Are Fetal-Type Posterior Cerebral Arteries Associated With an Increased Risk of Posterior Communicating Artery Aneurysms?

Are Fetal-Type Posterior Cerebral Arteries Associated With an Increased Risk of Posterior... Abstract BACKGROUND Fetal-type posterior cerebral arteries (F-PCAs) might result in alterations in hemodynamic flow patterns and may predispose an individual to an increased risk of posterior communicating artery aneurysms (PCoAAs). OBJECTIVE To determine the association between PCoAAs and the presence of ipsilateral F-PCAs. METHODS We retrospectively reviewed the radiographic findings from 185 patients harboring 199 PCoAAs that were treated at our institution between 2005 and 2015. Our study population consisted of 4 cohorts: (A) patients with 171 internal carotid arteries (ICAs) harboring unilateral PCoAAs; (B) 171 unaffected ICAs in the same patients from the first group; (C) 28 ICAs of 14 patients with bilateral PCoAAs; and (D) 180 ICAs of 90 patients with aneurysms in other locations. We then determined the presence of ipsilateral F-PCAs and recorded all aneurysm characteristics. RESULTS Group A had the highest prevalence of F-PCAs (42%) compared to 19% in group B, 3% in group C, and 14% in group D (odds ratio A : B = 3.041; A : C = 19.626; and A : D = 4.308; P < .001). PCoAAs were associated with larger diameters of the posterior communicating arteries (median value 1.05 vs 0.86 mm; P = .001). The presence of F-PCAs was associated with larger sizes of the aneurysm necks (median value 3.3 vs 3.0 mm; P = .02). CONCLUSION PCoAAs were associated with a higher prevalence of ipsilateral F-PCAs. This variant was associated with larger sizes of the aneurysm necks but was not associated with the sizes of the aneurysm domes or with their rupture statuses. Fetal-type posterior cerebral artery, Prevalence, Posterior communicating artery aneurysm ABBREVIATIONS ABBREVIATIONS CTA computed tomography angiography F-PCA fetal-type posterior cerebral artery ICA internal carotid artery MRA magnetic resonance angiography PCA posterior cerebral artery PCoA posterior communicating artery PCoAA posterior communicating artery aneurysm SAH subarachnoid hemorrhage A fetal-type posterior cerebral artery (F-PCA) is a variation of the posterior cerebral artery (PCA). Previous studies have reported the prevalence of F-PCA as ranging from 7% to 36%.1-7 This variant is named according to the persistence of the early fetal configuration of the PCA that originates in the internal carotid artery (ICA) instead of in the vertebrobasilar system.8 It is characterized by a larger size of the posterior communicating artery (PCoA) compared with the ipsilateral precommunicating segment of the PCA (P1). Thus, people who have this variant possess larger PCoAs than those with adult-type PCAs. The pathogenesis of cerebral aneurysms implicates many risk factors, for example, age,9 genetics,10-14 environment,15 and molecular factors.16,17 However, hemodynamic factors appear to play an important role in aneurysm formation, particularly in people who have variations in vascular anatomy. Previous studies suggested that persistent fetal intracranial arteries predispose individuals to an increased risk of intracranial aneurysms,18-20 likely due to hemodynamic alterations in intracranial circulation. Yamamoto et al18 found that 26% (40 of 155) of the reported cases of persistent hypoglossal arteries were associated with intracranial saccular aneurysms, and most of these presented with aneurysmal rupture. Similar findings were also found in persistent trigeminal arteries, with intracranial aneurysms being seen in 12% to 30% of the patients.19 FIGURE. View largeDownload slide Flow chart showing the study population and the allocation into the 4 cohorts. PCoAA, posterior communicating artery aneurysm; ICA, internal carotid artery. FIGURE. View largeDownload slide Flow chart showing the study population and the allocation into the 4 cohorts. PCoAA, posterior communicating artery aneurysm; ICA, internal carotid artery. Similarly, F-PCAs could be associated with an increased risk of ICA-posterior communicating artery aneurysm (PCoAA) development or aneurysmal rupture, but no studies have shown such a correlation. This study aimed to determine whether the presence of F-PCAs is associated with a higher risk of developing PCoAA. METHODS Study Subject and Data Collection We designed a case-control study using the neurovascular database from our institution, which is a single-defined neurosurgical center for the 2.2 million catchment population. The calculated sample size using the method of Fleiss with continuity correction was 152 cases for each group. To minimize any potential bias, we included all patients with ICA-PCoA aneurysms who were treated between November 2005 and November 2015. A total of 185 patients with 199 PCoAAs were identified. As a control group, 90 patients with other intracranial aneurysms treated in our institution in 2014 were randomly selected, of whom were 42 middle cerebral artery aneurysms, 20 anterior communicating artery aneurysms, 7 ophthalmic artery aneurysms, 13 posterior circulation aneurysms, 2 ICA bifurcation aneurysms, and 6 distal anterior cerebral artery aneurysms. These patients were divided into 4 groups: (A) 171 ICAs harboring the PCoAAs in the patients with unilateral PCoAAs; (B) 171 unaffected ICAs in the patients with unilateral PCoAAs; (C) 28 ICAs of 14 patients with bilateral PCoAAs; and (D) 180 ICAs in patients with aneurysms in the other locations (Figure). We identified 2 cases of true bilateral PCoAAs that originated from the bilateral F-PCA during the study period. However, we had to exclude true PCoAAs from our study because there was evidence that such aneurysms were associated with F-PCA approximately 81% of the time.21 Thus, this might have potentially biased our statistical analysis. In all the groups, we determined the presence of F-PCAs from preoperative radiographic images (computed tomography angiography, magnetic resonance angiography, or digital subtraction angiography). The hospital's digital archiving system (IMPAX, version 6.5.5.1608, Agfa, Mortsel, Belgium) provided all of the radiographic images; thus, the missing data are absent. Two neurosurgeons measured the diameters of the aneurysm's dome and neck, the ICA, and the PCoA for each patient. The presence of P1, if smaller than the PCoA, was classified as a partial F-PCA; a complete F-PCA was characterized by an atresia of P1, with the PCoA continually becoming the PCA. This study was approved by our Institutional Review Board; individual patient consent was not required, as this was a retrospective study. Statistical Analysis We used IBM SPSS statistics (IBM Inc, Armonk, New York), version 22.0.0 for the statistical analysis. For quantitative variables, the median was measured. We used Chi-square tests for qualitative variables and Mann–Whitney U-tests for the comparison of the medians of the nonparametric continuous variables. A P value <.05 was considered statistically significant. RESULTS Patients and Aneurysm Characteristics In 185 patients with 199 PCoAAs, the median aneurysm dome size was 5.3 mm, the median aneurysm neck size was 3.1 mm, and the median diameter of the PCoA was 1.30 ± 0.7 mm (Table 1). In comparison to the PCoAAs, aneurysms in other locations had lower rupture risks (Table 2). TABLE 1. Demographics and Characteristics of the Intracranial Aneurysms and the Diameter of Arteriesa   Overall (n = 185)  F-PCA (n = 85)  No F-PCA (n = 100)  P-value  Sex, no. (%)           Female  146 (79)  66 (78)  80 (80)     Male  39 (21)  19 (22)  20 (20)  .696  Age, yr, median ± SD  57 ± 13.9  58 ± 14.7  56 ± 13.2  .629  Rupture state, no. (%)  104(56)  50 (58)  54 (54)  .554  Aneurysm size, mm, median ± SD           Dome  5.3 ± 3.5  5.8 ± 3.5  5.0 ± 3.5  .774   Neck  3.1 ± 1.7  3.3 ± 1.5  3.0 ± 1.7  .021  Diameter of artery, mm, median ± SD          PCoA  1.3 ± 0.7  1.7 ± 0.2  0.8 ± 0.6  < .001  ICA  3.0 ± 0.6  3.2 ± 0.6  3.0 ± 0.6  .075    Overall (n = 185)  F-PCA (n = 85)  No F-PCA (n = 100)  P-value  Sex, no. (%)           Female  146 (79)  66 (78)  80 (80)     Male  39 (21)  19 (22)  20 (20)  .696  Age, yr, median ± SD  57 ± 13.9  58 ± 14.7  56 ± 13.2  .629  Rupture state, no. (%)  104(56)  50 (58)  54 (54)  .554  Aneurysm size, mm, median ± SD           Dome  5.3 ± 3.5  5.8 ± 3.5  5.0 ± 3.5  .774   Neck  3.1 ± 1.7  3.3 ± 1.5  3.0 ± 1.7  .021  Diameter of artery, mm, median ± SD          PCoA  1.3 ± 0.7  1.7 ± 0.2  0.8 ± 0.6  < .001  ICA  3.0 ± 0.6  3.2 ± 0.6  3.0 ± 0.6  .075  aF-PCA, fetal-type posterior cerebral artery; SD, standard deviation; PCoA, posterior communicating artery; ICA, internal carotid artery. View Large TABLE 1. Demographics and Characteristics of the Intracranial Aneurysms and the Diameter of Arteriesa   Overall (n = 185)  F-PCA (n = 85)  No F-PCA (n = 100)  P-value  Sex, no. (%)           Female  146 (79)  66 (78)  80 (80)     Male  39 (21)  19 (22)  20 (20)  .696  Age, yr, median ± SD  57 ± 13.9  58 ± 14.7  56 ± 13.2  .629  Rupture state, no. (%)  104(56)  50 (58)  54 (54)  .554  Aneurysm size, mm, median ± SD           Dome  5.3 ± 3.5  5.8 ± 3.5  5.0 ± 3.5  .774   Neck  3.1 ± 1.7  3.3 ± 1.5  3.0 ± 1.7  .021  Diameter of artery, mm, median ± SD          PCoA  1.3 ± 0.7  1.7 ± 0.2  0.8 ± 0.6  < .001  ICA  3.0 ± 0.6  3.2 ± 0.6  3.0 ± 0.6  .075    Overall (n = 185)  F-PCA (n = 85)  No F-PCA (n = 100)  P-value  Sex, no. (%)           Female  146 (79)  66 (78)  80 (80)     Male  39 (21)  19 (22)  20 (20)  .696  Age, yr, median ± SD  57 ± 13.9  58 ± 14.7  56 ± 13.2  .629  Rupture state, no. (%)  104(56)  50 (58)  54 (54)  .554  Aneurysm size, mm, median ± SD           Dome  5.3 ± 3.5  5.8 ± 3.5  5.0 ± 3.5  .774   Neck  3.1 ± 1.7  3.3 ± 1.5  3.0 ± 1.7  .021  Diameter of artery, mm, median ± SD          PCoA  1.3 ± 0.7  1.7 ± 0.2  0.8 ± 0.6  < .001  ICA  3.0 ± 0.6  3.2 ± 0.6  3.0 ± 0.6  .075  aF-PCA, fetal-type posterior cerebral artery; SD, standard deviation; PCoA, posterior communicating artery; ICA, internal carotid artery. View Large TABLE 2. Demographics of the Patients With PCoAAs and Other Aneurysmsa   Patients with PCoAA(s) (n = 185)  Patients with other aneurysm(s) (n = 90)  P-value  Sex, no. (%)      .153   Female  146 (79)  64 (71)     Male  39 (21)  26 (29)    Age, yr, median ± SD  57 ± 14  60 ± 13  .425  Rupture state, no. (%)  104 (56)  29 (32)  < .001    Patients with PCoAA(s) (n = 185)  Patients with other aneurysm(s) (n = 90)  P-value  Sex, no. (%)      .153   Female  146 (79)  64 (71)     Male  39 (21)  26 (29)    Age, yr, median ± SD  57 ± 14  60 ± 13  .425  Rupture state, no. (%)  104 (56)  29 (32)  < .001  aPCoAA, posterior communicating artery aneurysm; SD, standard deviation. View Large TABLE 2. Demographics of the Patients With PCoAAs and Other Aneurysmsa   Patients with PCoAA(s) (n = 185)  Patients with other aneurysm(s) (n = 90)  P-value  Sex, no. (%)      .153   Female  146 (79)  64 (71)     Male  39 (21)  26 (29)    Age, yr, median ± SD  57 ± 14  60 ± 13  .425  Rupture state, no. (%)  104 (56)  29 (32)  < .001    Patients with PCoAA(s) (n = 185)  Patients with other aneurysm(s) (n = 90)  P-value  Sex, no. (%)      .153   Female  146 (79)  64 (71)     Male  39 (21)  26 (29)    Age, yr, median ± SD  57 ± 14  60 ± 13  .425  Rupture state, no. (%)  104 (56)  29 (32)  < .001  aPCoAA, posterior communicating artery aneurysm; SD, standard deviation. View Large The median size of the aneurysm necks was significantly larger in patients with F-PCAs (3.3 vs 3.0 mm, respectively; P = .02). In contrast, the median size of the aneurysm domes in patients with F-PCAs was not significantly larger than the size in those without F-PCAs (5.8 vs 5.0 mm, respectively; P = .77). The patients presented with subarachnoid hemorrhage (SAH) in 100 (54%) cases. The median size of the ruptured aneurysms was significantly larger than that of the unruptured aneurysms (6.3 vs 5.1 mm, respectively; P = .03). The patients harboring PCoAAs with ipsilateral F-PCAs did not have a higher likelihood to present with SAH than those without F-PCAs did (odds ratio [OR] = 1.315; 95% confidence interval [CI] = 0.723-2.391; P = .45). The presence of PCoAAs was associated with a larger diameter of the PCoA (1.05 vs 0.86 mm, respectively; P = .001). For patients with PCoAAs, the ipsilateral absence of the PCoA was found in 38 (21%) patients. Incidence of F-PCA Of the 185 patients with PCoAAs, 85 (45%) had F-PCAs, which comprised 52 F-PCAs located ipsilateral to the PCoAAs, 13 F-PCAs located contralateral to the aneurysms and 20 patients with bilateral F-PCAs. Among these 20 bilateral F-PCAs, 16 patients had bilateral partial F-PCAs, 3 patients had complete ipsilateral F-PCAs, and 1 patient had a partial contralateral F-PCA. We observed 6 complete F-PCAs; 5 of these cases occurred ipsilateral to the aneurysms (Table 3). TABLE 3. Incidence of Partial and Complete Fetal-Type Posterior Cerebral Arteries in 185 Patients With Posterior Communicating Artery Aneurysmsa     Contralateral to aneurysm      No F-PCA  Partial F-PCA  Complete F-PCA  Ipsilateral to aneurysm  No F-PCA  100  13  0    Partial F-PCA  50  16  1    Complete F-PCA  2  3  0      Contralateral to aneurysm      No F-PCA  Partial F-PCA  Complete F-PCA  Ipsilateral to aneurysm  No F-PCA  100  13  0    Partial F-PCA  50  16  1    Complete F-PCA  2  3  0  aF-PCA, fetal-type posterior cerebral artery. View Large TABLE 3. Incidence of Partial and Complete Fetal-Type Posterior Cerebral Arteries in 185 Patients With Posterior Communicating Artery Aneurysmsa     Contralateral to aneurysm      No F-PCA  Partial F-PCA  Complete F-PCA  Ipsilateral to aneurysm  No F-PCA  100  13  0    Partial F-PCA  50  16  1    Complete F-PCA  2  3  0      Contralateral to aneurysm      No F-PCA  Partial F-PCA  Complete F-PCA  Ipsilateral to aneurysm  No F-PCA  100  13  0    Partial F-PCA  50  16  1    Complete F-PCA  2  3  0  aF-PCA, fetal-type posterior cerebral artery. View Large In group A, F-PCAs occurred in 71 (42%) ICAs; in group B, 33 (19%) ICAs; in group C, 1 (3%) ICA; and in group D, 26 (14%) ICAs. Thus, group A had a higher prevalence of F-PCAs than the other groups did (Table 4). TABLE 4. Univariate analysis Aassessing the Presence of Fetal-Type Posterior Cerebral Arteries in Group A and in the Other Groupsa   Patients with F-PCA, no. (%)  Odds Ratio  95% confidence interval  P-value  Group A  71 (42%)        171 Affected ICAs with unilateral PCoAA          Group B  33 (19%)  3.418  2.079–5.621  < .001  171 Unaffected ICAs with unilateral PCoAA          Group C  1 (3%)  19.170  2.546–144.361  < .001  28 ICAs with bilateral PCoAA          Group D  26 (14%)  4.205  2.513–7.038  < .001  180 ICAs without PCoAA            Patients with F-PCA, no. (%)  Odds Ratio  95% confidence interval  P-value  Group A  71 (42%)        171 Affected ICAs with unilateral PCoAA          Group B  33 (19%)  3.418  2.079–5.621  < .001  171 Unaffected ICAs with unilateral PCoAA          Group C  1 (3%)  19.170  2.546–144.361  < .001  28 ICAs with bilateral PCoAA          Group D  26 (14%)  4.205  2.513–7.038  < .001  180 ICAs without PCoAA          aF-PCA, fetal-type posterior cerebral artery; ICA, internal carotid artery; PCoAA, posterior communicating artery aneurysm. View Large TABLE 4. Univariate analysis Aassessing the Presence of Fetal-Type Posterior Cerebral Arteries in Group A and in the Other Groupsa   Patients with F-PCA, no. (%)  Odds Ratio  95% confidence interval  P-value  Group A  71 (42%)        171 Affected ICAs with unilateral PCoAA          Group B  33 (19%)  3.418  2.079–5.621  < .001  171 Unaffected ICAs with unilateral PCoAA          Group C  1 (3%)  19.170  2.546–144.361  < .001  28 ICAs with bilateral PCoAA          Group D  26 (14%)  4.205  2.513–7.038  < .001  180 ICAs without PCoAA            Patients with F-PCA, no. (%)  Odds Ratio  95% confidence interval  P-value  Group A  71 (42%)        171 Affected ICAs with unilateral PCoAA          Group B  33 (19%)  3.418  2.079–5.621  < .001  171 Unaffected ICAs with unilateral PCoAA          Group C  1 (3%)  19.170  2.546–144.361  < .001  28 ICAs with bilateral PCoAA          Group D  26 (14%)  4.205  2.513–7.038  < .001  180 ICAs without PCoAA          aF-PCA, fetal-type posterior cerebral artery; ICA, internal carotid artery; PCoAA, posterior communicating artery aneurysm. View Large DISCUSSION Morphological factors of the surrounding vascular tree22-24 and hemodynamic factors25-29 are important contributing factors to aneurysm formation. The presence of an F-PCA might result in a different hemodynamic flow pattern,30 particularly at the origin of the PCoA area. Therefore, F-PCAs might be associated with a higher incidence of PCoAAs. Currently, no study has determined a correlation between F-PCAs and PCoAAs. Previous articles on the prevalence of F-PCAs mostly studied normal brains or patients with cerebral infarctions. The estimated prevalence of unilateral F-PCAs ranged from 11% to 29% and that of bilateral F-PCA ranged from 1% to 9%.1-7 A previous study from our institution found an unusually high prevalence of F-PCAs, namely, 42%, in patients with PCoAAs.31 In our study, the higher prevalence of F-PCAs in group A may have indicated a correlation between F-PCAs and PCoAA formation. F-PCAs are a known risk factor for occipital lobe infarction in patients who undergo microsurgical clipping of the PCoAA because a PCoA might become entrapped by the clip.32,33 Thus, neurosurgeons should carefully determine the presence of F-PCAs from preoperative images, as up to 40% of patients with PCoAAs could have an F-PCA. When clipping a PCoAA that is associated with an ipsilateral F-PCA, the direction of the clip should be angled more laterally than usual to prevent F-PCA occlusion.31 Data regarding the prevalence of complete F-PCAs and partial F-PCAs were limited. Our results showed that the affected ICAs had a higher prevalence of complete F-PCAs than the unaffected arteries did. High wall shear stress is important in the development, continuous expansion, and eventual rupture of cerebral aneurysms.34-36 Kulcsar et al37 showed the important role in aneurysm formation due to a combination of high wall shear stress and a high positive spatial wall shear stress gradient on a small segment of an arterial wall. The present study indicated a correlation between the presence of F-PCAs and the size of an aneurysm neck but not of the aneurysm dome. Due to the wider diameter of an F-PCA, it could be postulated that the area of vessel wall remodelling is larger and results in a larger aneurysm neck.38,39 Morphological factors appear to be crucial risk factors for the rupture status of PCoAAs.40-42 Lv N et al43 reported factors that related to the rupture status of PCoAAs, which consist of a higher inflow angle and a higher percentage of low wall shear stress areas. Lindgren et al44 reported the association between irregular or multilobar aneurysm shapes and rupture status in intracranial aneurysms of all sizes and locations. In addition, prior studies have supported that hemodynamic alterations play an important role in the rupture status of intracranial aneurysms.28,45,46 Our findings revealed no association between the presence of F-PCAs and the rupture status of PCoAAs. The present results supported Can's findings that a larger PCoA diameter is associated with the presence of PCoAAs.47 Once blood flows from the proximal ICA to the larger cross-sectional area of the distal ICA and the large PCoA, the excess kinetic energy and momentum of the blood might cause a high stress impact on the arterial wall at the apical region, resulting in the formation of an aneurysm. We controlled for the effects of other risk factors, such as age, smoking, hypertension, and a family history of aneurysms by comparing the aneurysmal side with the unaffected side within the same patient for groups A and B of the study group. The aneurysmal side was significantly associated with a higher prevalence of F-PCA than the unaffected side and with the ICAs of patients with aneurysms in other locations. However, our findings of a lower prevalence of F-PCA in group C, the occurrence of PCoAAs contralateral to F-PCAs, and the absence of PCoAs ipsilateral to the PCoAAs appeared to contradict this association. One reason for these conflicting results might have been an inadequate sample size of group C. Another explanation is that other angioarchitectures, such as the angle between the ophthalmic segment and the communicating segment of the ICA or the symmetry of blood flow in the circle of Willis, were also associated with aneurysm formation.48,49 The impact of F-PCAs on hemodynamic characteristics, such as maximum wall shear stress, oscillatory wall shear stress distributions, the shear concentration index, and the mean oscillatory shear index, remains unclear. Increasing evidence has shown the formation of de novo and the growth of unruptured aneurysms in long-term follow-up clinical studies.50-52 Furthermore, a recent study using carbon dating to explore the age of intracranial aneurysms concluded that the average collagen age of the aneurysm wall is less than 5 yr.53 Therefore, in regard to F-PCA, a prospective study involving close long-term surveillance of these patients should be performed in order to determine the relative risk for the development of de novo PCoAAs. A cost-effectiveness study of the follow-up imaging would also be beneficial. Limitations An unavoidable bias of this study was that the ruptured aneurysms were included. Thus, the sizes of the PCoAs might have been affected by cerebral vasospasms. CONCLUSION Our findings that F-PCAs were associated with a higher risk of PCoAAs supported the hypothesis that hemodynamic factors might implicate the formation of an aneurysm. 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Morphological differences between the aneurysmal and normal artery in patients with internal carotid–posterior communicating artery aneurysm. J Clin Neurosci . 2010; 17( 11): 1395- 1398. Google Scholar CrossRef Search ADS PubMed  25. Charbel FT, Seyfried D, Mehta B, Dujovny M, Ausman JI. Dominant Al: angiographic and clinical correlations with anterior communicating artery aneurysms. Neurol Res . 1991; 13( 4): 253- 256. Google Scholar CrossRef Search ADS PubMed  26. Alnaes MS, Isaksen J, Mardal KA, Romner B, Morgan MK, Ingebrigtsen T. Computation of hemodynamics in the circle of Willis. Stroke . 2007; 38( 9): 2500- 2505. Google Scholar CrossRef Search ADS PubMed  27. Cebral JR, Mut F, Weir J, Putman CM. Association of hemodynamic characteristics and cerebral aneurysm rupture. Am J Neuroradiol . 2011; 32( 2): 264- 270. Google Scholar CrossRef Search ADS PubMed  28. Can A, Mouminah A, Ho AL, Du R. Effect of vascular anatomy on the formation of basilar tip aneurysms. Neurosurgery . 2015; 76( 1): 62- 66; discussion 66. Google Scholar CrossRef Search ADS PubMed  29. Fan J, Wang Y, Liu J et al.   Morphological-hemodynamic characteristics of intracranial bifurcation mirror aneurysms. World Neurosurg . 2015; 84( 1): 114- 120.e2. Google Scholar CrossRef Search ADS PubMed  30. Ren Y, Chen Q, Li ZY. A 3D numerical study of the collateral capacity of the circle of Willis with anatomical variation in the posterior circulation. BioMed Eng OnLine . 2015; 14( Suppl 1): S11. Google Scholar CrossRef Search ADS PubMed  31. Thiarawat P, Jahromi BR, Kozyrev DA et al.   Microneurosurgical management of posterior communicating artery aneurysm: A contemporary series from helsinki. World Neurosurgery . 2017; 101: 379- 388. Google Scholar CrossRef Search ADS PubMed  32. Wu HM, Chuang YM. The clinical relevance of fetal variant of the circle of Willis and its influence on the cerebral collateral circulation. Acta Neurol Taiwan . 2011; 20( 4): 379- 388. 33. Arjal RK, Zhu T, Zhou Y. The study of fetal-type posterior cerebral circulation on multislice CT angiography and its influence on cerebral ischemic strokes. Clin Imaging . 2014; 38( 3): 221- 225. Google Scholar CrossRef Search ADS PubMed  34. Steinman DA, Milner JS, Norley CJ, Lownie SP, Holdsworth DW. Image-based computational simulation of flow dynamics in a giant intracranial aneurysm. AJNR Am J Neuroradiol . 2003; 24( 4): 559- 566. Google Scholar PubMed  35. Cebral JR, Castro MA, Appanaboyina S, Putman CM, Millan D, Frangi AF. Efficient pipeline for image-based patient-specific analysis of cerebral aneurysm hemodynamics: technique and sensitivity. IEEE Trans Med Imaging . 2005; 24( 4): 457- 467. Google Scholar CrossRef Search ADS PubMed  36. Valencia AA, Guzman AM, Finol EA, Amon CH. Blood flow dynamics in saccular aneurysm models of the basilar artery. J Biomech Eng . 2006; 128( 4): 516- 526. Google Scholar CrossRef Search ADS PubMed  37. Kulcsar Z, Ugron A, Marosfoi M, Berentei Z, Paal G, Szikora I. Hemodynamics of cerebral aneurysm initiation: the role of wall shear stress and spatial wall shear stress gradient. Am J Neuroradiol . 2011; 32( 3): 587- 594. Google Scholar CrossRef Search ADS PubMed  38. Papaioannou TG, Stefanadis C. Vascular wall shear stress: basic principles and methods. Hellenic J Cardiol . 2005; 46( 1): 9- 15. Google Scholar PubMed  39. Katritsis D, Kaiktsis L, Chaniotis A, Pantos J, Efstathopoulos EP, Marmarelis V. Wall shear stress: theoretical considerations and methods of measurement. Prog Cardiovasc Dis . 2007; 49( 5): 307- 329. Google Scholar CrossRef Search ADS PubMed  40. Xu J, Yu Y, Wu X et al.   Morphological and hemodynamic analysis of mirror posterior communicating artery aneurysms. PLoS One . 2013; 8( 1): e55413. Google Scholar CrossRef Search ADS PubMed  41. Ho A, Lin N, Charoenvimolphan N et al.   Morphological parameters associated with ruptured posterior communicating aneurysms. PLoS One . 2014; 9( 4): e94837. Google Scholar CrossRef Search ADS PubMed  42. Matsukawa H, Fujii M, Akaike G et al.   Morphological and clinical risk factors for posterior communicating artery aneurysm rupture. J Neurosurg . 2014; 120( 1): 104- 110. Google Scholar CrossRef Search ADS PubMed  43. Lv N, Wang C, Karmonik C et al.   Morphological and hemodynamic discriminators for rupture status in posterior communicating artery aneurysms. PLoS One . 2016; 11( 2): e0149906. Google Scholar CrossRef Search ADS PubMed  44. Lindgren AE, Koivisto T, Bjorkman J et al.   Irregular shape of intracranial aneurysm indicates rupture risk irrespective of size in a population-based cohort. Stroke . 2016; 47( 5): 1219- 1226. Google Scholar CrossRef Search ADS PubMed  45. Takao H, Murayama Y, Otsuka S et al.   Hemodynamic differences between unruptured and ruptured intracranial aneurysms during observation. Stroke . 2012; 43( 5): 1436- 1439. Google Scholar CrossRef Search ADS PubMed  46. Matsukawa H, Uemura A, Fujii M, Kamo M, Takahashi O, Sumiyoshi S. Morphological and clinical risk factors for the rupture of anterior communicating artery aneurysms. J Neurosurg . 2013; 118( 5): 978- 983. Google Scholar CrossRef Search ADS PubMed  47. Can A, Ho AL, Emmer BJ, Dammers R, Dirven CM, Du R. Association between vascular anatomy and posterior communicating artery aneurysms. World Neurosurg . 2015; 84( 5): 1251- 1255. Google Scholar CrossRef Search ADS PubMed  48. Hu T, Wang D. Association between anatomical variations of the posterior communicating artery and the presence of aneurysms. Neurol Res . 2016; 12( 11): 1- 7. 49. Chung BJ, Doddasomayajula R, Mut F et al.   Angioarchitectures and hemodynamic characteristics of posterior communicating artery aneurysms and their association with rupture status. AJNR Am J Neuroradiol . 2017; 38( 11): 2111- 2118. Google Scholar CrossRef Search ADS PubMed  50. Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms: a long-term follow-up study. Stroke . 2001; 32( 2): 485- 491. Google Scholar CrossRef Search ADS PubMed  51. Ferns SP, Sprengers ME, van Rooij WJ et al.   De novo aneurysm formation and growth of untreated aneurysms: a 5-year MRA follow-up in a large cohort of patients with coiled aneurysms and review of the literature. Stroke . 2011; 42( 2): 313- 318. Google Scholar CrossRef Search ADS PubMed  52. Teo M, St George EJ. Radiologic surveillance of untreated unruptured intracranial aneurysms: A single surgeon's experience. World Neurosurg . 2016; 90: 20- 28. Google Scholar CrossRef Search ADS PubMed  53. Etminan N, Dreier R, Buchholz BA et al.   Exploring the age of intracranial aneurysms using carbon birth dating: preliminary results. Stroke . 2013; 44( 3): 799- 802. Google Scholar CrossRef Search ADS PubMed  COMMENTS The authors present the incidence of fetal posterior cerebral artery (PCA) in patients with posterior communicating artery (PCoA) aneurysms. This study included 185 patients harboring 199 PCoA aneurysms as well as 90 control patients with intracranial aneurysms in other locations. Of the patients with unilateral PCoA aneurysms, 71 (42%) had an ipsilateral fetal PCA and 33 (19%) had a contralateral fetal PCA. Fourteen patients presented with bilateral PCoA aneurysms, but of these, only 1 (3%) fetal PCA was present. Of the 180 ICAs studied in patients with aneurysms in other locations, 26 (14%) had fetal PCAs. Additionally, the authors note that the presence of an ipsilateral fetal PCA was significantly associated with a larger aneurysm neck (3.3 vs 3.0 mm, P = .02). They conclude that the presence of a fetal PCA is associated with a higher risk of developing PCoA aneurysms, likely due to increased hemodynamic stress. The notion that anatomical variations in the circle of Willis are associated with aneurysm formation is generally accepted, and well described, in the literature. In 1984, Kayembe et al.1 reported a post-mortem analysis of anatomical variations in the circle of Willis and cerebral aneurysms, finding that in patients with asymmetric PCoA arteries, aneurysms were more likely to be found on the side of a larger caliber vessel. More recently, a report on variations of the circle of Willis in 202 aneurysms revealed that of the 67 PCoAs, almost 50% were associated with fetal origin of the PCA, similar to the prevalence in the current series.2 Hemodynamic factors including flow patterns, wall shear stress, and oscillatory shear index have been implicated as key factors in the formation, growth, and rupture of intracranial aneurysms. The authors assert that the presence of a fetal PCA is associated with a higher risk of aneurysm formation likely due to an increase in local hemodynamic stress. While this finding would be consistent with the current literature, it is unclear if the data presented fully supports this conclusion. While the authors did find a significant increased incidence of fetal PCAs ipsilateral to unilateral PCoA aneurysms, patients with bilateral PCoA aneurysms actually had the lowest incidence of fetal PCAs (3%). Additionally, although PCoAs associated with fetal PCAs were slightly larger, they found no association between the presence of a fetal PCA and aneurysm rupture, an association which may have been expected in the setting of increased hemodynamic stress. These discrepancies highlight the lack of one simple anatomic predictor for risk of aneurysm formation, and challenge the notion that prospective surveillance of fetal PCA for de novo aneurysm, as proposed by the authors, is a clinically useful or warranted strategy. Ashley Barks Sepideh Amin-Hanjani Chicago, Illinois 1. Kayembe KN Sasahara M Hazama F. “ Cerebral aneurysms and variations in the circle of Willis”. Stroke  1984; 15( 5): 846– 850. Google Scholar CrossRef Search ADS PubMed  2. Songsaeng D Geibprasert S Willinsky R Tymianski M TerBrugge KG Krings T. “ Impact of anatomical variations of the circle of Willis on the incidence of aneurysms and their recurrence rate following endovascular treatment.” Clin Radiol . 2010; 65( 11): 895– 901. Google Scholar CrossRef Search ADS PubMed  The putative association of a fetal posterior cerebral artery (PCA) and posterior communicating artery (PCoA) aneurysm has been debated for a long time. The prevailing theory is that hemodynamic changes in the presence of a large PCoA might induce increased hemodynamic stress at the origin of the vessel, thus increasing the risk of aneurysm formation. In this study, the authors consider 4 different cohorts; Group A: 171 ICAs with unilateral PCoA aneurysms; group B: 171 contralateral unaffected ICAs; group C: 28 ICAs in patients with bilateral PCoA aneurysms, and group D: 180 ICAs in 90 patients with aneurysms in locations other than the PCoA. Overall, fetal PCA configuration was present in 42% of ICAs in group A, 19% in group B, 3% in group C, and 14% in group D. This observation would suggest that in patients with unilateral PCoA aneurysms, a fetal PCA configuration is more common than in control arteries. Although these findings might lend support to the theory that fetal PCA configuration is at increased risk of PCoA aneurysm formation, the practical implications of such observation are limited since it is impractical and not indicated to follow these patients over time to rule out aneurysm formation. Nevertheless, the presence of a fetal PCA in a patient with a PCoA aneurysm has important implications for surgical and endovascular therapy. When this anatomy is present, preservation of the fetal PCA is imperative from both a surgical and endovascular point of view. In this study, the presence of a fetal PCA was associated with a larger aneurysm neck, and this might make simple coil embolization more problematic. In addition, the presence of a true fetal PCA is a factor associated with lack of angiographic obliteration after flow diversion for PCoA aneurysms as suggested in a few recent series.1,2 Thomas Sorenson Giuseppe Lanzino Rochester, Minnesota 1. Kan P Duckworth E Puri A Velat G Wakhloo A. Treatment failure of fetal posterior communicating artery aneurysms with the pipeline embolization device. J Neurointerv Surg . 2016; 8( 9): 945- 948. Google Scholar CrossRef Search ADS PubMed  2. Wallace AN Kayan Y Austin MJ, et al. Pipeline embolization of posterior communicating artery aneurysms associated with a fetal origin posterior cerebral artery. Clin Neurol Neurosurg . 2017; 160: 83- 87. Google Scholar CrossRef Search ADS PubMed  Copyright © 2018 by the Congress of Neurological Surgeons This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurosurgery Oxford University Press

Are Fetal-Type Posterior Cerebral Arteries Associated With an Increased Risk of Posterior Communicating Artery Aneurysms?

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Congress of Neurological Surgeons
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Copyright © 2018 by the Congress of Neurological Surgeons
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0148-396X
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1524-4040
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10.1093/neuros/nyy186
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Abstract

Abstract BACKGROUND Fetal-type posterior cerebral arteries (F-PCAs) might result in alterations in hemodynamic flow patterns and may predispose an individual to an increased risk of posterior communicating artery aneurysms (PCoAAs). OBJECTIVE To determine the association between PCoAAs and the presence of ipsilateral F-PCAs. METHODS We retrospectively reviewed the radiographic findings from 185 patients harboring 199 PCoAAs that were treated at our institution between 2005 and 2015. Our study population consisted of 4 cohorts: (A) patients with 171 internal carotid arteries (ICAs) harboring unilateral PCoAAs; (B) 171 unaffected ICAs in the same patients from the first group; (C) 28 ICAs of 14 patients with bilateral PCoAAs; and (D) 180 ICAs of 90 patients with aneurysms in other locations. We then determined the presence of ipsilateral F-PCAs and recorded all aneurysm characteristics. RESULTS Group A had the highest prevalence of F-PCAs (42%) compared to 19% in group B, 3% in group C, and 14% in group D (odds ratio A : B = 3.041; A : C = 19.626; and A : D = 4.308; P < .001). PCoAAs were associated with larger diameters of the posterior communicating arteries (median value 1.05 vs 0.86 mm; P = .001). The presence of F-PCAs was associated with larger sizes of the aneurysm necks (median value 3.3 vs 3.0 mm; P = .02). CONCLUSION PCoAAs were associated with a higher prevalence of ipsilateral F-PCAs. This variant was associated with larger sizes of the aneurysm necks but was not associated with the sizes of the aneurysm domes or with their rupture statuses. Fetal-type posterior cerebral artery, Prevalence, Posterior communicating artery aneurysm ABBREVIATIONS ABBREVIATIONS CTA computed tomography angiography F-PCA fetal-type posterior cerebral artery ICA internal carotid artery MRA magnetic resonance angiography PCA posterior cerebral artery PCoA posterior communicating artery PCoAA posterior communicating artery aneurysm SAH subarachnoid hemorrhage A fetal-type posterior cerebral artery (F-PCA) is a variation of the posterior cerebral artery (PCA). Previous studies have reported the prevalence of F-PCA as ranging from 7% to 36%.1-7 This variant is named according to the persistence of the early fetal configuration of the PCA that originates in the internal carotid artery (ICA) instead of in the vertebrobasilar system.8 It is characterized by a larger size of the posterior communicating artery (PCoA) compared with the ipsilateral precommunicating segment of the PCA (P1). Thus, people who have this variant possess larger PCoAs than those with adult-type PCAs. The pathogenesis of cerebral aneurysms implicates many risk factors, for example, age,9 genetics,10-14 environment,15 and molecular factors.16,17 However, hemodynamic factors appear to play an important role in aneurysm formation, particularly in people who have variations in vascular anatomy. Previous studies suggested that persistent fetal intracranial arteries predispose individuals to an increased risk of intracranial aneurysms,18-20 likely due to hemodynamic alterations in intracranial circulation. Yamamoto et al18 found that 26% (40 of 155) of the reported cases of persistent hypoglossal arteries were associated with intracranial saccular aneurysms, and most of these presented with aneurysmal rupture. Similar findings were also found in persistent trigeminal arteries, with intracranial aneurysms being seen in 12% to 30% of the patients.19 FIGURE. View largeDownload slide Flow chart showing the study population and the allocation into the 4 cohorts. PCoAA, posterior communicating artery aneurysm; ICA, internal carotid artery. FIGURE. View largeDownload slide Flow chart showing the study population and the allocation into the 4 cohorts. PCoAA, posterior communicating artery aneurysm; ICA, internal carotid artery. Similarly, F-PCAs could be associated with an increased risk of ICA-posterior communicating artery aneurysm (PCoAA) development or aneurysmal rupture, but no studies have shown such a correlation. This study aimed to determine whether the presence of F-PCAs is associated with a higher risk of developing PCoAA. METHODS Study Subject and Data Collection We designed a case-control study using the neurovascular database from our institution, which is a single-defined neurosurgical center for the 2.2 million catchment population. The calculated sample size using the method of Fleiss with continuity correction was 152 cases for each group. To minimize any potential bias, we included all patients with ICA-PCoA aneurysms who were treated between November 2005 and November 2015. A total of 185 patients with 199 PCoAAs were identified. As a control group, 90 patients with other intracranial aneurysms treated in our institution in 2014 were randomly selected, of whom were 42 middle cerebral artery aneurysms, 20 anterior communicating artery aneurysms, 7 ophthalmic artery aneurysms, 13 posterior circulation aneurysms, 2 ICA bifurcation aneurysms, and 6 distal anterior cerebral artery aneurysms. These patients were divided into 4 groups: (A) 171 ICAs harboring the PCoAAs in the patients with unilateral PCoAAs; (B) 171 unaffected ICAs in the patients with unilateral PCoAAs; (C) 28 ICAs of 14 patients with bilateral PCoAAs; and (D) 180 ICAs in patients with aneurysms in the other locations (Figure). We identified 2 cases of true bilateral PCoAAs that originated from the bilateral F-PCA during the study period. However, we had to exclude true PCoAAs from our study because there was evidence that such aneurysms were associated with F-PCA approximately 81% of the time.21 Thus, this might have potentially biased our statistical analysis. In all the groups, we determined the presence of F-PCAs from preoperative radiographic images (computed tomography angiography, magnetic resonance angiography, or digital subtraction angiography). The hospital's digital archiving system (IMPAX, version 6.5.5.1608, Agfa, Mortsel, Belgium) provided all of the radiographic images; thus, the missing data are absent. Two neurosurgeons measured the diameters of the aneurysm's dome and neck, the ICA, and the PCoA for each patient. The presence of P1, if smaller than the PCoA, was classified as a partial F-PCA; a complete F-PCA was characterized by an atresia of P1, with the PCoA continually becoming the PCA. This study was approved by our Institutional Review Board; individual patient consent was not required, as this was a retrospective study. Statistical Analysis We used IBM SPSS statistics (IBM Inc, Armonk, New York), version 22.0.0 for the statistical analysis. For quantitative variables, the median was measured. We used Chi-square tests for qualitative variables and Mann–Whitney U-tests for the comparison of the medians of the nonparametric continuous variables. A P value <.05 was considered statistically significant. RESULTS Patients and Aneurysm Characteristics In 185 patients with 199 PCoAAs, the median aneurysm dome size was 5.3 mm, the median aneurysm neck size was 3.1 mm, and the median diameter of the PCoA was 1.30 ± 0.7 mm (Table 1). In comparison to the PCoAAs, aneurysms in other locations had lower rupture risks (Table 2). TABLE 1. Demographics and Characteristics of the Intracranial Aneurysms and the Diameter of Arteriesa   Overall (n = 185)  F-PCA (n = 85)  No F-PCA (n = 100)  P-value  Sex, no. (%)           Female  146 (79)  66 (78)  80 (80)     Male  39 (21)  19 (22)  20 (20)  .696  Age, yr, median ± SD  57 ± 13.9  58 ± 14.7  56 ± 13.2  .629  Rupture state, no. (%)  104(56)  50 (58)  54 (54)  .554  Aneurysm size, mm, median ± SD           Dome  5.3 ± 3.5  5.8 ± 3.5  5.0 ± 3.5  .774   Neck  3.1 ± 1.7  3.3 ± 1.5  3.0 ± 1.7  .021  Diameter of artery, mm, median ± SD          PCoA  1.3 ± 0.7  1.7 ± 0.2  0.8 ± 0.6  < .001  ICA  3.0 ± 0.6  3.2 ± 0.6  3.0 ± 0.6  .075    Overall (n = 185)  F-PCA (n = 85)  No F-PCA (n = 100)  P-value  Sex, no. (%)           Female  146 (79)  66 (78)  80 (80)     Male  39 (21)  19 (22)  20 (20)  .696  Age, yr, median ± SD  57 ± 13.9  58 ± 14.7  56 ± 13.2  .629  Rupture state, no. (%)  104(56)  50 (58)  54 (54)  .554  Aneurysm size, mm, median ± SD           Dome  5.3 ± 3.5  5.8 ± 3.5  5.0 ± 3.5  .774   Neck  3.1 ± 1.7  3.3 ± 1.5  3.0 ± 1.7  .021  Diameter of artery, mm, median ± SD          PCoA  1.3 ± 0.7  1.7 ± 0.2  0.8 ± 0.6  < .001  ICA  3.0 ± 0.6  3.2 ± 0.6  3.0 ± 0.6  .075  aF-PCA, fetal-type posterior cerebral artery; SD, standard deviation; PCoA, posterior communicating artery; ICA, internal carotid artery. View Large TABLE 1. Demographics and Characteristics of the Intracranial Aneurysms and the Diameter of Arteriesa   Overall (n = 185)  F-PCA (n = 85)  No F-PCA (n = 100)  P-value  Sex, no. (%)           Female  146 (79)  66 (78)  80 (80)     Male  39 (21)  19 (22)  20 (20)  .696  Age, yr, median ± SD  57 ± 13.9  58 ± 14.7  56 ± 13.2  .629  Rupture state, no. (%)  104(56)  50 (58)  54 (54)  .554  Aneurysm size, mm, median ± SD           Dome  5.3 ± 3.5  5.8 ± 3.5  5.0 ± 3.5  .774   Neck  3.1 ± 1.7  3.3 ± 1.5  3.0 ± 1.7  .021  Diameter of artery, mm, median ± SD          PCoA  1.3 ± 0.7  1.7 ± 0.2  0.8 ± 0.6  < .001  ICA  3.0 ± 0.6  3.2 ± 0.6  3.0 ± 0.6  .075    Overall (n = 185)  F-PCA (n = 85)  No F-PCA (n = 100)  P-value  Sex, no. (%)           Female  146 (79)  66 (78)  80 (80)     Male  39 (21)  19 (22)  20 (20)  .696  Age, yr, median ± SD  57 ± 13.9  58 ± 14.7  56 ± 13.2  .629  Rupture state, no. (%)  104(56)  50 (58)  54 (54)  .554  Aneurysm size, mm, median ± SD           Dome  5.3 ± 3.5  5.8 ± 3.5  5.0 ± 3.5  .774   Neck  3.1 ± 1.7  3.3 ± 1.5  3.0 ± 1.7  .021  Diameter of artery, mm, median ± SD          PCoA  1.3 ± 0.7  1.7 ± 0.2  0.8 ± 0.6  < .001  ICA  3.0 ± 0.6  3.2 ± 0.6  3.0 ± 0.6  .075  aF-PCA, fetal-type posterior cerebral artery; SD, standard deviation; PCoA, posterior communicating artery; ICA, internal carotid artery. View Large TABLE 2. Demographics of the Patients With PCoAAs and Other Aneurysmsa   Patients with PCoAA(s) (n = 185)  Patients with other aneurysm(s) (n = 90)  P-value  Sex, no. (%)      .153   Female  146 (79)  64 (71)     Male  39 (21)  26 (29)    Age, yr, median ± SD  57 ± 14  60 ± 13  .425  Rupture state, no. (%)  104 (56)  29 (32)  < .001    Patients with PCoAA(s) (n = 185)  Patients with other aneurysm(s) (n = 90)  P-value  Sex, no. (%)      .153   Female  146 (79)  64 (71)     Male  39 (21)  26 (29)    Age, yr, median ± SD  57 ± 14  60 ± 13  .425  Rupture state, no. (%)  104 (56)  29 (32)  < .001  aPCoAA, posterior communicating artery aneurysm; SD, standard deviation. View Large TABLE 2. Demographics of the Patients With PCoAAs and Other Aneurysmsa   Patients with PCoAA(s) (n = 185)  Patients with other aneurysm(s) (n = 90)  P-value  Sex, no. (%)      .153   Female  146 (79)  64 (71)     Male  39 (21)  26 (29)    Age, yr, median ± SD  57 ± 14  60 ± 13  .425  Rupture state, no. (%)  104 (56)  29 (32)  < .001    Patients with PCoAA(s) (n = 185)  Patients with other aneurysm(s) (n = 90)  P-value  Sex, no. (%)      .153   Female  146 (79)  64 (71)     Male  39 (21)  26 (29)    Age, yr, median ± SD  57 ± 14  60 ± 13  .425  Rupture state, no. (%)  104 (56)  29 (32)  < .001  aPCoAA, posterior communicating artery aneurysm; SD, standard deviation. View Large The median size of the aneurysm necks was significantly larger in patients with F-PCAs (3.3 vs 3.0 mm, respectively; P = .02). In contrast, the median size of the aneurysm domes in patients with F-PCAs was not significantly larger than the size in those without F-PCAs (5.8 vs 5.0 mm, respectively; P = .77). The patients presented with subarachnoid hemorrhage (SAH) in 100 (54%) cases. The median size of the ruptured aneurysms was significantly larger than that of the unruptured aneurysms (6.3 vs 5.1 mm, respectively; P = .03). The patients harboring PCoAAs with ipsilateral F-PCAs did not have a higher likelihood to present with SAH than those without F-PCAs did (odds ratio [OR] = 1.315; 95% confidence interval [CI] = 0.723-2.391; P = .45). The presence of PCoAAs was associated with a larger diameter of the PCoA (1.05 vs 0.86 mm, respectively; P = .001). For patients with PCoAAs, the ipsilateral absence of the PCoA was found in 38 (21%) patients. Incidence of F-PCA Of the 185 patients with PCoAAs, 85 (45%) had F-PCAs, which comprised 52 F-PCAs located ipsilateral to the PCoAAs, 13 F-PCAs located contralateral to the aneurysms and 20 patients with bilateral F-PCAs. Among these 20 bilateral F-PCAs, 16 patients had bilateral partial F-PCAs, 3 patients had complete ipsilateral F-PCAs, and 1 patient had a partial contralateral F-PCA. We observed 6 complete F-PCAs; 5 of these cases occurred ipsilateral to the aneurysms (Table 3). TABLE 3. Incidence of Partial and Complete Fetal-Type Posterior Cerebral Arteries in 185 Patients With Posterior Communicating Artery Aneurysmsa     Contralateral to aneurysm      No F-PCA  Partial F-PCA  Complete F-PCA  Ipsilateral to aneurysm  No F-PCA  100  13  0    Partial F-PCA  50  16  1    Complete F-PCA  2  3  0      Contralateral to aneurysm      No F-PCA  Partial F-PCA  Complete F-PCA  Ipsilateral to aneurysm  No F-PCA  100  13  0    Partial F-PCA  50  16  1    Complete F-PCA  2  3  0  aF-PCA, fetal-type posterior cerebral artery. View Large TABLE 3. Incidence of Partial and Complete Fetal-Type Posterior Cerebral Arteries in 185 Patients With Posterior Communicating Artery Aneurysmsa     Contralateral to aneurysm      No F-PCA  Partial F-PCA  Complete F-PCA  Ipsilateral to aneurysm  No F-PCA  100  13  0    Partial F-PCA  50  16  1    Complete F-PCA  2  3  0      Contralateral to aneurysm      No F-PCA  Partial F-PCA  Complete F-PCA  Ipsilateral to aneurysm  No F-PCA  100  13  0    Partial F-PCA  50  16  1    Complete F-PCA  2  3  0  aF-PCA, fetal-type posterior cerebral artery. View Large In group A, F-PCAs occurred in 71 (42%) ICAs; in group B, 33 (19%) ICAs; in group C, 1 (3%) ICA; and in group D, 26 (14%) ICAs. Thus, group A had a higher prevalence of F-PCAs than the other groups did (Table 4). TABLE 4. Univariate analysis Aassessing the Presence of Fetal-Type Posterior Cerebral Arteries in Group A and in the Other Groupsa   Patients with F-PCA, no. (%)  Odds Ratio  95% confidence interval  P-value  Group A  71 (42%)        171 Affected ICAs with unilateral PCoAA          Group B  33 (19%)  3.418  2.079–5.621  < .001  171 Unaffected ICAs with unilateral PCoAA          Group C  1 (3%)  19.170  2.546–144.361  < .001  28 ICAs with bilateral PCoAA          Group D  26 (14%)  4.205  2.513–7.038  < .001  180 ICAs without PCoAA            Patients with F-PCA, no. (%)  Odds Ratio  95% confidence interval  P-value  Group A  71 (42%)        171 Affected ICAs with unilateral PCoAA          Group B  33 (19%)  3.418  2.079–5.621  < .001  171 Unaffected ICAs with unilateral PCoAA          Group C  1 (3%)  19.170  2.546–144.361  < .001  28 ICAs with bilateral PCoAA          Group D  26 (14%)  4.205  2.513–7.038  < .001  180 ICAs without PCoAA          aF-PCA, fetal-type posterior cerebral artery; ICA, internal carotid artery; PCoAA, posterior communicating artery aneurysm. View Large TABLE 4. Univariate analysis Aassessing the Presence of Fetal-Type Posterior Cerebral Arteries in Group A and in the Other Groupsa   Patients with F-PCA, no. (%)  Odds Ratio  95% confidence interval  P-value  Group A  71 (42%)        171 Affected ICAs with unilateral PCoAA          Group B  33 (19%)  3.418  2.079–5.621  < .001  171 Unaffected ICAs with unilateral PCoAA          Group C  1 (3%)  19.170  2.546–144.361  < .001  28 ICAs with bilateral PCoAA          Group D  26 (14%)  4.205  2.513–7.038  < .001  180 ICAs without PCoAA            Patients with F-PCA, no. (%)  Odds Ratio  95% confidence interval  P-value  Group A  71 (42%)        171 Affected ICAs with unilateral PCoAA          Group B  33 (19%)  3.418  2.079–5.621  < .001  171 Unaffected ICAs with unilateral PCoAA          Group C  1 (3%)  19.170  2.546–144.361  < .001  28 ICAs with bilateral PCoAA          Group D  26 (14%)  4.205  2.513–7.038  < .001  180 ICAs without PCoAA          aF-PCA, fetal-type posterior cerebral artery; ICA, internal carotid artery; PCoAA, posterior communicating artery aneurysm. View Large DISCUSSION Morphological factors of the surrounding vascular tree22-24 and hemodynamic factors25-29 are important contributing factors to aneurysm formation. The presence of an F-PCA might result in a different hemodynamic flow pattern,30 particularly at the origin of the PCoA area. Therefore, F-PCAs might be associated with a higher incidence of PCoAAs. Currently, no study has determined a correlation between F-PCAs and PCoAAs. Previous articles on the prevalence of F-PCAs mostly studied normal brains or patients with cerebral infarctions. The estimated prevalence of unilateral F-PCAs ranged from 11% to 29% and that of bilateral F-PCA ranged from 1% to 9%.1-7 A previous study from our institution found an unusually high prevalence of F-PCAs, namely, 42%, in patients with PCoAAs.31 In our study, the higher prevalence of F-PCAs in group A may have indicated a correlation between F-PCAs and PCoAA formation. F-PCAs are a known risk factor for occipital lobe infarction in patients who undergo microsurgical clipping of the PCoAA because a PCoA might become entrapped by the clip.32,33 Thus, neurosurgeons should carefully determine the presence of F-PCAs from preoperative images, as up to 40% of patients with PCoAAs could have an F-PCA. When clipping a PCoAA that is associated with an ipsilateral F-PCA, the direction of the clip should be angled more laterally than usual to prevent F-PCA occlusion.31 Data regarding the prevalence of complete F-PCAs and partial F-PCAs were limited. Our results showed that the affected ICAs had a higher prevalence of complete F-PCAs than the unaffected arteries did. High wall shear stress is important in the development, continuous expansion, and eventual rupture of cerebral aneurysms.34-36 Kulcsar et al37 showed the important role in aneurysm formation due to a combination of high wall shear stress and a high positive spatial wall shear stress gradient on a small segment of an arterial wall. The present study indicated a correlation between the presence of F-PCAs and the size of an aneurysm neck but not of the aneurysm dome. Due to the wider diameter of an F-PCA, it could be postulated that the area of vessel wall remodelling is larger and results in a larger aneurysm neck.38,39 Morphological factors appear to be crucial risk factors for the rupture status of PCoAAs.40-42 Lv N et al43 reported factors that related to the rupture status of PCoAAs, which consist of a higher inflow angle and a higher percentage of low wall shear stress areas. Lindgren et al44 reported the association between irregular or multilobar aneurysm shapes and rupture status in intracranial aneurysms of all sizes and locations. In addition, prior studies have supported that hemodynamic alterations play an important role in the rupture status of intracranial aneurysms.28,45,46 Our findings revealed no association between the presence of F-PCAs and the rupture status of PCoAAs. The present results supported Can's findings that a larger PCoA diameter is associated with the presence of PCoAAs.47 Once blood flows from the proximal ICA to the larger cross-sectional area of the distal ICA and the large PCoA, the excess kinetic energy and momentum of the blood might cause a high stress impact on the arterial wall at the apical region, resulting in the formation of an aneurysm. We controlled for the effects of other risk factors, such as age, smoking, hypertension, and a family history of aneurysms by comparing the aneurysmal side with the unaffected side within the same patient for groups A and B of the study group. The aneurysmal side was significantly associated with a higher prevalence of F-PCA than the unaffected side and with the ICAs of patients with aneurysms in other locations. However, our findings of a lower prevalence of F-PCA in group C, the occurrence of PCoAAs contralateral to F-PCAs, and the absence of PCoAs ipsilateral to the PCoAAs appeared to contradict this association. One reason for these conflicting results might have been an inadequate sample size of group C. Another explanation is that other angioarchitectures, such as the angle between the ophthalmic segment and the communicating segment of the ICA or the symmetry of blood flow in the circle of Willis, were also associated with aneurysm formation.48,49 The impact of F-PCAs on hemodynamic characteristics, such as maximum wall shear stress, oscillatory wall shear stress distributions, the shear concentration index, and the mean oscillatory shear index, remains unclear. Increasing evidence has shown the formation of de novo and the growth of unruptured aneurysms in long-term follow-up clinical studies.50-52 Furthermore, a recent study using carbon dating to explore the age of intracranial aneurysms concluded that the average collagen age of the aneurysm wall is less than 5 yr.53 Therefore, in regard to F-PCA, a prospective study involving close long-term surveillance of these patients should be performed in order to determine the relative risk for the development of de novo PCoAAs. A cost-effectiveness study of the follow-up imaging would also be beneficial. Limitations An unavoidable bias of this study was that the ruptured aneurysms were included. Thus, the sizes of the PCoAs might have been affected by cerebral vasospasms. CONCLUSION Our findings that F-PCAs were associated with a higher risk of PCoAAs supported the hypothesis that hemodynamic factors might implicate the formation of an aneurysm. 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Kulcsar Z, Ugron A, Marosfoi M, Berentei Z, Paal G, Szikora I. Hemodynamics of cerebral aneurysm initiation: the role of wall shear stress and spatial wall shear stress gradient. Am J Neuroradiol . 2011; 32( 3): 587- 594. Google Scholar CrossRef Search ADS PubMed  38. Papaioannou TG, Stefanadis C. Vascular wall shear stress: basic principles and methods. Hellenic J Cardiol . 2005; 46( 1): 9- 15. Google Scholar PubMed  39. Katritsis D, Kaiktsis L, Chaniotis A, Pantos J, Efstathopoulos EP, Marmarelis V. Wall shear stress: theoretical considerations and methods of measurement. Prog Cardiovasc Dis . 2007; 49( 5): 307- 329. Google Scholar CrossRef Search ADS PubMed  40. Xu J, Yu Y, Wu X et al.   Morphological and hemodynamic analysis of mirror posterior communicating artery aneurysms. PLoS One . 2013; 8( 1): e55413. Google Scholar CrossRef Search ADS PubMed  41. Ho A, Lin N, Charoenvimolphan N et al.   Morphological parameters associated with ruptured posterior communicating aneurysms. PLoS One . 2014; 9( 4): e94837. Google Scholar CrossRef Search ADS PubMed  42. Matsukawa H, Fujii M, Akaike G et al.   Morphological and clinical risk factors for posterior communicating artery aneurysm rupture. J Neurosurg . 2014; 120( 1): 104- 110. Google Scholar CrossRef Search ADS PubMed  43. Lv N, Wang C, Karmonik C et al.   Morphological and hemodynamic discriminators for rupture status in posterior communicating artery aneurysms. PLoS One . 2016; 11( 2): e0149906. Google Scholar CrossRef Search ADS PubMed  44. Lindgren AE, Koivisto T, Bjorkman J et al.   Irregular shape of intracranial aneurysm indicates rupture risk irrespective of size in a population-based cohort. Stroke . 2016; 47( 5): 1219- 1226. Google Scholar CrossRef Search ADS PubMed  45. Takao H, Murayama Y, Otsuka S et al.   Hemodynamic differences between unruptured and ruptured intracranial aneurysms during observation. Stroke . 2012; 43( 5): 1436- 1439. Google Scholar CrossRef Search ADS PubMed  46. Matsukawa H, Uemura A, Fujii M, Kamo M, Takahashi O, Sumiyoshi S. Morphological and clinical risk factors for the rupture of anterior communicating artery aneurysms. J Neurosurg . 2013; 118( 5): 978- 983. Google Scholar CrossRef Search ADS PubMed  47. Can A, Ho AL, Emmer BJ, Dammers R, Dirven CM, Du R. Association between vascular anatomy and posterior communicating artery aneurysms. World Neurosurg . 2015; 84( 5): 1251- 1255. Google Scholar CrossRef Search ADS PubMed  48. Hu T, Wang D. Association between anatomical variations of the posterior communicating artery and the presence of aneurysms. Neurol Res . 2016; 12( 11): 1- 7. 49. Chung BJ, Doddasomayajula R, Mut F et al.   Angioarchitectures and hemodynamic characteristics of posterior communicating artery aneurysms and their association with rupture status. AJNR Am J Neuroradiol . 2017; 38( 11): 2111- 2118. Google Scholar CrossRef Search ADS PubMed  50. Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms: a long-term follow-up study. Stroke . 2001; 32( 2): 485- 491. Google Scholar CrossRef Search ADS PubMed  51. Ferns SP, Sprengers ME, van Rooij WJ et al.   De novo aneurysm formation and growth of untreated aneurysms: a 5-year MRA follow-up in a large cohort of patients with coiled aneurysms and review of the literature. Stroke . 2011; 42( 2): 313- 318. Google Scholar CrossRef Search ADS PubMed  52. Teo M, St George EJ. Radiologic surveillance of untreated unruptured intracranial aneurysms: A single surgeon's experience. World Neurosurg . 2016; 90: 20- 28. Google Scholar CrossRef Search ADS PubMed  53. Etminan N, Dreier R, Buchholz BA et al.   Exploring the age of intracranial aneurysms using carbon birth dating: preliminary results. Stroke . 2013; 44( 3): 799- 802. Google Scholar CrossRef Search ADS PubMed  COMMENTS The authors present the incidence of fetal posterior cerebral artery (PCA) in patients with posterior communicating artery (PCoA) aneurysms. This study included 185 patients harboring 199 PCoA aneurysms as well as 90 control patients with intracranial aneurysms in other locations. Of the patients with unilateral PCoA aneurysms, 71 (42%) had an ipsilateral fetal PCA and 33 (19%) had a contralateral fetal PCA. Fourteen patients presented with bilateral PCoA aneurysms, but of these, only 1 (3%) fetal PCA was present. Of the 180 ICAs studied in patients with aneurysms in other locations, 26 (14%) had fetal PCAs. Additionally, the authors note that the presence of an ipsilateral fetal PCA was significantly associated with a larger aneurysm neck (3.3 vs 3.0 mm, P = .02). They conclude that the presence of a fetal PCA is associated with a higher risk of developing PCoA aneurysms, likely due to increased hemodynamic stress. The notion that anatomical variations in the circle of Willis are associated with aneurysm formation is generally accepted, and well described, in the literature. In 1984, Kayembe et al.1 reported a post-mortem analysis of anatomical variations in the circle of Willis and cerebral aneurysms, finding that in patients with asymmetric PCoA arteries, aneurysms were more likely to be found on the side of a larger caliber vessel. More recently, a report on variations of the circle of Willis in 202 aneurysms revealed that of the 67 PCoAs, almost 50% were associated with fetal origin of the PCA, similar to the prevalence in the current series.2 Hemodynamic factors including flow patterns, wall shear stress, and oscillatory shear index have been implicated as key factors in the formation, growth, and rupture of intracranial aneurysms. The authors assert that the presence of a fetal PCA is associated with a higher risk of aneurysm formation likely due to an increase in local hemodynamic stress. While this finding would be consistent with the current literature, it is unclear if the data presented fully supports this conclusion. While the authors did find a significant increased incidence of fetal PCAs ipsilateral to unilateral PCoA aneurysms, patients with bilateral PCoA aneurysms actually had the lowest incidence of fetal PCAs (3%). Additionally, although PCoAs associated with fetal PCAs were slightly larger, they found no association between the presence of a fetal PCA and aneurysm rupture, an association which may have been expected in the setting of increased hemodynamic stress. These discrepancies highlight the lack of one simple anatomic predictor for risk of aneurysm formation, and challenge the notion that prospective surveillance of fetal PCA for de novo aneurysm, as proposed by the authors, is a clinically useful or warranted strategy. Ashley Barks Sepideh Amin-Hanjani Chicago, Illinois 1. Kayembe KN Sasahara M Hazama F. “ Cerebral aneurysms and variations in the circle of Willis”. Stroke  1984; 15( 5): 846– 850. Google Scholar CrossRef Search ADS PubMed  2. Songsaeng D Geibprasert S Willinsky R Tymianski M TerBrugge KG Krings T. “ Impact of anatomical variations of the circle of Willis on the incidence of aneurysms and their recurrence rate following endovascular treatment.” Clin Radiol . 2010; 65( 11): 895– 901. Google Scholar CrossRef Search ADS PubMed  The putative association of a fetal posterior cerebral artery (PCA) and posterior communicating artery (PCoA) aneurysm has been debated for a long time. The prevailing theory is that hemodynamic changes in the presence of a large PCoA might induce increased hemodynamic stress at the origin of the vessel, thus increasing the risk of aneurysm formation. In this study, the authors consider 4 different cohorts; Group A: 171 ICAs with unilateral PCoA aneurysms; group B: 171 contralateral unaffected ICAs; group C: 28 ICAs in patients with bilateral PCoA aneurysms, and group D: 180 ICAs in 90 patients with aneurysms in locations other than the PCoA. Overall, fetal PCA configuration was present in 42% of ICAs in group A, 19% in group B, 3% in group C, and 14% in group D. This observation would suggest that in patients with unilateral PCoA aneurysms, a fetal PCA configuration is more common than in control arteries. Although these findings might lend support to the theory that fetal PCA configuration is at increased risk of PCoA aneurysm formation, the practical implications of such observation are limited since it is impractical and not indicated to follow these patients over time to rule out aneurysm formation. Nevertheless, the presence of a fetal PCA in a patient with a PCoA aneurysm has important implications for surgical and endovascular therapy. When this anatomy is present, preservation of the fetal PCA is imperative from both a surgical and endovascular point of view. In this study, the presence of a fetal PCA was associated with a larger aneurysm neck, and this might make simple coil embolization more problematic. In addition, the presence of a true fetal PCA is a factor associated with lack of angiographic obliteration after flow diversion for PCoA aneurysms as suggested in a few recent series.1,2 Thomas Sorenson Giuseppe Lanzino Rochester, Minnesota 1. Kan P Duckworth E Puri A Velat G Wakhloo A. Treatment failure of fetal posterior communicating artery aneurysms with the pipeline embolization device. J Neurointerv Surg . 2016; 8( 9): 945- 948. Google Scholar CrossRef Search ADS PubMed  2. Wallace AN Kayan Y Austin MJ, et al. Pipeline embolization of posterior communicating artery aneurysms associated with a fetal origin posterior cerebral artery. Clin Neurol Neurosurg . 2017; 160: 83- 87. Google Scholar CrossRef Search ADS PubMed  Copyright © 2018 by the Congress of Neurological Surgeons This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

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NeurosurgeryOxford University Press

Published: May 21, 2018

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