Huimin Xu1, Ran Huo1, Ying Liu1, Lizhi Xie2, Ruijing Xin3, Tao Wang1, Huishu Yuan1, and Xihai Zhao4
1Peking University Third Hospital, Beijing, China, 2GE healthcare, Beijing, China, 3Southeastern University, Nanjing, China, 4Center for Biomedical Imaging Research, Beijing, China
Synopsis
The development of
secondary collaterals can be affected by the degree of luminal stenosis, which
is not parallel with plaque burden since the positive remodeling effect for
elastic arteries. This study aimed to determine the association of carotid
plaque burden with status of secondary collaterals in patients with severe
carotid stenosis. We found that patients with poor collaterals had
significantly larger Max WT than those with good collaterals (7.29 ±1.15 mm vs.
6.59 ± 0.93 mm; P=0.018) when the plaque is larger
than 5.45mm.
Background and Purpose
Collateral
circulations compensate blood flow for patients with decreased cerebral
perfusion. The status of collaterals is significantly associated with clinical
outcomes. Secondary collaterals, such as leptomeningeal anastomoses, may be
anatomically present, but the enhancement of their capacity likely requires
time to develop 1. It is believed that the development of collaterals is
heavily dependent on the diminished blood pressure in upstream vessels 2,
such as carotid artery luminal narrowing. Since there is positive remodeling
effect for elastic arteries, the progression of plaque burden may not be
parallel with degree of luminal stenosis 3. However, the relationship between
carotid plaque burden and status of secondary collaterals for patients with
similar degree of chronic carotid artery stenosis is still unknown. This study aimed to determine the
association of carotid plaque burden measured by MR vessel wall imaging with
status of secondary collaterals in patients with chronic carotid stenosis.
Methods
Study
sample:
Patients with carotid moderate to severe stenosis (50-99% stenosis) were
recruited and underwent CT and MR imaging. The exclusion criteria were as
follows: 1) hemorrhagic stroke; 2) cerebral neoplasms; 3) heart failure; 4) renal
dysfunction (GFR<60ml/min); 5) iodine contrast agent allergy; 4)
contraindications to MR examination. CT
perfusion: The whole brain CT perfusion was performed on a 256-row
wide-body detector CT scanner with 16 cm z-axis coverage, 0.5 mm slice
thickness. It was initiated 8s after contrast agent injection by 10 scans and a
2 s interval, followed by 7 scans and a 4 s interval. The total scan duration
was 56s. MR imaging: All
patients underwent carotid MR vessel wall imaging on a 3.0T MR scanner with
8-channel carotid coil to acquire the following sequences: 3D time-of-flight, TR/TE
17.6/6.7 ms, flip angle 8°, and slice thickness 2 mm; 2D T1-weighted: TR/TE
850/13.44 ms, slice thickness 2 mm; 2D T2-weighted: TR/TE 2000/96.6 ms, slice
thickness 2 mm; and Simultaneous Non-contrast Angiography intraplaque
hemorrhage (SNAP) imaging: TR/TE 9.6/4.0 ms, flip angle 12°, and slice
thickness 1 mm. The FOV, spatial resolution and longitudinal coverage was respectively
140×140 mm2, 0.55×0.55 mm2, and 32 mm for all imaging
sequences. Image review: The
collateral circulation score was calculated on multiphase CTA images using a 6-point
scale 4. The collaterals were divided into good collaterals (score=4-5) and
poor collaterals (score=0-3) status. The plaque components including lipid-rich
necrotic core (LRNC), intraplaque hemorrhage (IPH) and calcification (CA) were
identified and the Max WT and luminal stenosis were measured for the index
artery with most severe stenosis bilaterally. Statistics:
Carotid plaque features were compared between patients with good and poor
collaterals using Mann-Whitney U test or Chi-square. Univariate and
multivariate logistic regressions were used to determine the correlation
between plaque features and poor secondary collaterals.Results
Of 140 included subjects
(mean age, 65.5±7.8 years; 122 males), 121 (86.4%), 137 (97.9%), and 97 (69.3%)
had carotid CA, LRNC, and IPH, respectively. No significant differences were
found in prevalence of plaque components and Max WT between patients with poor
and good collaterals in all patients (all p>0.05,Table 1). Patients
were divided into 2 groups according to the median of Max WT (5.45 mm): large
plaque group (Max WT >5.45) and small plaque group (Max WT ≤5.45). In large
plaque group, patients with poor collaterals had significantly larger Max WT
than those with good collaterals (7.29 ±1.15 mm vs. 6.59 ± 0.93
mm; P=0.018, Fig. 1). Max WT was significantly
correlated with poor collaterals after (odds ratio, 2.07; 95% CI, 1.14 to 3.76,
P=0.018) adjusted for clinical risk
factors and carotid stenosis. No significant correlations were found between
other plaque features and poor collateral status (all P>0.05, Table 1). In small plaque group, no significant
correlations were found between plaque features and poor collateral status (all
P>0.05, Table 1).Discussions
This study
examined the association of carotid plaque features with status of secondary
collaterals in patients with chronic carotid stenosis. We found that there were
no significant correlations between plaque features and collateral status when the
plaque burden is relatively small (Max WT ≤5.45). In contrast, when the plaque burden
is large (Max WT >5.45), we found that patients with larger Max WT had poorer
collaterals. While the other plaque features will not influence the secondary
collaterals.Conclusions
When
the plaque burden reaches a certain level, carotid artery Max MT is
independently associated with secondary collateral status, suggesting that the
continually increase of plaque will worsen the secondary collateral status.Acknowledgements
No acknowledgementsReferences
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