ABSTRACT
Background
Intracranial High‐Resolution Vessel Wall (HRVW) MRI is sometimes used alongside standard ischemic stroke (IS) work‐up, yet its clinical and therapeutic interests remain debated. We aimed to assess the intracranial HRVW‐MRI findings in IS patients and their impact on the IS etiologic classification as well as on treatment modifications.
Methods
We retrospectively analyzed consecutive patients who underwent an intracranial HRVW‐MRI within 2 weeks from stroke onset at a single comprehensive stroke center. The HRVW‐MRI was considered for IS patients with intracranial stenosis or of undetermined origin following standard IS work‐up. We compared IS etiology according to the TOAST classification before and after HRVW MRI and identified treatment changes.
Results
Among the 316 included patients (mean age = 65 years ±16.9), HRVW‐MRI was performed to evaluate intracranial stenosis in 134 (42%), and IS of undetermined etiology without stenosis in 177 (56%). HRVW‐MRI modified the TOAST classification in 17% of cases. Following HRVW‐MRI, the proportion of strokes attributed to presumed atheromatous origin increased from 28.2% to 38.3% (p < 0.001), and those due to other determined etiologies rose from 7.3% to 12.7% (p < 0.001), while undetermined strokes decreased from 50.9% to 35.4% (p < 0.001). Etiological reclassifications were comparable in the subgroups of patients with intracranial stenosis and those with initially undetermined etiology. HRVW‐MRI prompted therapeutic changes in 7% of cases.
Conclusion
HRVW‐MRI significantly affected the IS etiologic classification and had implications in subsequent therapeutic management. Further prospective studies are warranted to determine the clinical utility of HRVW‐MRI in IS etiological work‐up.
Keywords: intracranial high‐resolution vessel wall MRI, intracranial stenosis, ischemic stroke, stroke of undetermined etiology, vasculitis
1. Introduction
Ischemic stroke (IS) has multiple underlying etiologies, including large vessel atheroma, cardioembolic sources, small vessel disease, dissection, arteritis/vasculitis, and hypercoagulability. Identifying IS etiology is essential for optimizing acute medical care and secondary prevention since IS prognosis, risk of recurrence, and overall outcome strongly depend on the etiology [1]. However, approximately one third of IS remain of undetermined etiology even after thorough investigations [1].
High‐Resolution Vessel Wall MRI (HRVWI), which provides information about the intracranial vessel wall and its lumen, may play a significant role to improve the identification of IS etiologies [2, 3, 4]. It may help to differentiate between intracranial vasculopathies such as atheroma, vasculitis, spasms, Moya‐Moya, and dissection [5, 6, 7, 8], but also identify culprit non‐stenotic vessel wall lesions that were not identified on arterial imaging such as CT‐angiography, MR‐angiography, or transcranial doppler. However, the impact of HRVW‐MRI on the etiological classification of ischemic stroke has been insufficiently studied [9, 10, 11, 12]. A few studies have suggested that HRVW‐MRI may alter the etiological classification in more than one‐third of cases, particularly by improving the detection of culprit non‐stenotic intracranial atherosclerosis. Nevertheless, these studies were limited by small to moderate sample sizes and were conducted primarily in very young populations, with a median age below 55 years in most studies [9, 10, 11, 12].
Here, we aimed to study the impact of intracranial HRVW‐MRI on IS etiological classification, as well as on therapeutic modifications in a large population of IS with intracranial stenosis or of undetermined etiology following standard IS work‐up.
2. Methods
2.1. Study Design, Data Sources, and Inclusion Criteria
We retrospectively collected data from IS patients from the prospective registry of our comprehensive stroke center (Rothschild Foundation Hospital, Paris, France) between January 2016 and December 2020. Inclusion criteria were patients aged ≥ 18 years with IS confirmed by positive diffusion‐weighted imaging and the realization of HRVW‐MRI within two weeks of IS onset. In our center, HRVW‐MRI is considered part of the IS workup in two main indications (1) to help differentiate between intracranial vasculopathies in patients with intracranial stenosis, and (2) for additional work‐up in IS of undetermined etiology following standard etiological work‐up and with no evidence of intracranial stenosis. However, the realization of HRVW‐MRI was not standardized, and the request was dependent on the physician in charge. Patients with MRI artifacts that hindered interpretation of HRVW‐MRI were excluded.
The study was approved by the Rothschild Foundation Hospital review board—IRB 00012801—under the study number CE_20210323_12_MOA. In accordance with French legislation, the ethics committee waived the requirement for informed consent, as the study involved analysis of anonymized data collected during routine clinical care. The data supporting the study findings are available from the corresponding author upon reasonable request.
2.2. Clinical Data
The following variables were collected: age, gender, vascular risk factors, previous vascular events, National Institute of Health Stroke Scale (NIHSS) score on admission, the vascular territory affected by the IS on diffusion‐weighted imaging, and the indication of the HRVW‐MRI (evaluation of an intracranial stenosis or additional work‐up for IS of undetermined origin).
All patients underwent an extensive stroke workup, including an EKG, full panel blood test including stroke‐specific blood tests for patients under 55 years of age, intracranial and cervical arterial workup (Doppler ultrasound, CT‐angiography or MR‐angiography), transthoracic echocardiography, and cardiac monitoring. Transesophageal echocardiography was performed for patients with a negative IS workup, and cerebrospinal fluid analysis was obtained for patients suspected of having intracranial vasculitis.
2.3. MR Imaging
HRVW‐MRI was performed using 3 Tesla Philips ELITION (Philips Medical Systems) device with a 32‐channel head coil. As recommended by the Vessel Wall Imaging Study Group of the American Society of Neuroradiology (ASNR) [13] the protocol included four HRVW sequences:
3D proton density‐weighted fat‐saturated sequences with blood‐suppression (spin‐echo) and CSF‐suppression, acquired before and after injection of a single intravenous bolus (0.1 mmol/kg) of gadobutrol (Gadovist, Bayer Healthcare), to detect vessel wall contrast‐enhancement and abnormalities,
3D proton density‐weighted fat‐saturated sequences with blood suppression (spin‐echo) without CSF suppression for morphological analysis of vessel wall abnormalities,
3D T1‐weighted fat‐saturated sequences with blood‐suppression (spin‐echo) and motion‐sensitized driven equilibrium (MSDE) pulse, which may sometimes allow better detection of vessel wall contrast‐enhancement than proton density‐weighted sequences. MSDE pulses allow better blood flow suppression [14, 15].
Additionally, to these HRVW sequences, the protocol included the following sequences:
3D time‐of‐flight MR angiography to characterize luminal abnormality,
Contrast‐enhanced MR angiography for low‐velocity flow caused by stenosis,
Diffusion‐weighted, 3D fluid‐attenuated inversion recovery (FLAIR), 3D susceptibility‐weighted imaging (SWI).
2.4. MR Analysis
HRVW‐MRI were reviewed by a neuroradiologist with 8 years of experience (AT) who was blinded to the clinical data. The patients were classified into six main groups depending on the HRVW MRI findings. First, no abnormalities. Second, intracranial atherosclerotic plaque defined as eccentric arterial wall thickening involving the circumference of the arterial wall, which may demonstrate enhancement. When the atheromatous plaque was located upstream of the corresponding infarct territory, it was deemed potentially causative of the IS and categorized as “Culprit atheroma” (see example in Figure 1). Third, vasculitis, defined as concentric arterial wall thickening and enhancement (see example in Figure 2). Fourth, dissection, defined as arterial wall thickening eccentrically involving the circumference of the arterial wall with spontaneous hyperintensity on T1‐weighted images and on PD‐weighted images with CSF‐suppression [14, 15]. The arterial wall abnormality extended relatively along the artery and was not focal like an atherosclerotic plaque and could exhibit enhancement. Fifth, unspecific enhancement, considered when the enhancement was at the site of an artery occlusion, or when thrombectomy was performed on that arterial segment [14, 15]. Last, other abnormalities, including spasms, thrombus, and other rare causes. Spasm was defined as a reduction in the caliber of an artery with no discernible vessel wall abnormality, at most a discrete, unenhanced vessel wall thickening.
FIGURE 1.
Example of culprit atheroma identified on HRVW‐MRI. Magnetic resonance imaging findings in a 62‐year‐old woman presenting with acute onset right hemiparesis and facial palsy. The standard MRI sequences (A, B) revealed a left paramedian pontine infarct, while MR angiogram (C) showed no arterial stenosis. To further investigate the possible cause, high‐resolution wall vessel imaging (HRWVI) was performed. HRWVI (D, E) revealed the presence of eccentric wall thickening and enhancement on PDT1W after gadolinium injection. These findings are suggestive of a culprit atheroma. PDT1W refers to pre‐contrast T1‐weighted imaging.
FIGURE 2.
Example of vasculitis identified on HRVW‐MRI. Radiographic image of a 36‐year‐old male presenting with sudden dysarthria and left facial palsy. Standard MRI sequences (A, C) revealed the presence of a right middle cerebral artery infarct, accompanied by a right middle artery stenosis. High‐resolution wall vessel imaging (HRWVI) was subsequently conducted (B, D, E, F) revealing the presence of circumferential wall thickening and enhancement on PDT1W after gadolinium injection, indicative of vasculitis. PDT1W refers to pre‐contrast T1‐weighted imaging.
2.5. TOAST Classification Before and After HRVW‐MRI
For the specific aim of this study, the full etiological work‐up was carefully reviewed for each patient to determine IS etiology according to the Trial of Org 10,172 in Acute Ischemic Stroke (TOAST) classification, by one stroke neurologist with 8 years of experience (GA) [16]. The classification was performed in two different sessions, a few weeks apart: (1) blinded to the results of the HRVW‐MRI, and (2) including the HRVW‐MRI results. For the diagnosis of CNS vasculitis, patients were required to have clinical suspicion for CNS vasculitis and tissue or biological support for the diagnosis, including either a positive brain biopsy, cerebrospinal fluid infection/inflammation, or evidence of systemic vasculitis.
Therapeutic changes before and after HRVW‐MRI, which included the introduction of dual antiplatelets, anticoagulants, corticosteroids, antibiotics, or antiviral drugs, were retrospectively reviewed from the medical chart of each patient.
2.6. Statistical Analysis
Continuous variables were described as mean (Standard deviation [SD]) or median (interquartile range [IQR]), as appropriate, and categorical variables as counts and percentages. The proportion of patients classified according to each TOAST subgroup (atheromatous, cardio‐embolic, small vessel disease, other determined, or undetermined stroke etiology) before and after HRVW‐MRI readings was compared using the Chi‐2 McNemar test for paired data. All tests were conducted with a two‐tailed formulation. Statistical analysis was performed using SPSS version 30.0 (IBM, Armonk, NY). A p value of < 0.05 was considered significant.
3. Results
3.1. Study Population
From January 2016 to December 2020, 327 acute stroke patients had an HRVW‐MRI in our study. Among them, 11 cases were excluded due to inadequate quality HRVW‐MRI, leaving 316 patients included in the study. Table 1 summarizes the baseline characteristics of the included patients. Median age was 65 years (SD 16.9), 103 (33%) patients were women, and median baseline NIHSS score was 4 (IQR 0–6). HRVW‐MRI was performed within a median of 5.4 (IQR 2–9) days following IS onset.
TABLE 1.
Baseline characteristics of included patients.
| Variables | Included patients (n = 316) |
|---|---|
| Women n, (%) | 103 (32.6%) |
| Median age ± SD | 65 ± 16.9 |
| NIHSS score (IQR, median) | 4 (0–6) |
| Previous medical history | |
| TIA n, (%) | 12 (3.7%) |
| Ischemic stroke n, (%) | 55 (17.4%) |
| Hemorrhagic stroke n, (%) | 8 (2.5%) |
| Risk factors | |
| Hypertension n, (%) | 158 (50%) |
| Diabetes mellitus n, (%) | 74 (23.4%) |
| Atrial Fibrillation n, (%) | 26 (8.22%) |
| Dyslipidemia n, (%) | 84 (26.6%) |
| Smoking n, (%) | 89 (28.2%) |
| Alcohol n, (%) | 50 (15.8%) |
| Drugs n, (%) | 16 (5%) |
| Acute phase treatment | |
| Thrombolysis n, (%) | 24 (7.6%) |
| Thrombectomy n, (%) | 17 (5.4%) |
| Ischemic stroke arterial territory | |
| Anterior circulation | 150 (47.5%) |
| Posterior circulation | 121 (38.3%) |
| Both | 43 (13.6%) |
HRVW‐MRI was performed for the characterization of an intracranial arterial stenosis in 134/316 (42%) patients, for the additional work‐up in IS of undetermined etiology without intracranial stenosis in 177/316 (56%) patients, and the indication of HRVW‐MRI was not specified in 5/316 (1.6%) patients.
3.2. HRVW‐MRI Findings
The description of the abnormalities observed on the HRVW‐MRI is provided in Figure 3.
FIGURE 3.
Abnormalities identified on the high resolution vessel wall MRI.
3.2.1. Overall Population
Following HRVW‐MRI review, the patients were classified as no abnormality in 155/316 (49%) cases, atheroma in 119/316 (34.7%), vasculitis in 19/316 (6.0%), dissection in 7/316 (2.2%), unspecific enhancement in 13/316 (4.1%), and other abnormality (vasospasm and moya moya) in 3/316 (1.0%).
3.2.2. Intracranial Arterial Stenosis Group
Among the 134 patients for whom the HRVW‐MRI was performed for intracranial stenosis characterization, patients were classified as atheroma in 98/134 (73.1%) of cases, vasculitis in 10/134 (7.5%), dissection in 3 (2.2%), and 23 (17.2%) patients had an unspecific enhancement or no abnormalities.
3.2.3. Stroke of Undetermined Etiology Group but Without Intracranial Arterial Stenosis
Among the 177 patients for whom the HRVW‐MRI was performed for additional workup for IS of undetermined origin, patients were classified as atheroma in 21 (11.9%), vasculitis in 9 (5.1%), dissection in 3 (1.69%), and 144 (81.35%) had an unspecific enhancement or no abnormalities.
3.3. Contribution of HRVW‐MRI for IS Etiological Classification
The etiological classification of IS according to the TOAST classification without, then with HRVW‐MRI finding in the entire cohort are provided in Table 2. The etiologic classification changed following HRVW‐MRI in 53/316 (16.8%) cases. These changes were observed in 29/177 patients (16.4%) with stroke of undetermined etiology and in 24/134 (17.9%) in those with intracranial arterial stenosis. The rate of IS of presumed atheromatous origin increased from 28.2% to 38.3% following HRVW‐MRI (p < 0.001), and the rate of IS due to another determined etiology increased from 7.3% to 12.7% (p < 0.001). HRVW‐MRI had no impact on the proportion of strokes attributed to cardioembolic sources or small vessel disease. The rate of IS of undetermined etiology decreased from 50.9% to 35.4% following HVRW‐MRI (p < 0.001).
TABLE 2.
TOAST classification with and without high resolution vessel wall MRI findings in the overall population.
| TOAST a | Without HRVWI findings | Including HRVWI findings | p |
|---|---|---|---|
| I (atheroma) | 89 (28.2%) | 121 (38.3%) | p < 0.001 |
| II (cardioembolic) | 33 (10.4%) | 33 (10.4%) | p > 0.99 |
| III (small vessel disease) | 10 (3.2%) | 10 (3.2%) | p > 0.99 |
| IV (other determined) | 23 (7.3%) | 40 (12.7%) | p < 0.001 |
| V (undetermined) | 161 (50.9%) | 112 (35.4%) | P < 0.001 |
TOAST I: large vessel atherothromboembolic, TOAST II: cardioembolic, TOAST III: small vessel disease, TOAST IV: stroke of other determined etiology, TOAST V: stroke of undetermined etiology.
The etiological classification of IS according to the TOAST classification without, then with HRVW‐MRI findings for the subgroups of patients with intracranial stenosis and those with undetermined etiology but no intracranial stenosis is presented in Tables 3 and 4. Similar to the results observed in the overall cohort, HRVW‐MRI significantly increased the proportion of strokes classified as atherothrombotic or of other determined etiology, while reducing the proportion of strokes categorized as of undetermined origin.
TABLE 3.
TOAST classification with and without high resolution vessel wall MRI findings in the intracranial arterial stenosis group.
| TOAST a | Without HRVWI findings | Including HRVWI findings | p |
|---|---|---|---|
| I (atheroma) | 81 (60.4%) | 95 (70.9%) | p = 0.001 |
| II (cardioembolic) | 10 (7.5%) | 10 (7.5%) | p > 0.99 |
| III (small vessel disease) | 2 (1.5%) | 2 (1.5%) | p > 0.99 |
| IV (other determined) | 11 (8.2%) | 19 (14.2%) | p = 0.008 |
| V (undetermined) | 30 (22.4%) | 8 (6.0%) | p < 0.001 |
TOAST I: large vessel atherothromboembolic, TOAST II: Cardioembolic, TOAST III: small vessel disease, TOAST IV: stroke of other determined etiology, TOAST V: stroke of undetermined etiology.
TABLE 4.
TOAST classification with and without High resolution Vessel Wall MRI findings in the subgroup of patients with stroke of undetermined etiology but without intracranial stenosis.
| TOAST a | Without HRVWI findings | Including HRVWI findings | p |
|---|---|---|---|
| I (atheroma) | 5 (2.8%) | 23 (13.0%) | p < 0.001 |
| II (cardioembolic) | 22 (12.4%) | 22 (12.4%) | p > 0.99 |
| III (small vessel disease) | 8 (4.5%) | 8 (4.5%) | p > 0.99 |
| IV (other determined) | 11 (6.2%) | 20 (11.3%) | p = 0.004 |
| V (undetermined) | 131 (74.0%) | 104 (58.8%) | p < 0.001 |
TOAST I: large vessel atherothromboembolic, TOAST II: Cardioembolic, TOAST III: small vessel disease, TOAST IV: stroke of other determined etiology, TOAST V: stroke of undetermined etiology.
3.4. Subgroup of Patients With Clinical or HRVW‐MRI Features Suggestive of Vasculitis
3.4.1. HRVW‐MRI Features Suggestive of Vasculitis
HRVW MRI found radiological features suggestive of vasculitis in 19 patients (10 patients from the intracranial stenosis group and 9 from the group of stroke of undetermined etiology). Among those 19 patients, there was also a clinical suspicion of vasculitis in 13 (60%) patients. The diagnosis of vasculitis was confirmed based on clinical, biological, and radiological criteria in 11/19 patients (58%).
Among the 297 patients without HRVW MRI features suggestive of vasculitis, none had a final diagnosis of vasculitis based on the full etiological work‐up.
3.4.2. Clinical Features Suggestive of Vasculitis
HRVW‐MRI was performed in 82 patients with a clinical suspicion of vasculitis, to assess for radiological features consistent with the diagnosis. This included 26 patients with intracranial stenosis and 56 without. Among them, 13/82 patients (16%) had HRVW‐MRI findings suggestive of vasculitis. The diagnosis of vasculitis was eventually confirmed in 7/13 patients (54%). No patients without HRVW‐MRI findings of vasculitis had a final diagnosis of vasculitis.
3.5. Therapeutic Changes Following HRVW‐MRI
Therapeutic changes were made in 22/316 patients (7%) following HRVW‐MRI. These changes included the introduction of dual antiplatelet therapy in 8 patients, anticoagulation in 2, corticosteroids in 9, and an antibiotic or antiviral treatment in 3.
4. Discussion
In our study of 316 IS patients with intracranial stenosis or of undetermined etiology following standard IS work‐up, we found that HRVW‐MRI modified the etiological classification in 17% of cases. This was mainly due to a +10% increase of atherosclerotic etiology, but also to the increase of stroke from another determined cause. The proportion of IS of undetermined etiology was reduced by 15%. These modifications were similar in the subgroups of patients with intracranial stenosis and those with undetermined etiology but no intracranial stenosis. Therapeutic changes occurred in 7% of cases based on the HRVW findings. The main changes were the introduction of dual antiplatelet therapy.
While many studies have focused on the impact of HRVWI on the characterization of intracranial arterial stenosis [4, 5], few have specifically examined its broader impact on stroke etiological classification and its implications for therapeutic decision‐making. Our results align with other studies, showing that HRVW MRI increases the likelihood of identifying IS of atheromatous origin. In one study on a Chinese population, the authors showed that HRVW MRI changed the etiologic stroke classification in 39% of cases regardless of the presence of intracranial stenosis. This change was mainly driven by an increase in stroke of atheromatous origin from 29% to 58% [10]. Another study also found that HRVW MRI increased the diagnosis of stroke of atheromatous origin in 34% of cases regardless of the presence of an intracranial stenosis [9]. These studies were limited by smaller sample sizes and were conducted primarily in very young populations, which might explain the lower rate of etiological reclassification seen in our study [9, 10, 11, 12].
The contribution of HRVW‐MRI to stroke etiology reclassification stems from its ability to detect vulnerable atherosclerotic plaques not only in patients with intracranial stenosis or occlusion visible on conventional luminal imaging, but also in those with mild stenosis or even normal angiographic findings. In our study, HRVW‐MRI led to etiological reclassification in both subgroups: patients with visible intracranial stenosis and those initially categorized with undetermined etiology despite the absence of luminal stenosis.
In cases of intracranial stenosis or occlusion, HRVW‐MRI provides critical insights into the underlying vasculopathy. Atherosclerotic lesions are typically characterized by eccentric wall thickening involving the arterial circumference and may exhibit contrast enhancement. Notably, features such as plaque enhancement and intraplaque hemorrhage suggest active inflammation, neovascularization, and plaque instability—hallmarks of symptomatic plaques associated with atherothrombotic events and increased risk of stroke recurrence [17, 18, 19]. HRVW‐MRI also aids in clarifying the underlying mechanism of intracranial occlusions. The presence of peri‐thrombus plaque along with distal residual flow favors an atherosclerotic origin over a cardioembolic one [20].
Beyond its role in evaluating intracranial stenosis or occlusion, our study shows that HRVW‐MRI provides valuable insights into the etiological assessment in patients with mild or no stenosis. This finding is in line with former studies focusing on embolic strokes of undetermined source (ESUS), which showed that HRVW‐MRI enables direct visualization of non‐stenotic intracranial atherosclerotic plaques, which may harbor vulnerable features such as focal enhancement, eccentric wall thickening, or intraplaque hemorrhage suggesting a high‐risk, unstable plaque phenotype [21, 22, 23, 24]. This mechanism supports the concept of artery‐to‐artery embolism arising from non‐stenotic yet active intracranial atheromatous plaques. Detecting such lesions can therefore reclassify a subset of ESUS as being of atherothrombotic origin, rather than truly cryptogenic. Moreover, HRVW‐MRI helps at detecting non‐stenotic atheromatous plaques that obstruct perforating arteries—contributing to perforator occlusions [25, 26]. This capacity is especially valuable in distinguishing lacunar strokes due to small vessel disease from those caused by branch atheromatous disease.
HRVW‐MRI also contributes to the reclassification of IS to other determined causes, such as arterial dissection or vasculitis [27, 28, 29]. Notably, this diagnostic benefit was observed in both patients with intracranial stenosis and those initially classified as having a stroke of undetermined etiology but no detectable stenosis. HRVW‐MRI enables improved detection of intramural hematoma during the subacute phase of intracranial arterial dissection, even when conventional imaging fails to identify the lesion. Additionally, HRVW‐MRI is valuable in diagnosing intracranial vasculitis, which typically presents with homogeneous, concentric, and moderate arterial wall enhancement. In our study, these imaging characteristics were strongly suggestive of vasculitis. In patients with arterial stenosis, our findings are consistent with previous studies: one study reported that HRVW‐MRI helped identify intracranial vasculitis in 21% and 5% of cases [11], while another demonstrated that HRVW‐MRI helped to classify 33% of acute stroke patients with intracranial stenosis, primarily to a vasculitic etiology [12]. To our knowledge, this is the first study evaluating the use of HRVW‐MRI in the diagnosis of IS of undetermined etiology without stenosis.
The increased identification of ischemic strokes of atherothrombotic and other determined etiologies resulted in a corresponding reduction in strokes classified as of undetermined origin, both among patients with intracranial stenosis and those initially categorized as having a stroke of undetermined etiology without detectable stenosis. Such reduction is clinically relevant as identifying IS etiology is essential for optimizing acute medical care and secondary prevention. We observed therapeutic changes in only 22 out of 316 patients (7%). The main therapeutic change was the initiation of dual antiplatelet therapy. This typically involved patients who were initially on single antiplatelet treatment prior to imaging and were escalated to dual therapy after the identification of a culprit atheromatous plaque. However, the number of such changes was relatively limited, as the majority of patients were already receiving dual antiplatelet therapy at admission, in combination with high‐dose statins—either due to minor stroke severity (median NIHSS score: 4, IQR 0–6) or the presence of intracranial stenosis. Additionally, HRVWI proved valuable in diagnosing vasculitis when clinical, biological, and imaging indicators were insufficient. It facilitated the initiation of corticosteroid treatment in 9 patients by confirming the presence of inflammatory vasculitis, and it also guided the appropriate use of antiviral or antibiotic therapy in cases of infectious vasculitis.
This study has several limitations. First, its monocentric design and retrospective data collection may introduce selection bias and limit the generalizability of the findings. The patient population and clinical practices may not fully reflect those of other centers, particularly in settings with different access to advanced imaging modalities or variations in stroke management protocols. Second, there was no standardized indication for performing HRVW‐MRI, which may have led to variability in patient selection. The decision to perform HRVW‐MRI was left to the discretion of the treating neurologist, potentially introducing a selection bias favoring more diagnostically challenging or atypical cases. Third, the initial interpretation of HRVW‐MRI findings was not blinded to the clinical context, which could have influenced diagnostic attribution. Although a secondary, blinded review of the imaging was conducted, it was performed by a single expert neuroradiologist, and inter‐observer variability was not assessed, thus making generalizability limited. Finally, therapeutic changes were modest (7%) and the decisions based on HRVW‐MRI findings were not standardized and were left to the judgment of individual treating neurologists; as a result, treatment modifications may have been influenced by clinical context, physician experience, or institutional preferences. In addition, clinical outcome data were not collected. All the following complicates the assessment of the direct impact of HRVW‐MRI on clinical management and limits the generalizability of the findings.
5. Conclusion
High‐resolution vessel wall MRI significantly contributes to the etiological classification of acute ischemic stroke and has the potential to influence therapeutic decision‐making. Further prospective, multicenter studies including outcome measures and cost‐effectiveness evaluations are warranted to better define the added clinical value of this approach in the diagnostic work‐up and management of patients with acute ischemic stroke.
Author Contributions
All authors designed the study and developed the methodology. Grace Adwane and Alexia Tran collected the data. Grace Adwane and Pierre Seners analyzed the data and created the tables and the figures. Grace Adwane wrote the manuscript. All authors reviewed and approved the final version of the manuscript.
Funding
The authors have nothing to report.
Ethics Statement
The study was approved by the Rothschild Foundation Hospital review board—IRB 00012801—under the study number CE_20210323_12_MOA. In accordance with French legislation, the ethics committee waived the requirement for informed consent, as the study involved analysis of anonymized data collected during routine clinical care.
Conflicts of Interest
The authors declare no conflicts of interest.
Data Availability Statement
The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.