Proximal hyper-intense vessel sign on initial FLAIR MRI in hyper-acute middle cerebral artery ischemic stroke: a retrospective observational study

Abstract

Background

A hyper-intense vessel sign on fluid attenuated inversion recovery magnetic resonance imaging (FHV) represents slow blood flow in the cerebral arteries.

Purpose

To investigate the relationship between the proximal FHV (pFHV) on initial magnetic resonance imaging (MRI) and the status of the culprit vessel (stenosis, obstruction) in hyper-acute strokes affecting the territory of the middle cerebral artery (MCA).

Material and Methods

The study participants consisted of 105 patients presenting to the emergency department (ED) with acute MCA infarction within 4.5 h of onset of symptoms. Patients underwent brain MRI within 45 min of arrival at the ED and angiography within 2 h of arrival. Culprit vessel status and presence of a pFHV on initial MRI were investigated retrospectively.

Results

The pFHV was observed in 71/105 (67.6%) patients who presented with a hyper-acute MCA infarction. All patients with hyper-acute MCA infarction caused by internal carotid artery (90.6% caused by M1 occlusion, 92.9% caused by M2 occlusion) showed a pFHV on initial MRI. After logistic regression analysis, the presence of a pFHV showed significant positive correlation with large vessel occlusion (adjusted odds ratio [OR] 34.533, 95% confidence interval [CI] 9.781–121.926; P < 0.001). A pFHV was not associated with severe large vessel stenosis.

Conclusion

A pFHV is independently representative of the acute occlusion of intervention-eligible proximal arteries within the territory of the MCA. If a patient with a hyper-acute MCA infarction shows a pFHV, aggressive flow augmentation strategies and early activation of intervention team should be warranted for best patient outcome.

Keywords

Cerebral arterial disease fluid-attenuated inversion recovery magnetic resonance imaging hyperintense vessel middle cerebral artery infarction

Introduction

The usefulness of fluid-attenuated inversion recovery (FLAIR) imaging in the detection of ischemic brain lesions has been well known since before 2000 and is now a recommended part of the routine stroke magnetic resonance imaging (MRI) protocol (1 –3). Parenchymal FLAIR hyper-intensity is known to be caused by vasogenic edema associated with ischemic lesions and requires some time to appear on MRI. It was demonstrated that if FLAIR imaging showed no parenchymal hyper-intense signals, the stroke onset was within 4.5 h (4). Contrary to parenchymal FLAIR changes, vascular FLAIR changes can sometimes be observed during the hyper-acute phase of an ischemic stroke (5 –7). The hyper-intense vessel sign (HVS) on FLAIR is reported to be observed in nearly half of all cases of acute ischemic stroke, primarily in strokes involving the middle cerebral artery (MCA) territory (8).

The HVS is presumed to reflect stationary blood flow and slow antegrade or retrograde collateral circulation (6,9,10). In previous studies, the HVS was variably divided into proximal versus distal HVS, subtle versus prominent HVS, and extensive versus less pronounced HVS (6,11 –13). However, determining the presence of a less pronounced HVS and a subtle HVS may subject to ambiguity or subjectivity. Moreover, in the case of a distal HVS, cranial nerves, venous structures, or cerebrospinal fluid, flow artifacts can often be mistaken for arterial hyperintensities. Contrary to a distal HVS, the presence of a proximal HVS is not ambiguous and can easily be determined by a novice interpreter. If the proximal HVS indicates the occlusion or severe stenosis of intervention-eligible large sized arteries, it may be of huge clinical significance. The aim of the present study was to investigate the relationship between the presence of a proximal HVS on FLAIR MRI (pFHV) as determined by emergency physicians and the status of the proximal MCA territory culprit blood vessel among patients presenting to an emergency department (ED) with clinically significant hyper-acute MCA territory ischemic stroke.

Material and Methods

This is a retrospective observational study conducted at a tertiary teaching hospital located in the center of Seoul, South Korea. The study hospital has 671 beds and an average of 35,000 patients visit its ED annually. After approval by the Institutional Review Board of our institute (IRB number: 2019-03-006-001), ED patients with acute ischemic stroke were investigated between January 2016 and March 2020.

During the study period and to date, our ED runs a separate fast-track protocol for prompt treatment of patients with suspected acute stroke. An initial brain imaging is scheduled to be completed and interpreted within 45 min of patient arrival, and either brain non-contrast computed tomography (CT) or diffusion MR (usually test with shorter waiting time is selected among CT or MR) will be performed. Use of intravenous (IV) recombinant tissue plasminogen activator (rtPA) is determined based on clinical feature and findings of initial brain imaging. After initial brain imaging and determining the use of IV rtPA, patients usually undergo an additional CT angiography (CTA) or cerebral angiogram to evaluate the vessel status and possible indication of endovascular intervention. In some cases, CTA was performed simultaneously with initial brain imaging before use of IV rtPA.

Participants

We included adult patients aged >18 years who: (i) had a final diagnosis of acute MCA territory ischemic stroke; (ii) presented to the ED within 4.5 h of symptom onset; (iii) were treated with IV rtPA (use of rtPA was arbitrarily considered equivalent to clinically significant ischemic stroke); (iv) underwent brain MRI within 45 min of arrival at the ED; (v) had angiographic findings (CTA or cerebral angiography) within 2 h of arrival at the ED.

Exclusion criteria were as follows: (i) age <18 years; (ii) acute ischemic stroke other than that of the MCA territory, i.e. isolated anterior cerebral artery territory or posterior circulation infarction; (iii) no initial brain MRI (those who only underwent brain CT as their initial brain imaging); (iv) insufficient image quality with which to assess HVS; (v) no available initial angiographic findings (no CTA or cerebral angiography, or no formal report by intervention radiologist or intervention neurosurgeon).

In the present study, large vessels were defined as internal carotid artery (ICA), MCA M1, and MCA M2. Participants were divided into groups with occlusion in large vessels (LVO) and without occlusion in large vessels (non-LVO) according to occlusion sites identified in initial angiography. Case matching was not performed because there was no difference between the two groups in the potential confounding variables, such as age, sex, the time from onset of symptoms to the ED visit, the time from arrival at the ED to MRI, and the time from arrival at the ED to CTA.

Image acquisition

MRI examinations were performed utilizing 1.5-T scanners (Intera, Philips Medical Systems, Best, The Netherlands). FLAIR parameters were as follows: TR/TE = 8000/121 ms; TI = 2500 ms; field of view (FOV) = 23 × 23 cm; matrix size = 256 × 145; slice thickness = 5 mm; inter-slice gap = 1.5 mm. Diffusion-weighted imaging (DWI) was obtained using the following parameters: TR/TE = 5320/74 ms; FOV = 23 × 23 cm; matrix size = 128 × 128; slice thickness =4 mm; interslice gap = 0 mm; b value = 1000 s/mm². The resulting voxel volumes of FLAIR were 1.80 mm³. CTA or cerebral angiography was obtained within 2 h of arrival at the ED and within 1 h of initial MRI. CTA was obtained by Brilliance iCT–SP 128 (Philips Medical Systems, Best, The Netherlands), and cerebral angiography was obtained by a bipolar angiographic unit, Allura Xper (Phillips Medical System, Best, The Netherlands).

Imaging analysis and data collection

The pFHV was defined as a linear or serpentine hyper-intensity on FLAIR imaging corresponding to a typical arterial course (i.e. corresponding to the MCA M1 or M2 segments) and which was proximal to or within the Sylvian fissure. The pFHV was graded as either absent or present (Fig. 1a and b). Distal HVS was not investigated in the present study. In the case of ICA or carotid T lesions, a pFHV was considered to be present when an HVS was observed on the vascular course corresponding to the ICA. Two board-certified emergency physicians blinded to the patient’s diagnosis determined the presence of the pFHV on initial FLAIR images at the same time, according to the definition of the pFHV in the present study. In the event of discrepancies, the result was reached by consensus.

Fig. 1.

A proximal hyper-intense vessel sign on initial FLAIR MRI. (a) An 82-year old woman presented to the ED 39 min after onset of symptoms. MRI was performed 53 min after onset of symptoms. Arrows indicate linear hyper-intensity on FLAIR imaging corresponding to the arterial course of MCA M1 proximal to the Sylvian fissure (proximal HVS). (b) B-1000 imaging of the same patient showing hyper-intensity in MCA territory indicating acute ischemic infarction. (c, d) CTA of the same patient performed 2.2 h after onset of symptoms. Arrowheads indicate the obstructed segment of MCA M1. CTA, computed tomography angiography ED, emergency department; FLAIR, fluid-attenuated inversion recovery; HVS, hyper-intense vessel sign; MCA, middle cerebral artery; MRI, magnetic resonance imaging.

Information regarding vascular status was investigated by two investigators who did not participate in determining the presence or absence of the pFHV. Arterial occlusion or stenosis of large vessels were investigated by referencing pre-existing formal radiology reports and reviewing CTA or cerebral angiography images. Arterial occlusion was graded as either absent or present (Fig. 1c and d). Arterial stenosis was categorized as mild (<50%), moderate (50%–69%), or severe (≥70%) (14). The percentage of stenosis was measured by visual inspection based on the method used in the North American Symptomatic Carotid Endarterectomy Trial (15). When acute ischemic lesions were present in both hemispheres, only the status of the culprit vessel responsible for the acute symptom was included for analysis.

Demographic data (diabetes, hypertension, hyperlipidemia, previous stroke, atrial fibrillation [AF], smoking, excessive alcohol use, use of anti-thrombotics, etc.) were obtained by reviewing the electronic medical records. Smoking was based on current smoking and excessive use of alcohol was defined according to the Center for Disease Control definition of excessive use of alcohol (16).

Outcome measures

The primary outcome was the presence of a pFHV on the initial MRI according to the presence of occlusion or stenosis of the ICA, M1, M2, or distal MCA.

Statistical analysis

Statistical analysis was performed using STATA 13.0 for Windows (StataCorp, College Station, TX, USA). The continuous variables were presented as median and interquartile ranges, and the categorical variables were described in terms of frequency (%). We compared the continuous variables using the Mann–Whitney test, and the categorical variables using the Chi-square or Fisher’s exact test, according to the expected frequency. Logistic regression analysis was performed to investigate the relationship between the pFHV and the occlusion or severe stenosis of the culprit vessel.

Results

During the study period, 226 adult patients were treated with IV rtPA for acute ischemic stroke in the ED. Of them, 18 patients were excluded because there was no initial MRI, 10 patients were excluded as there were no available angiography findings, and 25 patients were excluded due to the delays in MRI or angiography. The remaining 173 patients underwent both initial MRI and angiography (either CTA or cerebral angiography). Of them, 47 further patients were excluded because of a non-MCA territory infarction and 21 patients were excluded because of poor imaging quality due to patient movement or other artifacts. Finally, 105 patients were included in this study (Fig. 2). There were no missing data among finally included cases.

Fig. 2.

Patient selection. FLAIR, fluid attenuated inversion recovery; IV rtPA, intravenous recombinant tissue plasminogen activator; LVO, large vessel occlusion; MCA, middle cerebral artery; MRI, magnetic resonance imaging.

Of the 105 participants, 62 (59%) had LVO. The median age of the participants was 74 years and 74 were men, which was more than double the number of women. The average time interval from onset of symptoms to ED visit was 44 min. The average time interval from arrival at the ED to initial MRI study and to initial angiography (either CTA or cerebral angiography) were 17 min and 61 min, respectively. The characteristics of the individuals are presented in Table 1. When comparing the characteristics of the participants between the LVO group and the non-LVO group, there was no significant difference in most demographic data such as age, sex, onset of symptoms to ED time, medical history, but AF was significantly higher in the LVO group (27/62 vs. 5/43, P < 0.001), and the initial National Institutes of Health Stroke Scale (NIHSS) was approximately twice as high in the LVO group (16 vs. 8, P < 0.001). The pFHV was observed significantly more in the LVO group than in the non-LVO group (94% vs. 30%, P < 0.001).

Table 1.

Demographic and clinical parameters.

Variables	All (n = 105)	LVO (n = 62)	Non-LVO (n = 43)	P
Age (years)	74 (62–79)	72.5 (65–82)	74 (58–78)	0.444
Male	74 (70.5)	44 (71)	30 (69.8)	0.895
Clinical features and medical history
Initial NIHSS	10 (7–17)	15.5 (9–18)	8 (6–10)	<0.001
Atrial fibrillation	32 (30.5)	27 (43.5)	5 (11.6)	<0.001
Diabetes	27 (25.7)	18 (29)	9 (20.9)	0.350
Hypertension	61 (58.1)	35 (56.5)	26 (60.5)	0.682
Hyperlipidemia	8 (7.6)	3 (4.8)	5 (11.6)	0.268
Previous stroke	16 (15.2)	7 (11.3)	9 (20.9)	0.177
Use of anti-thrombotics	15 (14.3)	8 (12.9)	7 (16.3)	0.627
Current smoker	22 (21)	11 (17.7)	11 (25.6)	0.332
Excessive alcohol user	19 (18.1)	13 (21)	6 (14)	0.359
Time from
Symptom onset to ED (min)	44 (32–91)	41.5 (31–91)	53 (34–101)	0.440
ED to MRI (min)	17 (13–25)	16 (13–24)	18 (14–26)	0.415
ED to angiography* (min)	61 (36–82)	60 (33–78)	64 (38–86)	0.473
ED to rtPA administration (min)	44 (35–53)	42 (33–53)	46 (35–53)	0.602
MRI to angiography* (min)	46 (19–60)	46 (18–58)	45 (29–69)	0.571
Angiography* after rtPA administration	78 (74.3)	44 (71)	34 (79.1)	0.350
Initial angiography
CTA	96 (91.4)	53/62 (85.5)	43/43 (100)	0.010
Cerebral angiography	9 (8.6)	9/62 (14.5)	0/43 (0)
Mechanical thrombectomy	37 (35.2)	37 (59.7)	0 (0)	<0.001
Successful mechanical thrombectomy		34/37 (91.9)
pFHV	71 (67.6)	58 (93.5)	13 (30.2)	<0.001

Values are given as n (%) or median (interquartile range).

*CTA or cerebral angiography.

CTA, computed tomography angiography; ED, emergency department; LVO, large vessel occlusion; MRI, magnetic resonance imaging; NIHSS, National Institutes of Health Stroke Scale; pFHV, proximal hyper-intense vessel sign on fluid-attenuated inversion recovery magnetic resonance imaging; rtPA, recombinant tissue plasminogen activator.

When patients’ characteristics were compared according to pFHV, there were significant differences in AF, initial NIHSS, mechanical thrombectomy, and LVO (Table 2). Mechanical thrombectomy was performed significantly more for patients with pFHV (49% vs. 6%, P < 0.001).

Table 2.

Comparison of characteristics of patients based on pFHV.

Variables	pFHV (n = 71)	No pFHV (n = 34)	P
Age (years)	74 (64–81)	74.5 (54–79)	0.401
Male	51 (71.8)	23 (67.6)	0.660
Clinical features and medical history
Initial NIHSS	13 (8–18)	8 (6–12)	0.005
Atrial fibrillation	28 (39.4)	4 (11.8)	0.004
Diabetes	21 (29.6)	6 (17.6)	0.191
Hypertension	41 (57.7)	20 (58.8)	0.917
Hyperlipidemia	3 (4.2)	7 (20.6)	0.012
Previous stroke	9 (12.7)	7 (20.6)	0.291
Use of anti-thrombotics	11 (15.5)	4 (11.8)	0.769
Current smoker	12 (16.9)	10 (29.4)	0.140
Excessive alcohol user	12 (16.9)	7 (20.6)	0.646
Time from
Symptom onset to ED (min)	44 (30–101)	49 (36–90)	0.588
ED to MRI (min)	16 (13–24)	19 (14–27)	0.236
ED to angiography* (min)	61 (34–76)	63.5 (36–89)	0.455
ED to rtPA administration (min)	42 (33–52)	47 (36–54)	0.364
MRI to angiography* (min)	46 (19–57)	47 (20–71)	0.610
Angiography* after rtPA administration (min)	53 (74.6)	25 (73.5)	0.902
Mechanical thrombectomy (min)	35 (49.3)	2 (5.9)	<0.001
Angiographic findings
Any occlusion	61 (85.9)	6 (17.6)	<0.001
Large vessel occlusion	58 (81.7)	4 (11.8)	<0.001
Severe large vessel stenosis	11 (55)	60 (70.6)	0.180
Moderate to severe large vessel stenosis	16 (61.5)	55 (69.6)	0.445

Values are given as n (%) or median (interquartile range).

*CTA or cerebral angiography.

After initial MRI, 96 patients underwent a CTA (the pFHV was correlated with the CTA report) and nine patients directly underwent cerebral angiography without CTA (the pFHV was correlated with the cerebral angiography report). IV rtPA was used before initial angiography (either CTA or cerebral angiography) in 78 patients. In 27 patients, IV rtPA was administered after CTA (Fig. 3).

Fig. 3.

Timing of angiography regarding use of IV rtPA. CA, cerebral angiography; CTA, computed tomography angiography; IV rtPA, intravenous recombinant tissue plasminogen activator; MRI, magnetic resonance imaging.

Occlusion of the culprit vessel from the ICA to the distal MCA was observed in 67 (63.8%) patients. All patients with ICA (100%) showed a pFHV sign; 29/32 (90.6%) with M1 occlusion and 13/14 (92.9%) with M2 occlusion also showed a pFHV sign (Table 3). Stenotic lesions were observed in 48 patients, of which 20 were severe degree stenosis. All cases of severe stenosis were large vessel lesions; 11/20 (55%) patients with severe stenosis showed a pFHV (Table 4).

Table 3.

Relationship between the occlusion of MCA territory culprit vessels and the pFHV on the initial MRI.

Occlusion of culprit vessels	All (n = 105)	pFHV (n = 71)	No pFHV (n = 34)	P
No occlusion	38/105 (36.2)	10/71 (14.1)	28/34 (82.4)	–
Occlusion	67/105 (63.8)	61/71 (85.9)	6/34 (17.6)	<0.001
Location of lesion
ICA	16	16	0
MCA M1	32	29	3
MCA M2	14	13	1
Distal MCA	5	3	2

Values are given as n or n (%).

ICA, internal carotid artery; MCA, middle cerebral artery; MRI, magnetic resonance imaging; pFHV, proximal hyper-intense vessel sign on fluid-attenuated inversion recovery magnetic resonance imaging.

Table 4.

Relationship between the stenosis of MCA territory culprit vessels and the pFHV on the initial MRI.

	Mild stenosis (30%–50%)			Moderate stenosis (50%–69%)			Severe stenosis (≥70%)
	All	pFHV	No pFHV	All	pFHV	No pFHV	All	pFHV	No pFHV
Cases (n)	22	11 (50)	11 (50)	6	5 (83.3)	1 (16.7)	20	11 (55)	9 (45)
Location of lesion
ICA	14	7	7	4	3	1	12	8	4
MCA M1	6	3	3	1	1	0	7	3	4
MCA M2	1	0	1	1	1	0	1	0	1
Distal MCA	1	1	0	0	0	0	0	0	0

Values are given as n or n (%).

ICA, internal carotid artery; MCA, middle cerebral artery; MRI, magnetic resonance imaging; pFHV, proximal hyper-intense vessel sign on fluid-attenuated inversion recovery magnetic resonance imaging.

In logistic regression analysis, the presence of a pFHV showed a significant correlation with vessel occlusion in particular, LVO (adjusted odds ratio [OR] = 34.533, 95% confidence interval [CI] = 9.781–121.926; P < 0.001, adjusted for AF) (Table 5). However, the presence of a pFHV had no correlation with severe large vessel stenosis (adjusted OR = 0.597, 95% CI = 0.214–1.668; P = 0.325) (Table 5). The sensitivity, specificity, positive predictive value, and negative predictive value of pFHV for LVO were 93.6%, 69.8%, 81.7%, and 88.2%, respectively.

Table 5.

Logistic regression analysis for the relationship between the presence of a pFHV and the occlusion or stenosis of culprit vessels.

pFHV	OR (95% CI)	P	Adjusted OR (95% CI)	P
Occlusion, any location	28.467 (9.413–86.085)	<0.001	27.475 (7.494–100.723)*	<0.001
Occlusion
Large vessel^†	40.600 (11.700–140.883)	<0.001	34.533 (9.781–121.926)^‡	<0.001
Distal MCA	4.200 (0.610–28.918)	0.145	4.739 (0.676–33.233)^‡	0.117
Large vessel stenosis
More than moderate degree (≥50%)	0.698 (0.277–1.759)	0.446	0.597 (0.214–1.668)*	0.325
Severe degree (≥70%)	0.509 (0.188–1.380)	0.185	0.485 (0.163–1.440)*	0.193

*Adjusted for AF and initial National Institutes of Health Stroke Scale.

^†Included ICA, MCA M1, and MCA M2.

^‡Adjusted for AF.

AF, atrial fibrillation; CI, confidence interval; ICA, internal carotid artery; MCA, middle cerebral artery; OR, odds ratio; pFHV, proximal hyper-intense vessel sign on fluid-attenuated inversion recovery magnetic resonance imaging.

The timing of angiography (angiography after IV rtPA versus angiography before IV rtPA) did not affect the association between the pFHV and the LVO (adjusted OR = 2.061, 95% CI = 0.523–8.124; P = 0.302).

Discussion

Previous studies have reported that an FHV is observed in 10%–97% of patients with acute ischemic cerebral infarction (6,8,9,11,13,17,18). This large difference in the incidence of HVS is probably because the definition of HVS differed between studies. In some previous studies, HVS was variably divided into distal versus proximal, subtle versus prominent, or extensive versus less pronounced (6,11 –13). The present study only targeted the pFHV, and the pFHV was observed in 67.6% of patients with a clinically important (eligible for IV rtPA) acute MCA territory infarction. The pFHV, unlike the distal FHV, can be easily and objectively judged by novice interpreters, which can be an advantage in the emergency medicine setting.

The most important feature of the present study was that the analysis of vascular status was based on angiography findings, which were taken within 1 h of the initial MRI. The main findings of the present study clearly show that the presence of a pFHV on initial MRI indicates the occlusion of proximal culprit vessels in an MCA territory infarction. The main finding of this study is consistent with that of previous reports that the presence of a proximal HVS is a marker of arterial occlusion (6,11,13). It further corroborates the hypothesis that the HVS is attributable to slow arterial flow and is more likely to be observed in proximal vessels due to the Bernoulli effect. All study participants with hyper-acute ischemic stroke caused by ICA or M1 occlusion showed a pFHV on initial MRI. Therefore, a pFHV may be of great clinical significance in determining the occlusion of large vessels, which could potentially undergo mechanical recanalization procedures. If a patient with a hyper-acute MCA territory ischemic stroke shows a pFHV on initial MRI, early activation of the intervention team may be a reasonable strategy because the pFHV may be reflective of those patients who need more than IV rtPA to achieve recanalization.

There were 13 patients with pFHV but without LVO. In the sub-analysis of the non-LVO group, there were no variables related to the presence or absence of pFHV. There were five patients with distal occlusion without proximal occlusion, and distal occlusion was not related to pFHV. However, there were too few pure distal occlusion cases included in this study, making it difficult to draw any conclusions.

Unlike other clinical parameters, AF was higher in the LVO group than in the non-LVO group. When further analyzed according to the occlusion site, AF showed a significant correlation with M1 or M2 occlusion (OR = 6.05, 95% CI = 2.005–18.252; P = 0.001) than ICA occlusion (OR = 3, 95% CI = 0.729–12.349; P = 0.128). AF itself does not mean cardioembolic infarction; however, considering that AF is a major risk factor for cardioembolic infarction, higher incidence of MCA lesions in patients with AF is understandable (19,20). In the present study, it was not possible to collect data on stroke etiology due to the limitations of the retrospective study. However, it seems likely that AF is associated with pFHV, because the frequency of embolic infarction in AF is high and the predominant occlusion site of embolic infarction is a large vessel.

The main difference between the results of the present study and those of previous studies is the link between the HVS and stenosis. Several previous studies asserted that a HVS is associated with stenosis (6,8,12); however, stenosis (even severe stenosis) showed no significant association with the presence of a pFHV in this study. This conflicting result is probably because this study only included pFHV and not distal FHV. Speed of flow was not investigated in this retrospective study; we cannot explain why approximately half of patients with stenosis showed a pFHV, while the other half did not. One thing that is clear about the findings of this study is that culprit vessel stenosis is not associated with a pFHV.

Although the physiopathology of the HVS is thought to reflect stationary blood and slow antegrade or retrograde collateral circulation (6,9,10), the clinical significance of HVS still needs to be investigated. Several previous studies have presumed that the HVS on FLAIR MRI is an indicator of severe ischemia as a result of large vessel occlusion or stenosis and poor collateralization (6,8,12), but other studies have asserted that the HVS may be reflective of increased leptomeningeal collateral blood flow and less ischemic injury to tissue supplied by the occluded artery (11,13,17,21,22). The apparent contradictions between these studies may stem from the difference between the proximal and distal HVS. Previous studies indicate that a proximal HVS is associated with more severe ischemia and worse outcome (8,12), while a distal HVS indicates collateral circulation and less ischemic injury (11,13,21). Although beyond the scope of the present study, the main finding (the independently strong relationship between the pFHV and LVO) is in accordance with a previous study showing that the pFHV is associated with larger ischemic lesions and worse clinical outcomes. We recommend that physicians who treat hyper-acute ischemic stroke patients in the ED should carefully monitor for the presence of a pFHV in the initial MRI.

The present study has some limitations. First, the degree of stenosis and occlusion was determined based on radiology reports. The flow speed was not reported and it was not possible to determine whether the blood flow in the stenosis area was faster or slower than normal. However, the most important result of the study is the clear association between a pFHV and the obstruction of medium- to large-sized arteries. Second, not all patients with acute ischemic MCA territory stroke were selected for the study, but only those for whom the use of IV rtPA was indicated. Therefore, the results of the study may be difficult to apply to minor stroke. However, the fact that the study was conducted only on patients who were targeted for the use of IV rtPA may be an advantage in that only patients with clinically important ischemic stroke were studied. Third, the vascular status was based on the results of two imaging tests, CTA and cerebral angiography, rather than one imaging test. Data on the vascular status in patients who only underwent CTA may not be 100% reliable. Finally, it may be difficult to generalize the pFHV results read by two board-certified emergency physicians to all other novice interpreters.

In conclusion, the pFHV represents acute arterial occlusion of intervention eligible proximal arteries such as of ICA, MCA M1, and MCA M2 segment.

Footnotes

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Ji Ung Na

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