He and Wan found an incidence of 22% of intracranial aneurysm in fPCA., Hypoplastic A1 segment of ACA was noticed in 23% of our subjects, which was similar to the observation made by He and Wan. In this study, 56% were found to have small vessel ischaemic changes, which was similar to observations made by Indiran and Maduraimuthu, in which 65% were found to have small vessel ischaemic changes. The incidence of ischaemic stroke among fPCA was 127 patients (51%), which were slightly lower as compared to a study done by Arjal et al., where they noticed incidence to be 64%. Among patients with ischaemic stroke, 34% had large vessel disease, whereas Indiran and Maduraimuthu, noticed 51% with large vessel disease. In a similar study conducted by Shaban et al., 34% had large vessel disease, 19% with lacunar infarct, 21% had a cardioembolic stroke and 15% with cryptogenic stroke, but in our study majority had lacunar infarct (41%), followed by 34% with large vessel disease, 18% with cryptogenic stroke and 7% had a cardioembolic stroke. In our study, 55% of patients had MCA territory, and 13% had PCA territory infarct which is similar to observations made by Indiran and Maduraimuthu, where 35% had MCA, and 15% had PCA infarct. The presence of a higher incidence of MCA infarct in fPCA could be due to poor collateral formation in ICA or MCA occlusion. On analysis of fPCA with the side of an infarct, 45% of patients had fPCA in the symptomatic side, 28% of patients had fPCA in the asymptomatic side and 27% patients had bilateral fPCA or infarcts in the bilateral hemisphere. The above finding is discordant to study by Monye et al., where he has noticed 17% of fPCA in the symptomatic side, 22% in the asymptomatic side and 6% had bilateral fPCA concluding that there is an increased incidence of infarct ipsilateral to the side of fPCA in our study.
On subgroup analysis, 50% of patients with ischaemic stroke in fPCA had hypoplastic vertebral artery, whereas only 15% of patients had stroke with fPCA and hypoplastic vertebral artery in a study by Lochner et al., among which only 4 had brainstem stroke.
The hypoplastic vertebral artery is present in 42% with anterior circulation strokes and 63% with posterior circulation strokes compared to a study conducted by Park et al., where 27% of patients with anterior circulation strokes and 45% of patients with posterior circulation strokes had hypoplastic vertebral artery.
Comparison of various types of strokes with normal PCA was not made in this study, which could have provided a better analysis.
Although we were able to draw some conclusive findings, our study was not statistically significant.
The sample size is limited to a particular region. (Very few studies have been done– more such studies should be encouraged over a broad geographical region, to have a clear understanding of the prevalence of fPCA and its association with vascular anomalies).
| Conclusions|| |
In this study, we conclude that patients with fPCA had increased risk of MCA infarct probably due to poor collaterals from posterior circulation. Furthermore, patients with bilateral hypoplastic vertebral artery are more prone for embolic stroke of unknown source. Moreover, we have also noticed that fPCA is not associated with increased risk of aneurysms or AV malformations
Future studies should be done on assessing the neurological outcome in patients with fPCA.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2]