ORIGINAL RESEARCH

ADULT BRAIN

Hyperintense Vessels on FLAIR: Hemodynamic Correlates and

Response to Thrombolysis
A. Kufner, I. Galinovic, V. Ambrosi, C.H. Nolte, M. Endres, J.B. Fiebach, and M. Ebinger

ABSTRACT
BACKGROUND AND PURPOSE: Hyperintense vessels on baseline FLAIR MR imaging of patients with ischemic stroke have been linked to
leptomeningeal collateralization, yet the ability of these to maintain viable ischemic tissue remains unclear. We investigated whether
hyperintense vessels on FLAIR are associated with the severity of hypoperfusion and response to thrombolysis in patients treated with
intravenous tissue-plasminogen activator.

MATERIALS AND METHODS: Consecutive patients with ischemic stroke with an MR imaging before and within 24 hours of treatment,
with proved vessel occlusion and available time-to-maximum maps were included (n 62). The severity of hypoperfusion was charac-
terized on the basis of the hypoperfusion intensity ratio (volume with severe/mild hypoperfusion [time-to-maximum 8 seconds /
time-to-maximum 2 seconds]). The hypoperfusion intensity ratio was dichotomized at the median to differentiate moderate (hypo-
perfusion intensity ratio 0.447) and severe (hypoperfusion intensity ratio 0.447) hypoperfusion. Good outcome was dened as a
modied Rankin Scale score of 2.

RESULTS: Hyperintense vessels on FLAIR were identied in 54 patients (87%). Patients with extensive hyperintense vessels on FLAIR (4 sections)
had higher NIHSS scores, larger baseline lesion volumes, higher rates of perfusion-diffusion mismatch, and more severe hypoperfusion (hypo-
perfusion intensity ratio). In stepwise backward multivariate regression analysis for the dichotomized hypoperfusion intensity ratio (including
stroke etiology, age, perfusion decit, baseline lesion volume, smoking, and extent of hyperintense vessels on FLAIR), extensive hyperintense
vessels on FLAIR were independently associated with severe hypoperfusion (OR, 6.8; 95% CI, 1.1 42.7; P .04). The hypoperfusion intensity ratio
was an independent predictor of a worse functional outcome at 3 months poststroke (OR, 0.2; 95% CI, 0.5 0.6; P .01).

CONCLUSIONS: Hyperintense vessels on FLAIR are associated with larger perfusion decits, larger infarct growth, and more severe
hypoperfusion, suggesting that hyperintense vessels on FLAIR most likely indicate severe ischemia as a result of insufcient
collateralization.

ABBREVIATIONS: FHV hyperintense vessels on FLAIR; HIR hypoperfusion intensity ratio; IQR interquartile range; Tmax time-to-maximum; TOAST Trial
of Org 10172 in Acute Stroke Treatment

W hile most studies agree that hyperintense vessels on FLAIR

(FHV) are highly associated with large-vessel occlusion,
results on the underlying pathophysiology are seemingly split.1
ingeal collateralization and found an association with smaller le-
sions, slower infarct progression, and better prognosis.6-10
The apparent contradiction of these studies may stem from the
Several studies suggest FHV to be indicative of hemodynamic use of different methodologies and the diversity of populations
stress, inadequate collateralization, and poor functional recov- studied, making the plethora of results challenging to analyze.
ery.2-5 Conversely, others attributed FHV to increased leptomen- Nevertheless, 2 critical questions remain due to lack of compre-
hensive imaging data and long-term clinical follow-up: Do FHV
represent good collateralization or indicate the insufficiency of
Received September 23, 2014; accepted after revision January 8, 2015. established collaterals to maintain ischemic tissue? Second, does
From the Klinik und Hochschulambulanz fu r Neurologie (A.K., C.H.N., M. Endres,
M. Ebinger), International Graduate Program Medical Neurosciences (A.K., V.A.),
FHV have clinical relevance in terms of functional recovery?
and Cluster of Excellence NeuroCure (M. Endres), ChariteUniversitatsmedizin
Berlin, Berlin, Germany; and Center for Stroke Research Berlin (I.G., C.H.N., M. En-
Please address correspondence to Anna Kufner, MSc, Klinik und Hochschulambu-
dres, J.B.F., M. Ebinger), Berlin, Germany.
lanz fu
r Neurologie, ChariteUniversitatsmedizin Berlin, Chariteplatz 1, Berlin-10117,
This work was funded by the Federal Ministry of Education and Research via the Germany; e-mail: anna.kufner@charite.de
grant Center for Stroke Research Berlin (01 EO 0801), the Volkswagen Foundation Indicates open access to non-subscribers at www.ajnr.org
(Lichtenberg program to Matthias Endres), the EU (EUSTROKE, ARISE), and the Ger-
man Research Foundation (NeuroCure, SFB-TR 43). http://dx.doi.org/10.3174/ajnr.A4320

1426 Kufner Aug 2015 www.ajnr.org

 The difficulty in determining collateral status poses a major Postprocessing of DWI was performed by using MRIcro (Ad-
challenge in answering these questions because digital subtraction vanced Brain Imaging; McCausland Center for Brain Imaging,
angiography is not always readily available and associated risks Columbia, South Carolina) to assess lesion volumes on acute and
may not be justified in most cases. Bang et al11 used a hypoperfu- second-scan images to determine infarct growth (DWI lesion vol-
sion intensity ratio (HIR: time-to-maximum [Tmax] 8 sec- ume after thrombolysis DWI baseline lesion volume). Stroke-
onds/Tmax 2 seconds) on baseline MR perfusion imaging as a tool (Digital Image Solutions; Frechen, Germany) was used to
surrogate marker of collateral status and found that excellent and assess acute perfusion deficit volume (MTT 6 seconds). Perfu-
intermediate collateral grades were highly associated with lower sion-diffusion mismatch was assessed as a binary variable defined
HIRs. as follows: (perfusion deficit DWI lesion volume)/DWI lesion
In the PRE-FLAIR study, patients with FHV had larger initial volume 100 20%. Tmax maps of acute perfusion imaging
lesion volumes and more severe clinical impairment12; therefore, images were created in Stroketool. The severity of the hypoperfu-
we hypothesized that patients with FHV would have more severe sion was characterized on the basis of HIR (Fig 1), defined as
hypoperfusion, suggesting the insufficiency of established collat- tissue volume with severe hypoperfusion (Tmax 8 seconds)
erals to maintain ischemic tissue before reperfusion is achieved. In divided by volume with mild hypoperfusion (Tmax 2 seconds).
this study, we investigated whether the extent of FHV is correlated HIR was dichotomized at the median to differentiate moderate
with the severity of hypoperfusion by using Tmax perfusion maps (HIR 0.447) and severe (HIR 0.447) hypoperfusion.
and whether this plays a role in response to thrombolysis in pa- Arterial occlusion was evaluated on time-of-flight MRA. Arte-
tients with arterial occlusion treated with intravenous recombi- rial occlusions were categorized on the basis of the size of the
nant tissue plasminogen activator. occluded vessel: large-vessel occlusions (internal carotid artery
and carotid-T occlusions), medium-vessel occlusions (ie, M1,
MATERIALS AND METHODS M2, P1, P2, and vertebral occlusions), and small-vessel occlusions
This was a retrospective study conducted at the Center for Stroke (ie, occlusion in distal arterial branches).15 Recanalization was
Research Berlin at Charite University Hospital. Consecutive pa- defined as an increase in at least 2 Thrombolysis in Myocardial
tients with acute stroke recruited between March 2008 and De- Infarction points within 24 hours of treatment based on acute and
cember 2012 (1000Plus study registered with clinicaltrials.gov; follow-up MRA.
NCT 00715533) were selected for analysis on the basis of the fol- For all 2-group analyses, we used the Fisher exact test and
lowing criteria: received IV-tPA within 4.5 hours of symptom Mann-Whitney U test as appropriate. We chose a stepwise back-
onset, had MR imaging before and within 24 hours after treat- ward regression model with a binary dependent variable (dichot-
ment, and had proved vessel occlusion and acute perfusion maps omized HIR and outcome) for multivariate regression analyses;
of sufficient quality to postprocess into Tmax maps. MR imaging all parameters that reached a significance of .1 in univariate
(3T, Tim Trio; Siemens, Erlangen, Germany) protocol included analysis based on the dependent variable were included for
T2*, FLAIR (TE 100 ms, TR 8000 ms, TI 2370.5 ms, analysis.
FOV 220 mm, matrix 256 232, 5-mm section thickness Stepwise backward multivariate regression analysis was per-
with a 0.5-mm intersection gap), diffusion-weighted imaging formed to determine independent predictors of the severity of
(TE 93.1 ms, TR 7600 ms, FOV 230 mm, matrix 192 hypoperfusion. We included the following parameters: TOAST
192, 2.5-mm section thickness with no intersection gap), MR an- criteria, the size of the vessel occlusion, smoking, baseline perfu-
giography (TE 3.86 ms, TR 22.0 ms, FOV 200 mm, ma- sion deficit, baseline lesion volume, and extent of FHV. Analo-
trix 384 268, 0.65-mm section thickness with a 7.2 mm in- gously, stepwise backward regression analysis was performed for
tersection gap), and perfusion imaging (TE 29 ms, TR 1390 favorable outcome, with the only change being that age was also
ms, FOV 230 mm, matrix 128 128, 5-mm section thick- dichotomized at older than 70 years to increase external compa-
ness with a 0.5-mm intersection gap). rability13 (age [older than 70 years], smoking, atrial fibrillation,
The following cerebrovascular risk factors were evaluated on HIR [0.447], NIHSS score on admission, baseline lesion vol-
admission by using previously published definitions13: smoking, ume, and extent of FHV [4 sections]). All statistical analyses
arterial hypertension, diabetes mellitus, hypolipoproteinemia, were performed by using SPSS, Version 19 (IBM, Armonk,
and atrial fibrillation. Stroke severity was assessed by using the New York).
National Institutes of Health Stroke Scale. Stroke etiology was
determined by using the Trial of Org 10172 in Acute Stroke Treat- RESULTS
ment (TOAST) criteria.14 Functional outcome was assessed 3 Sixty-two patients were included for final analysis (mean age,
months poststroke by using the modified Rankin Scale score; fa- 71.4 13.9 years; 48.4% female; median NIHSS score on admis-
vorable outcome was defined as mRS of 2. sion, 11; interquartile range [IQR], 4.8 16); 87% had visible FHV
Blinded to acute perfusion imaging, 2 raters (A.K., I.G.) inde- on acute FLAIR (n 54). Interrater reliability for the presence of
pendently counted the number of FLAIR sections with FHV, de- FHV was high ( 0.86; P .01); in 9 cases, raters differed in 2
fined as focal, linear, or serpentine hyperintensities distal to the sections when counting the number of sections with FHV.
main occluded artery. In case of disagreement, raters met for con- Patients with extensive FHV (4 sections) had higher NIHSS
sensus. The number of sections with FHV was dichotomized at scores on admission, larger baseline lesion volumes, higher rates
the median ( or 4 sections) to distinguish between less pro- of perfusion-diffusion mismatch, and more severe hypoperfusion
nounced versus more extensive FHV. (ie, HIR) (Table 1). Patient groups also differed in terms of stroke
AJNR Am J Neuroradiol 36:1426 30 Aug 2015 www.ajnr.org 1427
FIG 1. MR imaging (left-to-right: acute FLAIR, acute DWI, acute Tmax, dichotomized Tmax, follow-up DWI) of patients with middle cerebral
artery occlusions (M1). Patient A (82 years of age; baseline NIHSS score, 13; baseline lesion volume, 1.4 mL; HIR, 0.031; recanalization to Throm-
bolysis in Myocardial Infarction 2 following treatment; absolute infarct growth, 3.3 mL) had FLAIR hyperintense vessels on 3 sections (FHV 4;
not visible on the depicted section) and patient B (76 years of age; baseline NIHSS score, 23; baseline lesion volume, 63.8 mL; HIR, 0.53; no
recanalization following treatment [Thrombolysis in Myocardial Infarction, 0]; absolute infarct growth, 80.2 mL) had FHV on 8 sections (arrows;
FHV 4).

Table 1: Comparison of baseline parameters and response to thrombolysis based on the baseline lesion volumes, and lower rates
number of sections with FLAIR hyperintense vesselsa of a favorable outcome (Table 2). Stroke
Visible FHV Visible FHV etiology based on the TOAST criteria
on 4 Sections on >4 Sections P Value
did not differ between groups.
No. 30 32
In multivariate regression analysis
Age (yr) (mean) (SD) 71 (10.8) 71.9 (16.5) .42
Time to MRI in min (median) (IQR) 88.5 (72103) 93.5 (61121) .98 for HIR, the extent of FHV was associ-
NIHSS score on admission (median) (IQR) 5 (413) 14.5 (1118) .001 ated with severe hypoperfusion (OR,
NIHSS score on day 2 (median) (IQR) 3 (15) 5 (217) .03 6.8; 95% CI, 1.1 42.7; P .04; Table 3).
TOAST .05 In multivariate regression analysis for
Cardioembolic (%) (No.) 40.7 (11) 36.7 (11)
outcome, only baseline lesion volume
Macroangiopathic (%) (No.) 37 (10) 63.3 (19)
Microangiopathic (%) (No.) 0 (0) 0 (0) (OR, 0.95; 95% CI, 0.9 1.0; P .05) and
Other (%) (No.) 7.4 (2) 0 (0) dichotomized HIR (OR, 0.17; 95% CI,
Competing causes (%) (No.) 14.8 (4) 0 (0) 0.05 0.57; P .01) remained in the
Baseline lesion volume (mL) (median) (IQR) 1.6 (.34.9) 8.1 (2.420.6) .01 model (Table 4). Last-step multivariate
Infarct growth (median) (IQR) 1.2 (0.212.7) 12.8 (2.543.9) .01
r2 increased from 0.42 to 0.49 when age
Perfusion-diffusion mismatch (%) (No.) 67.7 (21) 96.9 (31) .01
Baseline perfusion decit (mL) (median) (IQR) 24.8 (14.554.6) 118 (82175) .001 was included in the model as a continu-
Tmax 2 sec 30 (16.797.1) 155 (115.7191.2) .001 ous variable.
Tmax 8 sec 10.3 (3.727.2) 87.2 (62.5123.7) .001
HIR 0.28 (0.070.47) 0.61 (0.440.73) .01
Vessel occlusion size: .29
DISCUSSION
Large (%) (No.) 20 (6) 9.4 (3) The extent of FHV is not only associated
Medium (%) (No.) 80 (24) 90.6 (29) with larger perfusion deficits1,16 but is
Small (%) (No.) 0 (0) 0 (0) also an independent predictor of more
Recanalization (%) (No.) 53.3 (16) 74.2 (23) .11 severe hypoperfusion, resulting in larger
Favorable outcome at 3 months (%) (No.) 66.7 (20) 38.7 (12) .02
infarct growth. Although we found no
a
A Fisher exact test and Mann-Whitney U test were used for categoric and continuous variables, respectively.
independent association between the
extent of FHV and functional recovery,
etiology, in which patients with extensive FHV more often had the severity of hypoperfusion was independently associated with a
macroangiopathic strokes. Despite the similarity of vessel-occlu- worse functional recovery 3 months poststroke (Table 2).
sion size and recanalization rates, patients with extensive FHV Similar to results from a multicenter observational study,12
had larger infarct growth and a worse functional recovery 3 approximately 87% of patients with proved vessel occlusion had at
months poststroke. least 1 section with FHV on acute examination. Patients with exten-
Patients with severe hypoperfusion were significantly older sive FHV (4 sections) had comparatively higher NIHSS scores on
and less often smokers and had higher NIHSS scores on admis- admission, more severe hypoperfusion, larger infarct growth, and a
sion, more sections with FHV, larger perfusion deficits, higher worse functional outcome 3 months poststroke. While patient
1428 Kufner Aug 2015 www.ajnr.org
Table 2: Univariate analysis comparing patients with moderate hypoperfusion (HIR < 0.447) ing, this study found that low HIR
with patients with severe hypoperfusion (HIR > 0.447)a (moderate hypoperfusion) was highly
Low HIR (0.447) High HIR (>0.447) P Value associated with good collateral grades.
No. 31 31 This finding is in line with our hypothe-
Age (yr) (mean) (SD) 67.5 (13.2) 75.4 (13.7) .02
Female (%) (No.) 51.6 (16) 45.2 (14) .8 sis that FHV are indicative of severe hy-
Arterial hypertension (%) (No.) 80.6 (25) 87.1 (27) .73 poperfusion and insufficient collateral-
Diabetes mellitus (%) (No.) 16.1 (5) 25.8 (8) .53 ization. These results stand in contrast
Smoking (%) (No.) 38.7 (12) 9.7 (3) .02 to previous studies suggesting that FHV
Hypolipoproteinemia (%) (No.) 54.8 (17) 46.4 (15) .9 represent increased leptomeningeal col-
Atrial brillation (%) (No.) 35.5 (11) 45.2 (14) .6
No. of sections with FHV (median) (IQR) 3 (17) 7 (410) .01 lateralization6,7,10,17; these studies, how-
NIHSS score on admission (median) (IQR) 5 (413) 15 (1118) .001 ever, did not report perfusion status or
Baseline lesion volume (mL) (median) (IQR) 1.5 (0.275.8) 6.7 (2.328.2) .01 clinical follow-up.
Infarct growth (median) (IQR) 1.6 (0.210.6) 6.2 (1.439.0) .01 Peripheral collateralization is an in-
Baseline perfusion decit (mL) (median) (IQR) 41.2 (15.8101.7) 117.1 (56.0171.6) .01 herent defense mechanism following
Tmax 2 sec 75.6 (24.7179.4) 143.1 (70.5170.2) .08
Tmax 8 sec 10.5 (3.761.9) 88.2 (43.7122.6) .001 proximal vessel occlusion; collaterals
Vessel-occlusion size: .47 can prolong tissue viability if blood flow
Large (%) (No.) 19.4 (6) 9.7 (3) is sufficient to keep hypoperfusion mod-
Medium (%) (No.) 80.6 (25) 90.3 (28) erate until reperfusion is achieved. Ves-
Small (%) (No.) 0 (0) 0 (0) sels become hyperintense on FLAIR
Recanalization (%) (No.) 70 (21) 58.1 (18) .43
Favorable outcome at 3 months (%) (No.) 75.9 (22) 32.3 (10) .01 when blood flow is so slow that there is a
a loss of the flow-void phenomenon.
A Fisher exact test and Mann-Whitney U test were used for categoric and continuous variables, respectively.
Here, we observe an independent asso-
Table 3: Stepwise multivariate regression analysis for severity of hypoperfusion ciation between the extent of FHV and
(dichotomized at median)
severe hypoperfusion (Table 3); how-
Odds
2 ever, the link to collateral flow is not yet
Ratio 95% CI P Value Univariate r
clear. On the one hand, one might imag-
First step (multivariate r 0.68)
2

Age 1.2 1.01.3 .01 0.12 ine that slow flow in collaterals directly
TOAST 0.76 0.154.2 .77 0.004 causes arterial hyperintensities on
Baseline lesion volume 1.1 1.01.2 .04 0.12 FLAIR, suggesting that FHV directly de-
Baseline perfusion decit 1.0 0.991.0 .06 0.12 pict insufficient or sluggish flow in col-
Sections with FHV (4) 6.7 1.041.9 .04 0.26
lateral pathways.7,8 On the other hand,
Smoking 0.04 0.0010.99 .05 0.14
Last step (multivariate r 0.68)
2 vessel occlusion and subsequent isch-
Age 1.2 1.01.3 .01 emia cause cerebral swelling, which
Baseline lesion volume 1.1 1.01.2 .05 likely compresses distal collateral ves-
Baseline perfusion decit 1.01 0.91.0 .06 sels, slowing blood flow. Regardless,
Smoking 0.04 0.0010.96 .05
FHV most likely reflect slow flow in dis-
Sections with FHV (4) 6.8 1.142.7 .04
tal collateral pathways distributed over a
large ischemic area, resulting in larger
Table 4: Stepwise multivariate regression analysis for favorable outcome (mRS <2)
ischemic lesions. Hence, this frequently
Odds
2 observed MR imaging feature may be
Ratio 95% CI P Value Univariate r
useful as a tool to assess the severity of
First step (multivariate r 0.42)
2

Age (older than 70 years) 1.0 0.235.8 .95 0.0 hypoperfusion over an ischemic area as
Smoking 0.84 0.204.5 .83 0.02 a result of poor collateralization.
Atrial brillation 0.41 0.101.6 .21 0.14 Of note, patients with large-vessel
Sections with FHV (4) 0.89 0.23.9 .88 0.12 occlusion had less pronounced FHV
HIR (0.447) 0.24 0.051.1 .07 0.24
(4) and more moderate hypoperfu-
NIHSS score on admission 0.93 0.831.0 .12 0.25
Baseline lesion volume 0.96 0.901.0 .12 0.21 sion (low HIR), though these did not
Last step (multivariate r2 0.36) reach the level of significance (Tables 1
HIR (0.447) 0.17 0.050.57 .01 and 2). Carotid occlusions are fre-
Baseline lesion volume 0.95 0.901.0 .05 quently the end result of chronic occlu-
sive disease, and the recruitment of col-
groups based on FHV differed in terms of stroke etiology, TOAST laterals often happens before acute stroke takes place. Thus,
criteria showed neither association with the severity of hypoperfu- one might imagine that the longer large-vessel disease has been
sion nor functional recovery in univariate analysis. in existence before the index event, the greater the likelihood of
Bang et al11 used the same Tmax HIR ratio to determine the excellent flow in collaterals. These collaterals might maintain
severity of the perfusion deficit and found similar results in terms good flow without visible FHV; however, this is mere
of NIHSS scores on admission and infarct volume. Most interest- speculation.

AJNR Am J Neuroradiol 36:1426 30 Aug 2015 www.ajnr.org 1429

 Although HIR was an independent predictor of functional re- by HMG-CoA reductase inhibitors (US patent number 6,147,109). Jochen B. Fiebach
RELATED: Consulting Fee or Honorarium: Boehringer; UNRELATED: Board Member-
covery, we observed no independent associations of the extent of
ship: Lundbeck, Sygnis, Synarc, Comments: Head of Imaging Board of the Desmo-
FHV and outcome (Table 4). A possible explanation may lie in the toplase in Acute Ischemic Stroke Trial (DIAS) 3&4 and Imaging Board DIAS J; central
heterogeneity of vessel occlusion size observed in this cohort; an reader AXIS 2 trial; central reader i.a. Thrombolysis trial; Consultancy: Lundbeck,
Comments: DIAS 3&4; Payment for Lectures (including service on Speakers Bu-
independent analysis including only patients with middle cerebral
reaus): Boehringer Ingelheim, Siemens, Comments: stroke imaging; OTHER: He re-
artery occlusions is suggested. ports the following board memberships, consultancies and/or payments for lectures
In multivariate analysis for outcome, baseline lesion volume including service on speakers bureaus: Boehringer-Ingelheim, Lundbeck, Siemens,
Sygnis, Synarc. *Money paid to the institution.
remained in the model, accounting for 21% of the variance; this is
to be expected because initial infarct volume may reflect collateral
status. While FHV may be indicative of insufficient collateral REFERENCES
flow, the clinical relevance of this MR imaging sign in terms of 1. Azizyan A, Sanossian N, Mogensen MA, et al. Fluid-attenuated in-
predicting response to treatment remains unclear. A study by version recovery vascular hyperintensities: an important imaging
Olindo et al9 found extensive FHV associated with smaller infarcts marker for cerebrovascular disease. AJNR Am J Neuroradiol
2011;32:177175
pre- and posttreatment, as well as a better prognosis in patients
2. Ebinger M, Kufner A, Galinovic I, et al. Fluid-attenuated inversion
with MCA occlusion. The discordance of these results may lie in recovery images and stroke outcome after thrombolysis. Stroke
the use of different MR imaging units (1T versus 3T), the charac- 2012;43:539 42
teristics of populations studied, and the question at hand. In this 3. Girot M, Gauvrit JY, Cordonnier C, et al. Prognostic value of hyper-
study, we focused primarily on the acute hemodynamic correlates intense vessel signals on fluid-attenuated inversion recovery se-
quences in acute cerebral ischemia. Eur Neurol 2007;57:7579
of FHV, which show a clear independent association with more
4. Hohenhaus M, Schmidt WU, Brunecker P, et al. FLAIR vascular hy-
severe hypoperfusion; the prognostic value of FHV remains perintensities in acute ICA and MCA infarction: a marker for mis-
unresolved. match and stroke severity? Cerebrovasc Dis 2012;34:63 69
Most interesting, smoking was independently associated 5. Kamran S, Bates V, Bakshi R, et al. Significance of hyperintense ves-
with moderate hypoperfusion, suggesting better collateraliza- sels on FLAIR MRI in acute stroke. Neurology 2000;55:265 69
6. Huang X, Liu W, Zhu W, et al. Distal hyperintense vessels on FLAIR:
tion in patients with this risk factor. Bang et al11 also found an
a prognostic indicator of acute ischemic stroke. Eur Neurol
association between smoking status and low HIR. Studies have 2012;68:214 20
suggested that long-term smoking-induced atherosclerosis 7. Lee KY, Latour LL, Luby M, et al. Distal hyperintense vessels on
leads to increased collateralization,18 which may explain this FLAIR: an MRI marker for collateral circulation in acute stroke?
observed phenomenon. Neurology 2009;72:1134 39
8. Liu W, Xu G, Yue X, et al. Hyperintense vessels on FLAIR: a useful
This study has limitations. Most important, it is a retrospective
non-invasive method for assessing intracerebral collaterals. Eur J
observational study. Furthermore, lack of DSA did not allow di- Radiol 2011;80:786 91
rect assessment of collateral grade; the use of HIR only partially 9. Olindo S, Chausson N, Joux J, et al. Fluid-attenuated inversion re-
compensated for this limitation. Finally, due to small numbers, covery vascular hyperintensity: an early predictor of clinical out-
this study runs the risk of type 2 errors, and multivariable regres- come in proximal middle cerebral artery occlusion. Arch Neurol
2012;69:1462 68
sion analyses may lead to overfitting.
10. Perez de la Ossa N, Hernandez-Perez M, Domenech S, et al. Hyper-
intensity of distal vessels on FLAIR is associated with slow progres-
CONCLUSIONS sion of the infarction in acute ischemic stroke. Cerebrovasc Dis
The extent of FHV on baseline MR imaging is an independent 2012;34:376 84
predictor of severe hypoperfusion in patients with acute ischemic 11. Bang OY, Saver JL, Alger JR, et al. Determinants of the distribution
and severity of hypoperfusion in patients with ischemic stroke.
stroke. FHV were highly associated with more severe strokes and
Neurology 2008;71:1804 11
larger infarct growth, suggesting that this frequently observed MR 12. Cheng B, Ebinger M, Kufner A, et al. Hyperintense vessels on acute
imaging feature most likely indicates severe ischemia due to the stroke fluid-attenuated inversion recovery imaging: associations
insufficiency of established collaterals to maintain ischemic tissue with clinical and other MRI findings. Stroke 2012;43:2957 61
before recanalization is achieved. 13. Kufner A, Nolte CH, Galinovic I, et al. Smoking-thrombolysis
paradox: recanalization and reperfusion rates after intravenous tis-
sue plasminogen activator in smokers with ischemic stroke. Stroke
Disclosures: Christian H. NolteUNRELATED: Consultancy: Bristol-Myers Squibb,
2013;44:40713
Pzer, Bayer Pharma; Payment for Lectures (including service on Speakers Bureaus):
Pzer, Boehringer Ingelheim; OTHER: payment for lectures and travel grants from
14. Adams HP Jr, Bendixen BH, Kappelle LJ, et al; TOAST Investigators.
Boeheringer-Ingelheim and Takeda-Pharma. Matthia EndresRELATED: Grant: DFG: Classification of subtype of acute ischemic stroke: definitions for
Excellence Cluster NeuroCure,* Federal Ministry of Education and Research: Center use in a multicenter clinical trial. Stroke 1993;24:35 41
for Stroke Research,* EU: WakeUp,* Volkswagen Foundation: Lichtenberg-Program*; 15. TIMI Study Group. The Thrombolysis in Myocardial Infarction
UNRELATED: Board Membership: Bayer, Boehringer Ingelheim, Pzer, BMS, MSD, (TIMI) trialphase I findings. N Engl J Med 1985;312:93236
Sano, Comments: Advisory Board; Grants/Grants Pending: DFG,* EU,* Astra- 16. Schellinger PD. Diagnostic accuracy and relevance of early MRI ves-
Zeneca,* Roche,* Sano,* Comments: DFG: SFB TR43, KFO 247, KFO 213, EU: ESN, sel signs are highly overrated. Cerebrovasc Dis 2006;21:215; author
Counterstroke (an EU-funded research project in which specialists collaborate to reply 21516
develop novel therapies to treat stroke); Payment for Lectures (including service on
17. Liu W, Xu G, Yue X, et al. Hyperintense vessels on FLAIR: a useful
Speakers Bureaus): Astra Zeneca, Bayer, Boston Scientic, Bristol-Myers Squibb,
Boehringer-Ingelheim, Ever, Glaxo Smith Kline, MSD, Novartis, Pzer, Sano; OTHER:
non-invasive method for assessing intracerebral collaterals. Eur J
He reports the following consultancies, grants and/or payments for lectures includ- Radiol 2011;80:786 91
ing service on speakers bureaus: Astra Zeneca, Bayer, Berlin Chemie, BMS, Boehr- 18. Koerselman J, de Jaegere PP, Verhaar MC, et al. Coronary collateral
inger-Ingelheim, Glaxo Smith Kline, Novartis, Pzer, Sano-Aventis, Trommsdorff; he circulation: the effects of smoking and alcohol. Atherosclerosis 2007;
holds a patent for the upregulation of type III endothelial cell nitric oxide synthase 191:19198

1430 Kufner Aug 2015 www.ajnr.org