Pericarotid fat stranding at CT angiography:a marker of the short-term prognosis of acute ischemic stroke

doi:10.21203/rs.3.rs-2243590/v2

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Pericarotid fat stranding at CT angiography:a marker of the short-term prognosis of acute ischemic stroke

https://doi.org/10.21203/rs.3.rs-2243590/v2

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Purpose

Perivascular epicardial fat stranding detected in the coronary CT angiography was associated with culprit lesion and provided helpful information of risk for ACS. This study aimed to evaluate the potential clinical significance of pericarotid fat stranding (PCFS) and investigate the association between PCFS and short-term prognosis of acute stroke with head and neck CT angiography (CTA).

Methods

This study included 80 patients (mean age 69.69士11.03; 58 men) who underwent both head and neck CTA and magnetic resonance imaging (MRI) within 2 weeks. Baseline characteristics, PCAT attenuation, plaque characteristics, ischemic penumbra, infarct core volume, infarct core growth rate (CGR) and grade of collateral status between PCFS group and non-PCFS group were recorded, these data were compared by using two-sample t,Mann-Whitney U,Fisher tests and Spearman’s correlation test.

Results

We found that patients with PCFS had a significantly higher PCAT density than non-PCFS patients (-55.75 ± 5.53 vs -65.82 ± 9.65;P༜0.001 ). Those with PCFS showed a larger infarct core volume (166.43 ± 73.07 vs 91.43 ± 55.03;P = 0.001 ) and faster CGR (39.57 ± 12.01 vs 19.83 ± 32.77;P༜0.001), and that the frequency of adverse prognosis was more significant than in control subjects (83.33% vs 19.11%). The difference was statistically significant.

Conclusions

We discovered that individuals with PCFS had greater CGR, which was substantially related with a worse outcome in acute stroke patients with ipsilateral carotid atherosclerosis. Recognition of PCFS may help to predict stroke prognosis and allow doctors to take early action to improve patient prognosis.

pericarotid adipose tissue

atherosclerosis

plaque

pericarotid fat stranding

short-term prognosis

stroke

Carotid atherosclerosis is a chronic progressive disease [1], and may result in symptoms of cerebral ischemia such as transient attack or acute stroke. Inflammation has long been considered to be a central driver of atherogenesis [2], as well as being a key element in the development of the vulnerable atherosclerotic plaque. Recently studies [3] found that pericarotid adipose tissue (PCAT) behaved as a sensor of signal that comes from the inflammatory vascular wall, allowing for non-invasive detection of vascular inflammation.

The attenuated changes in the inflammatory PCAT lipid gradient can be detected in CT angiography. Fat stranding is an imaging feature of inflammatory and/or neoplastic infiltration [4], which manifests as irregular strip increased attenuation accompanied by signs of blurred fat space. Sandeep et al. [5] conducted a retrospective study and found that the sign of perivascular fat stranding in the coronary could be used as an imaging marker to assess coronary plaque vulnerability and risk of acute coronary syndrome.

Inflammatory PCAT secrets some adipocytokines to regulate metabolism, such as fatty acid binding protein (A-FABP) [6], which was proven to be a key factor in associated PCAT inflammation and inflammatory cell regulating. Increased circulating A-FABP can damage the blood-brain barrier and aggravate cerebral ischemia symptoms, which is significantly positively correlated with poor prognosis of acute stroke.

For acute ischemic stroke (AIS), core growth rate (CGR) is an independent predictor of clinical outcomes according to the previous reports [7], and relates closely with collateral circulation status. The relationship between time after stroke and core growth appears to be a nearly linear one in the first 24 hours. Therefore, the identification of pericarotid adipose inflammation may be used as an imaging indicator to evaluate the severity of cerebral ischemia in patients with acute ischemic brain injury.

Given that perivascular epicardial fat stranding is a meaningful predictor of risk for acute coronary syndrome [5], it is unknown the clinical significance of pericarotid fat stranding (PCFS), we therefore hypothesize that AIS patients accompanying with ipsilateral PCFS correlates with rate of core growth and collateral circulation status.

Consent

General data

We retrospectively identified consecutive patients (N=80) with carotid atherosclerosis with moderate-to-severe stenosis who diagnosed with ipsilateral AIS between February 2019 to February 2022, including 58 males and 22 females. Head and neck CT angiography is a key part of routine emergency procedure screening for stroke, and patients with suspicious stroke symptoms shall be examined after exclusion of relevant contraindications.

Medical personal history like hypertension, diabetes and clinical data such as sex, age, blood pressure, blood glucose, triglyceride (TG), cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), lipoprotein A, homocysteine (Hcy), and smoking history were recorded.

CTA protocol

The patient was required to remove the metal objects from the body before the examination and keep a needle in the median cubital vein. The contrast medium was injected with Iodixanol contrast agent (Loversol Injection,320 mg I/ml, 80mL, Jiangsu Hengrui Pharmaceutical Co., Ltd., China) at a flow rate of 5.0mL/s. On this basis, normal saline (50mL) was injected at the same rate.

CTA was performed using a standard protocol with the following parameters: 100 kV, automated tube current modulation using a 125mA reference value, and a 0.75 mm reconstructed section thickness (A Simens Somatom Definition Flash dual-source CT scanner). The scans were conducted from the aortic arch to the cranial apex before and after contrast injection, and the scanning time was 8.5±1.5 s.

Patient population

Eligibility criteria

1.The patient was age 40-80 years old.

2.Completed head and neck CTA examination.

3.The patient with unilateral internal carotid artery stenosis between 50% and 99% according to NASCET (North American Symptomatic Carotid Endarterectomy Trial) complicating internal carotid artery terminus/middle cerebral artery M1 occlusion.

4.Acute cerebral infarction which detected in MRI on the ipsilateral side of the carotid plaque, and the lesion area diameter>1.5cm.

5.Clear nervous system symptoms and national Institutes of Health Stroke Scale (NIHSS) score ≥2.

6.The interval between the CT angiography and MRI examinations was less than 1 week.

Exclusion criteria:

1.The patents with carotid artery dissection or carotid web.

2.Patients had been made a definite diagnosis of cardiogenic embolism or had atrial fibrillation.

3.Patients after a surgery of carotid stenting or carotid endarterectomy.

4.Patients with moyamoya disease.

5.Patients who had a history of malignant tumour.

6.Poor image quality and incomplete medical record.

7.Prior history of stroke especially caused clinical symptoms.

They were divided into two groups according to the presence or absence of streaks. Cases were defined as patients with pericarotid fat stranding; a control cohort was identified from within the study population but without associated fat stranding.

Image analysis

1 Pericarotid fat stranding (PCFS) was defined as irregular obscuration of adipose tissue adjacent to a carotid artery wall when the presence of plaque (Figure 1).

2 PCAT was defined as the adipose tissue surrounding the carotid artery, whose radial distance from the outer vessel wall is equal to the diameter of the vessel. All adipose density measurements are reported in Hu within the range −190 to −30 HU.

3 When PCFS was detected, it was quantified by measuring the attenuation within the involved fat tissue. The ROIs (diameter 1mm) were drawn carefully at least 1mm and no more than 5mm from the adventitia of the carotid artery according to the site of maximum stenosis, the location of the carotid plaque, and the location of PCAT pads. With the carotid bifurcation as the base point, the upper and lower longitudinal ranges were within 5cm.The results were rechecked by another experienced researcher. For comparison, Hounsfield unit values of the adjacent unaffected carotid fat and subcutaneous fat were recorded by placing a region of interest of equivalent size. Associated findings, including degree of stenosis by the plaque associated with fat stranding, and features of high-risk plaque like napkin ring sign or contrast plaque enhancement, were also recorded. A GPACS system was used to analyze the segments with plaques to the carotid srtery bifurcation. We set the standard window width and window level to 800 and 300 respectively, but the reviewers were allowed to modify the window width and window level for better observation of PCFS.

All images were independently evaluated by two experienced researchers, both of whom were blinded to the clinical data and CGR calculation results of the population in the study. Any disagreement during evaluation were resolved by consensus.

CGR calculation

It is calculated in a dual-source CT workstation (Simens Somatom Definition Flash dual-source CT) (Figure 2). The infarct core is defined as a decrease in CBF in the infarct area, less than 30% of the contralateral normal value. It is currently believed that the infarct core shows a linear growth pattern within 24h after stroke onset, therefore the formula is as follows: CGR = acute ischemic infarct core volume / time to onset.

Collateral status grade

We used collateral score (CS) system proposed by Souza et al. [8] to evaluate the grade of collateral status:

Grade 0: absent collaterals >50% of an M2 territory;

Grade 1: diminished collaterals >50% M2 territory;

Grade 2: diminished collaterals ＜50% M2 territory;

Grade 3: collaterals equal to contralateral side;

Grade 4: increased collaterals.

Prognosis definition

We reviewed the electronic medical records and excluded the patients with history of any prior stroke especially caused clinical symptoms.

Patients were followed up by telephone until 30 days after the onset of illness. According to clinical symptoms of subjects, we applied National Institutes of Health Stroke Scale score (NIHSS) to assess the degree of stroke severity. Functional outcome was assessed on the Barthel index (BI) and the modified Rankin Scale (mRS) [9]. A favorable outcome was defined as mRS score of 0 to 2 or a BI ≥95, and poor outcome was defined as mRS ≥3 or BI <60.

Statistical analysis

Results were analyzed with a statistical software (version SPSS 26.0). Continuous parametric variables are expressed as means ±standard deviations. The normality of each continuous variable group was tested using the Kolmogorov-Smirnov Z-test. Categorical variables are expressed as frequencies and percentages. Paired Wilcoxon was used to test skewness distribution of counting data (blood lipid, lipoprotein A, blood glucose, etc.). The independent sample t-test was used to analyse the differences between the two groups, the Fisher exact test was used to test the differences of probability of poor prognosis and the Mann-Whitney U test for comparing Hounsfield unit. Spearman’s correlation test was used to analyze the correlation between the grade of collateral status and PCFS, infarct core volume, CGR, ischemic penumbra. P values were two-sided, and P <0.05 was considered indicative of a statistically significant difference.

Baseline characteristics

After all exclusion based on the predetermined eligibility criteria and exclusion criteria, of 80 eligible subjects (mean age, 69.69士11.03 years), 58 (72.5%) were males and 22 (27.5%) were females; and 12 patients were assigned to the PCFS group and 68 to the Control group,46 (57.5%) had hypertension,39 (39.8%) had diabetes,22 (27.5%) had hyperlipidemia,23 (28.75%) had smoke history. Head and neck CT Angiography showed moderate stenosis 8 (10%), severe stenosis in 36 (45%), and occlusion in 36 (45%). Five (41.67%) of the twelve cases in PCFS group had carotid artery occlusion, compared with thirty-one (45.59%) of the control group.

No significant statistical differences were found in clinical characteristics between two groups. The demographics and clinical data in the study population are shown in Table 1.

Table 1

Demographics(n = 80)
Characteristic	PCFS group(n = 12)	Control group(n = 68)	P value
Sex(male),n(%)	6(50%)	52(76.5%)	0.058
Age(means ± standard)	70.83 ± 10.44	69.13 ± 11.11	0.287
Smoking,n(%)	3(25%)	20(29.4%)	0.756
Systolic pressure(means ± standard)	160.42 ± 30.62	147.85 ± 20.39	0.074
Diastolic pressure(mmol/L,means ± standard)	83.00 ± 19.65	82.72 ± 11.89	0.947
Blood glucose(mmol/L,means ± standard)	7.88 ± 2.93	6.38 ± 2.39	0.056
Triglyceride(mmol/L,means ± standard)	2.22 ± 2.91	1.69 ± 1.59	0.359
High-density lipoprotein(mmol/L,means ± standard)	1.23 ± 0.30	1.14 ± 0.29	0.266
Low-density lipoprotein(mmol/L,means ± standard)	2.54 ± 0.69	2.49 ± 0.85	0.868
Lipoprotein A(mmol/L,means ± standard)	190.35 ± 88.69	267.98 ± 275.54	0.339
Homocysteine(mmol/L,means ± standard)	13.14 ± 7.28	13.02 ± 8.82	0.968

Plaque characteristics and CGR analysis

In the analysis of AIS subjects (Table 2), we found that patients with PCFS had a significantly higher PCAT density compared with non-PCFS patients (-55.75 ± 5.53 vs -65.82 ± 9.65;P༜0.001 ) .As shown in Table 2,compared with the group without PCFS, those with PCFS showed a larger infarct core volume (166.43 ± 73.07 vs 91.43 ± 55.03;P = 0.001) and faster CGR (39.57 ± 12.01 vs 19.83 ± 32.77; P༜0.001). Ischemic penumbra, plaque area, plaque burden and lumen stenosis were not significantly different with and without PCFS.

Table 2

Plaque characteristics and CGR analysis
Characteristic	PCFS group(n = 12)	Control group(n = 68)	P value
Ischemic penumbra(mmol/L,means ± standard)	57.34 ± 33.47	82.60 ± 58.82	0.198
Infarct core volume(mmol/L,means ± standard)	166.43 ± 73.07	91.43 ± 55.03	0.001
CGR	39.57 ± 12.01	19.83 ± 32.77	༜0.001
PCATattenuation(Hounsfield)	-55.75 ± 5.53	-65.82 ± 9.65	༜0.001
Plaque area(mm2)	47.03 ± 18.55	51.66 ± 24.61	0.635
Plaque burden	7.42 ± 6.51	13.38 ± 15.33	0.572
Lumen stenosis(%)	89.30 ± 12.13	89.90 ± 13.59	0.887

The grade of collateral status

There was a weak negative correlation between the grade of collateral status and PCFS (r₁=-0.42, P༜0.001). The correlation coefficient between the collateral grade and infarct core volume, CGR were r₂=-0.666 (P༜0.001), r₃=-0.749 (P༜0.001), respectively.

PCFS and adverse prognosis

Our data indicate that the frequency of adverse prognosis was greater in cases with PCFS (83.33%,10 of 12 cases) than in control subjects (19.11%, 13 of 68 cases), and the difference was statistically significant (P༜0.001).

In a cohort of patients who underwent head and neck CT angiography for acute ischemic stroke due to internal carotid artery terminus/middle cerebral artery M1 occlusion, while they have moderate or greater ipsilateral internal carotid artery stenosis, we found that AIS patients with ipsilateral PCFS will have a higher rate of core growth and relatively poorer collateral circulation than those without imaging suggestive of PCFS. When comparing the PCAT density changes between the two groups, it is obviously that PCFS group trends to show increased attenuation more significantly. Additionally, PCFS was found to be significantly related to a poor prognosis, including delirium, drowsiness, herniation of brain and severe neurological dysfunction of the limbs affecting the quality of daily life.

Given recent studies supporting the role of the PCAT attenuation increased as a helpful radiographic indication for localized inflammation, we have found that the degree of PCATattenuation is significantly correlated with the severity degree of local adipose inflammation in previous study [10]. Our data in this study suggests that AIS patients accompanying with ipsilateral PCFS are inclined to have acute inflammatory exudation of the carotid artery adipose tissue, which is likely more severer than the relatively mild, focal chronic fat tissue inflammation. The inflammatory adipose tissue became dysfunctional gradually, which is characterized by infiltration of inflammatory cells and aberrant production of adipokines [11]. Several adipokines such as lipocalin [11] and adipocyte fatty acid binding protein (A-FABP) [12] are identified to mediate the cross talk between adipose tissue and cardiovascular and cerebrovascular system. A-FABP has been elucidated to play an important role in dysfunctional PCAT associated inflammatory and correlate with carotid atherosclerosis, plaque vulnerability [11]. Elevated circulating level of A-FABP in patients with carotid atherosclerosis can causes cerebral embolization and acute ischemic stroke and relate positively with infarct volume and poor clinical outcomes. Boya Liao et al. [6] reported that circulating and cerebral A-FABP were increased in mice after acute ischemic stroke and cerebral ischaemic injury in mice were ameliorated after genetic ablation of A-FABP. These data from genetic ablation and pharmacological inhibition in mice supported that A-FABP is involved in the progress of acute ischemic stroke. In their study, A-FABP was identified as a novel factor that regulate the Blood-brain barrier disruption after acute ischemic stroke and exacerbate symptoms of cerebral ischemia and we speculate that it may be related to the core growth rate of AIS patients with ipsilateral PCFS.

We further found a negative correlation between the grade of collateral status and infarct core volume, CGR. It implies AIS patients with poor collateral status may probably have large infarct core volume and faster CGR. Collateral status has been reported [13] to play an important role in the infarct core volume. Good collateral flow, which ustains brain viability distal to arterial occlusion, correlates with small ischemic core volume [14–17]. Campbell BC et al. [18] correlated leptomeningeal collateral flow with simultaneous assessment of perfusion parameters using novel perfusion magnetic resonance imaging (MRI) processing at baseline and 3 to 5 days, highlighting the importance of collateral flow as a key determinant of infract evolution and reporting the association of the existence of fluctuations in collateral flow over time with ischemic core growth. Similarly, Longting Lin et al. [7] have validated that collateral status is a major determinant for core growth. These findings are relevant for clinical practice because CTA is more widely available in the emergency setting than MR imaging examination.

Our study showed that there was a weak negative correlation between the grade of collateral status and PCFS, while the relationship between PCFS and intracranial collateral circulation has not been confirmed by relevant studies at present. We speculate that this may be because atherosclerosis is a chronic disease that affects arteries throughout the whole-body, and the chronic inflammation of the vessel wall affects the regeneration of terminal vascular branches.

In addition, our study showed PCFS correlates with larger ischemic core volume and CGR. The frequency of adverse prognosis was greater in cases with PCFS (83.33%,10 of 12 cases) than in control subjects (19.11%,13 of 68 cases). The prevalence of occlusive diseases was higher in patients with PCFS than that in the control group, which revealed the PCFS is a meaningful CT finding of acute carotid atherosclerotic lesion and alert the doctors to a critically stroke patient or a probably poor-prognosis. According to previous studies [19, 20], CGR was demonstrated to have large variability within 24 hours after onset and may continue to grow for up to 72 hours after stroke without any treatment to restore the blood supply, he ischemic core may grow into the whole ischemic region and result in a diminishing of the penumbra. GR has demonstrated [21] an independent predictor of adverse outcome, which is not only a biomarker of large infraction but also an assessment of the ongoing ischemic process.

Rupture of high-risk plaques is the major contributing etiology of acute stroke. The pathophysiology of atherosclerotic plaque or atherosclerotic tumor is the increase of microemboli or macroemboli, thrombus or platelet emboli in situ. Thrombi often originates at the internal carotid artery stump and embolize to downstream circulation, thus causing symptoms of acute cerebral ischemia. Saba et al. [22] proposed that the degree of plaque enhancement is positively correlated with the increase of pericarotid adipose tissue density (PFD), which can be an indirect marker of plaque stability. In addition, high-risk plaques tend to rupture are generally large with a lipid-rich necrotic core, neovascularity (contrast plaque enhancement), intraplaque hemorrhage and inflammatory cell infiltration [23–25]. Recently, researchers [26] have verified the correlation between carotid intraplaque hemorrhage (IPH) and increased attenuation of PVAT. IPH is caused by damaged neovascularization in plaques due to vascular inflammation and oxidative stress, suggesting that PCATinflammation may play a crucial role in IPH. However, the differences between two groups in plaque area, plaque burden and lumen stenosis were not statistic significantly. In the cases we included in this study, the plaques at the carotid bifurcation caused moderate degree or severe carotid stenosis and were all classified as high-risk plaque, and our small sample size study was not able to achieve statistically significant results.

One patient with carotid artery dissection was excluded from consideration for inclusion, although he had significant PCFS. Carotid artery dissection is one of the causes of acute carotid occlusion, but our study focused on acute ischemic stroke patients with carotid atherosclerosis.

The retrospective study is limited by its single-center design and small sample size, and there is inevitable selection bias; thus, these findings are preliminary and need larger studies to confirm. We were unable to quantitative analysis of the levels of fatty acid binding proteins in the patients and could not assess their association with PCFS because of its a retrospective study. More importantly, application of this study is currently limited to patients with large vessel occlusions on ICA/MCA.

In AIS patients with carotid artery stenosis investigated by CTA, the study highlights the importance of PCFS as a critical factor associated with the rate of infarct core growth and infarct core volume in patients with acute stroke, which is significantly associated with poor prognosis. Our study suggests that PCFS can be used as suggestive imaging markers to predict stroke progression and prognosis.

-Ethics approval and consent to participate

This study protocol was approved by the Ethics Committee of the First People's Hospital of Lianyungang (KY-20210416001-01). Informed consent was waived by our review board for this single-center retrospective analysis. All methods in this study have been performed in accordance with the Declaration of Helsinki.

-Consent for publication

Not Applicable.

-Availability of Data and Materials

The datasets used and/or analysed during the current study available from the corresponding author on reasonable request.

-Competing interests

The authors do not have any possible conflicts of interest.

-Funding

This study received funding from the General Program of China Postdoctoral Science

Foundation (2020M681534).

-Authors' contributions

Ying Liu:Conceptualization,Writing-Original Draft.

Yinan Zhao:Formal analysis.

Zhongping Guo:Edit the manuscript.

Mengshuang Li:Visualization.

Hangsheng Shan:Methodology.

Yonggang Zhang:Data Curation

Chongchang Miao:Supervision.

Yan Gu:Writing-Review&Editing,Funding acquisiton.

All authors agree to be accountable for the content of the work.

-Acknowledgements

The authors wish to acknowledge Dr Gu for her help in experiment design and thesis

writing of this study.

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AIS=acute ischemic stroke, A-FABP=fatty acid binding protein, BI=Barthel index, CGR=core growth rate, CS=collateral score, CTA=CT angiography, HDL=high-density lipoprotein, LDL=low-density lipoprotein, MRI=magnetic resonance imaging, mRS=modified Rankin Scale, NIHSS=National Institutes of Health Stroke Scale score, PCAT=pericarotid adipose tissue, PCFS=pericarotid fat stranding, TC=cholesterol, TG=triglyceride

No competing interests reported.

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Pericarotid fat stranding at CT angiography:a marker of the short-term prognosis of acute ischemic stroke

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Abstract

Purpose

Methods

Results

Conclusions

Figures

Introduction

Material And Methods

Consent

General data

CTA protocol

Patient population

Eligibility criteria

Exclusion criteria:

Image analysis

CGR calculation

Collateral status grade

Prognosis definition

Statistical analysis

Result

Baseline characteristics

Plaque characteristics and CGR analysis

The grade of collateral status

PCFS and adverse prognosis

Discussion

Conclusions

Declarations

References

Abbreviations

Additional Declarations

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