Authors: Mohamad Abdalkader (Department of Radiology, Boston Medical Center, Boston University‐School of Medicine, Boston, MA), Anurag Sahoo (Department of Neurology, Boston Medical Center, Boston University‐School of Medicine, Boston, MA), Adam A. Dmytriw (Neuroendovascular Program, Massachusetts General Hospital ‐ Harvard Medical School, Boston, MA), Waleed Brinjikji (Department of Radiology, Mayo Clinic, Rochester, MN), Guilherme Dabus (Interventional Neuroradiology, Miami Cardiac & Vascular Institute and Baptist Neuroscience Center, Miami, FL), Eytan Raz (Department of Radiology, New York University Langone Medical Center, New York, NY), Leonardo Renieri (Interventional Neuroradiology Unit, University Hospital Careggi, Firenze, Toscana, Italy), Antonio Laiso (Interventional Neuroradiology Unit, University Hospital Careggi, Firenze, Toscana, Italy), Alberto Maud (Department of Neurology, Texas Tech University Health Sciences Center El Paso, El Paso, TX), Mario Martínez‐Galdámez (Interventional Neuroradiology/Endovascular Neurosurgery, Hospital Clínico Universitario de Valladolid, Valladolid, Spain), Jorge Galván‐Fernández (Interventional Neuroradiology/Endovascular Neurosurgery, Hospital Clínico Universitario de Valladolid, Valladolid, Spain), Miguel Schüller‐Arteaga (Interventional Neuroradiology/Endovascular Neurosurgery, Hospital Clínico Universitario de Valladolid, Valladolid, Spain), Fawaz Al‐Mufti (Department of Neurosurgery, Westchester Medical Center at New York Medical College, Valhalla, NY), Krishna Amuluru (Division of Interventional Neuroradiology, Goodman Campbell Brain and Spine, Ascension St. Vincent Medical Center, Indianapolis, IN), Johanna T. Fifi (Department of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY), Shahram Majidi (Department of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY), Priyank Khandelwal (Department of Neurosurgery, Rutgers University, Newark, NJ), Justin M. Moore (Division of Neurosurgery, Beth Israel Deaconess Medical Center, Boston, MA), Santiago Ortega‐Gutierrez (Department of Neurology, Radiology and Neurosurgery, The University of Iowa Hospitals and Clinics, Iowa City, IA), Ameer E. Hassan (Department of Neurology, University of Texas Rio Grande Valley, Valley Baptist Medical Center, Harlingen, TX), James E. Siegler (Cooper Neurological Institute, Cooper University Hospital, Camden, NJ), Simon Nagel (Department of Neurology, University Hospital Heidelberg, Heidelberg, Germany), Osama O. Zaidat (Neuroscience Institute, St Vincent Mercy Hospital, Toledo, OH), Thanh N. Nguyen (Department of Radiology, Boston Medical Center, Boston University‐School of Medicine, Boston, MA; Department of Neurology, Boston Medical Center, Boston University‐School of Medicine, Boston, MA; Department of Neurosurgery, Boston Medical Center, Boston University‐School of Medicine, Boston, MA)
Categories: Original Research, acute stroke, fetal posterior cerebral artery, mechanical thrombectomy
Source: Stroke: Vascular and Interventional Neurology
Authors: Mohamad Abdalkader, Anurag Sahoo, Adam A. Dmytriw, Waleed Brinjikji, Guilherme Dabus, Eytan Raz, Leonardo Renieri, Antonio Laiso, Alberto Maud, Mario Martínez‐Galdámez, Jorge Galván‐Fernández, Miguel Schüller‐Arteaga, Fawaz Al‐Mufti, Krishna Amuluru, Johanna T. Fifi, Shahram Majidi, Priyank Khandelwal, Justin M. Moore, Santiago Ortega‐Gutierrez, Ameer E. Hassan, James E. Siegler, Simon Nagel, Osama O. Zaidat, Thanh N. Nguyen
Fetal posterior cerebral artery (FPCA) occlusion is a rare but potentially disabling cause of stroke. While endovascular treatment is established for acute large vessel occlusion stroke, FPCA occlusions were excluded from acute ischemic stroke trials. We aim to report the feasibility, safety, and outcome of mechanical thrombectomy in acute FPCA occlusions.
We performed a multicenter retrospective review of consecutive patients who underwent mechanical thrombectomy of acute FPCA occlusion. Primary FPCA occlusion was defined as an occlusion that was identified on the pre‐procedure computed tomography angiography or baseline angiogram whereas a secondary FPCA occlusion was defined as an occlusion that occurred secondary to embolization to a new territory after recanalization of a different large vessel occlusion. Demographics, clinical presentation, imaging findings, endovascular treatment, and outcome were reviewed.
There were 25 patients with acute FPCA occlusion who underwent mechanical thrombectomy, distributed across 14 centers. Median National Institutes of Health Stroke Scale on presentation was 16. There were 76% (19/25) of patients who presented with primary FPCA occlusion and 24% (6/25) of patients who had a secondary FPCA occlusion. The configuration of the FPCA was full in 64% patients and partial or “fetal‐type” in 36% of patients. FPCA occlusion was missed on initial computed tomography angiography in 21% of patients with primary FPCA occlusion (4/19). The site of occlusion was posterior communicating artery in 52%, P2 segment in 40% and P3 in 8% of patients. Thrombolysis in cerebral infarction 2b/3 reperfusion was achieved in 96% of FPCA patients. There were no intraprocedural complications. At 90 days, 48% (12/25) were functionally independent as defined by modified Rankin scale≤2.
Endovascular treatment of acute FPCA occlusion is safe and technically feasible. A high index of suspicion is important to detect occlusion of the FPCA in patients presenting with anterior circulation stroke syndrome and patent anterior circulation.
This is the first multicenter study showing that thrombectomy of FPCA occlusion is feasible and safe.
During embryological life, the caudal internal carotid artery (ICA) supplies the posterior cerebral artery (PCA) territory and later regresses as the PCA annexes with the basilar artery. ^1^ Failure of the caudal ICA to regress results in a fetal configuration of the fetal posterior cerebral artery (FPCA). ^1^ , ^2^ In a full FPCA, the P1 segment is absent whereas in partial or fetal‐type FPCA, the P1 segment is smaller or equivalent in diameter to the posterior communicating artery (PCOM). ^1^ , ^3^ This variant is common and seen in 16% to 40% of the population. ^3^ , ^4^ In the presence of FPCA, the vascularization of the PCA territory relies on the ICA and thromboembolism in the anterior circulation may result in PCA territory infarction. ^3^ , ^5^ Acute ischemic stroke due to proximal FPCA occlusion may be disabling. ^6^ It can lead to impairments in cognition, vision, language, and motor function ^5^ and can mimic middle cerebral artery (MCA) occlusion syndromes. ^5^ , ^7^
While there is strong and growing evidence that reperfusion of large and medium vessels occlusions leads to better clinical outcomes, ^6^ , ^8^ , ^9^ , ^10^ , ^11^ , ^12^ data of endovascular therapy of FPCA occlusion is lacking. Considering the unique anatomy of a fetal circulation, and the potentially disabling deficits of FPCA occlusion, we conducted a retrospective multicenter analysis looking at the safety and efficacy of mechanical thrombectomy (MT) in FPCA occlusions.
We performed a multicenter retrospective observational study of consecutive patients who presented with acute ischemic stroke and underwent MT of FPCA occlusion. Data was consolidated from 14 centers in the USA and Europe. Each center queried their database to identify consecutive patients who met inclusion criteria from January 2015 to January 2021 (FPCA occlusion who underwent trans‐circulation MT). Trans‐circulation thrombectomy was defined as navigation through the PCOM from the ICA to perform the endovascular treatment.
FPCA was classified as partial (also known as fetal‐type) or full FPCA depending on whether the P1 segment was small or absent, respectively. ^3^ Patients diagnosed with FPCA occlusion but who did not undergo endovascular therapy or who underwent intraarterial tissue plasminogen activator without MT were excluded. Institutional review board approval was obtained in each contributing center. Patient consent was waived given the retrospective and anonymous data analysis. Data are available with reasonable request to the corresponding author.
Demographics details (age, sex), comorbidities, stroke risk factors, clinical presentation (last known well, stroke symptoms, and National Institutes of Health Stroke Scale [NIHSS] score), and imaging findings and procedural details were collected. All patients underwent computed tomography (CT) head without contrast and CT angiogram of the head and neck before the procedure. FPCA occlusion was identified on CT angiography and/or digital subtraction angiography. FPCA occlusion was defined as primary if the occlusion was identified on the pre‐procedure computed tomography angiography (CTA) or baseline angiogram. Secondary FPCA occlusion was defined as FPCA occlusion that occurred secondary to embolization to a new territory (ENT) after recanalization of another large vessel occlusion (LVO). FPCA occlusion was either isolated or associated with LVO of the internal carotid artery or the MCA.
The choice of endovascular technique and anesthesia modality were at the discretion of the treating neurointerventionalist. The primary outcome was the rate of successful reperfusion defined as modified thrombolysis in cerebral infarction (TICI) Scale 2b/3 in the territory of the FPCA. ^13^ For primary isolated FPCA, TICI 2b was defined as >2/3 of the territory of the FPCA reperfused and TICI 3 was full reperfusion of the FPCA territory. The secondary outcome was the rate of good outcome defined as 90‐days modified Rankin scale score 0–2. Safety evaluation included procedure‐related complications such as dissection, contrast extravasation, subarachnoid hemorrhage, and symptomatic intracranial hemorrhage (sICH) defined as clinical deterioration after treatment with 4 points increase in the NIHSS from baseline. ^14^ The procedure time was defined as the time from arterial access to vessel recanalization.
The data that support the findings of this study are available from the corresponding author upon reasonable request.
There were 25 patients (44% [11/25] female and 56% [14/25] male patients) who underwent MT of FPCA occlusion in the setting of acute ischemic stroke. Three out of the included 25 patients were already published as separate case reports. ^15^ , ^16^ The median age was 75 years (interquartile range [IQR] 59–77 years). Stroke risk factors included hypertension (76%), atrial fibrillation (36%), and diabetes mellitus (24%).
Overall, the median NIHSS on presentation was 16 (IQR 11–20). There were 48% (12/25) patients who presented with aphasia, 96% (24/25) patients with motor deficits (62% were hemiplegic and 38% were hemiparetic), and 68% (17/25) who had sensory loss. There were 92% (23/25) patients who had a visual deficit of which 91% (21/23) had a hemianopsia and 9% (2/23) with quadrantanopia. Behavioral manifestations (agitation) were noted in 24% (6/25) of patients. Among patients who presented with isolated fetal PCA occlusion (i.e., no other associated vessel occlusion) (8/25), median NIHSS was 10 (IQR 4–14). In this group, there were 38% (3/8) patients who presented with aphasia, 88% (7/8) patients with motor deficits (4 were hemiplegic and 3 were hemiparetic), and 63% (5/8) had sensory loss. There were 88% (7/8) who had a visual deficit of which 86% (6/7) had a hemianopsia and 17% (1/6) had a quadrantanopia.
Median time from “last known well” to groin puncture was 335 minutes (IQR 240–480). There were 44% (11/25) who received intravenous tissue plasminogen activator prior to MT. Patient demographics, main risk factors, and imaging characteristics are provided in Table 1.
Anatomically, 64% (16/25) of patients had a full FPCA and 36% (9/25) of patients had a partial or “fetal‐type” PCA configuration. There were 76% (19/25) of patients who presented with FPCA occlusion (primary FPCA occlusion) and 24% (6/25) of patients had a secondary FPCA occlusion. Of the primary FPCA occlusion, there were 42% (8/19) patients who had an isolated FPCA occlusion and 58% (11/19) patients who had an associated ipsilesional occlusion at presentation (36% [4/11] had an intracranial ICA occlusion and 64% [7/11] had an MCA territory occlusion).
The FPCA occlusion was missed on initial CTA but then detected on cerebral angiogram in 21% of patients with primary FPCA occlusion (4/19). The site of occlusion was PCOM in 52% (13/25), P2 segment in 40% (10/25), and P3 segment in 8% (2/25) of patients. In all cases with secondary FPCA occlusions, the fetal or fetal type posterior cerebral artery was identified on the pre‐procedure CT angiogram and there was no occlusion detected of these vessels before interventions.
MT was performed using a combination of stent retriever and aspiration technique in 60% (15/25) of interventions, aspiration in 28% (7/25), and stent retriever in 12% (3/25). The Solitaire 4×40 mm (Medtronic; ev3 Neurovascular, Irvine, CA) was the most commonly used in 17% (3/18) of stent retriever cases. The most common catheter used was the Sofia (MicroVention, Inc) catheters in 67% (14/21) of cases. Balloon Guide Catheter was used in 28% of cases (7/25). The median procedure time was 53 minutes (IQR 36–78). General anesthesia was used in 40% of cases (10/25).
There were no intraprocedural complications, including vessel dissection, spasm, perforation, or recurrent embolism. One patient had sICH related to hemorrhagic transformation of infarcted tissue in a “rapid progressor” despite successful reperfusion of the MCA and FPCA territories.
The primary outcome of successful recanalization (TICI 2b/3) was achieved in 96% (24/25) patients. Median discharge NIHSS was 7 (IQR 4–11). At 3 months, a good outcome (tissue plasminogen activator≤2) was achieved in 48% (12/25) of patients and 16% (4/25) patients died. All 4 patients who died presented initially with severe stroke (NIHSS>20) and had FPCA associated with MCA or ICA occlusion. More technical details and outcomes are provided in Table 1. An example of the endovascular treatment of acute PCOM occlusion is illustrated in Figure 1.

Our multicenter study indicates that MT in patients with acute FPCA occlusion is feasible, safe and carries a high rate of successful reperfusion with half of patients achieving functional independence. To our knowledge, this is the first multicenter study of FPCA thrombectomy. Trials that established endovascular treatment as standard of care in LVO acute ischemic stroke ^17^ , ^18^ , ^19^ , ^20^ , ^21^ as well as the growing literature of endovascular treatment of medium occlusion stroke ^6^ , ^9^ , ^11^ , ^12^ , ^22^ , ^23^ did not include acute FPCA or PCOM occlusions. Even though the deficits from this type of stroke may be disabling, ^5^ , ^7^ , ^24^ only a few cases of endovascular FPCA recanalization have been reported in the literature. ^15^ , ^16^ , ^25^ , ^26^ Patients in our series presented with severe deficits that were often associated with anterior circulation stroke such as aphasia, motor, or sensory deficits with a median NIHSS of 16 in all patients. In isolated FPCA occlusions (ie, no other associated vessel occlusion), patients presented with motor deficits (88%), visual deficits (88%), sensory loss (63%), and aphasia (38%) with a median NIHSS of 10, highlighting the potentially disabling deficits of this stroke syndrome. An isolated FPCA occlusion may mimic MCA occlusion syndromes from infarction of the cerebral peduncle, posterior limb of the internal capsule, or ventral thalamus resulting in hemiparesis and/or hemisensory loss, and may produce hemispatial neglect or aphasia due to thalamic involvement. ^5^ , ^7^ , ^27^ The association of FPCA occlusion with an ICA or MCA occlusion accounts for a more severe presentation as a larger area is infarcted by the addition of the FPCA territory to the MCA or ICA territory. Furthermore, the lack of leptomeningeal collateral formation between the anterior and posterior circulations in simultaneous FPCA and ICA/MCA occlusions lends to a greater ischemic area. ^3^ , ^5^ , ^24^
The detection of FPCA occlusion may be challenging on initial CTA as this was missed in 4 of our patients on baseline CTA (1 isolated FPCA and 3 FPCA with associated ICA/MCA occlusion). This could be explained by the location of the FPCA occlusion occurring flush as a branch of the carotid terminus. Alternatively, an associated ICA/MCA occlusion can result in a “satisfaction of search” error in which detection of 1 target diminishes detection of subsequent targets, thereby overlooking the FPCA occlusion. ^28^
In the setting of an absent or hypoplastic P1 segment with FPCA occlusion, trans‐circulation flow restoration across the PCOM represents the primary pathway for access. Theoretically, this may pose a higher risk of complications because of the relatively smaller caliber of the PCOM and the need to catheterize acute angles such as the ICA/PCOM junction. While there may be reluctance to catheterize the FPCA, the mean diameter of the PCOM is estimated to be 2 mm which is comparable to the distal M1 or proximal M2 diameter. ^4^ In our series, there were no procedural or postprocedural complications related to the procedure. One patient had sICH postprocedure which was related to hemorrhagic transformation of infarcted tissue despite successful recanalization. Our results are in line with other studies looking at MT in nonfetal PCA occlusions which found low rates of sICH and procedural complications. ^6^ , ^23^ , ^29^ However, a meta‐analysis looking at multiple registries with M2 thrombectomies found a higher rate of sICH compared to more proximal occlusions ^12^ signifying that caution is warranted when intervening in these distal and fragile vessels. ^30^ , ^31^ , ^32^
Our series included cases from different institutions with varying techniques. Despite this variability, 96% of patients had a TICI≥2b reperfusion and 48% patients reached functional independence at 90 days. This is comparable to reperfusion rates and functional outcomes seen in trials for anterior circulation LVOs as well as cohorts for posterior circulation vessel occlusions. ^10^ , ^33^ The median procedure time was 53 minutes which is comparable to a separate multicenter cohort across 10 centers that looked at procedural times for thrombectomy where median time was 57 minutes. ^34^ This was in light of the fact the procedures were performed with a trans‐circulation approach and frequently had other vessel occlusions which also needed to be treated.
Due to the retrospective nature of this study, we cannot exclude the possibility of bias in case selection. A lack of a control group limits the conclusions we draw about the efficacy of treatment. Lastly the rarity of the condition limits the sample size available for analysis. However, the results of our study may be generalizable due to its international and multicenter design.
Acute fetal posterior cerebral occlusion can be as disabling as anterior circulation hemispheric infarction, but recanalization using MT is technically feasible, safe and is associated with a high probability of long‐term functional independence. A high level of clinical suspicion is important to detect these patients who often present with anterior circulation stroke syndromes but with patent anterior carotid circulation on initial review of CTA. Further investigation is needed to compare the efficacy of different management considerations for this condition.
Dr Siegler reports consulting fees for Ceribell. Dr. Amuluru performs consulting at Medtronic. Dr. Hassan performs consulting for Medtronic, Microvention, Stryker, Pneumbra, Cerenovus, Genentech, Scientia, GE healthcare, Balt, Viz.ai, Insera therapeutics, Proximie, Novasignal, Vesalio; Grants from GE healthcare. He also serves as PI for COMPLETE and LVO SYNCHRONISE and is part of the steering committee for SELECT, DAWN, SELECT 2, EXPEDITE II, EMBOLISE, CLEAR, DELPHI. Dr. Nguyen reports a grant from Medtronic.