High-Intensity Signal in Carotid Plaque on Routine 3D-TOF-MRA Is a Risk Factor of Ischemic Stroke

Yamada, Kiyofumi; Kawasaki, Masanori; Yoshimura, Shinichi; Shirakawa, Manabu; Uchida, Keiji; Shindo, Seigo; Nishida, Shuji; Iwamoto, Yasuhiro; Nakahara, Shigehiro; Sato, Yoshikazu

doi:10.1159/000441094

Cited by 29 publications

(21 citation statements)

References 38 publications

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“…Moreover, TEE has only limited capabilities in evaluation of the internal structure of plaques, which is relevant for differentiating between stable and potentially vulnerable plaques [18,19]. In this context, MRI [20] and CT imaging [21] or dedicated ultrasound techniques [22,23] may provide additional information; however, those techniques are mostly designed for carotid plaque imaging and not suitable for the aorta. Furthermore, it is beyond the boundaries of this study to establish a causal link between complex plaques in the proximal DAo and stroke, because no control group was included in our study and patients were not followed up prospectively.…”

Section: Discussionmentioning

confidence: 99%

Aortic Atherosclerosis Determines Increased Retrograde Blood Flow as a Potential Mechanism of Retrograde Embolic Stroke

Wehrum

Guenther²,

Vach³

et al. 2017

Cerebrovasc Dis

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Background: Retrograde brain embolization from complex plaques of the proximal descending aorta (DAo) has been identified as a new potential mechanism of stroke. Our purpose was to identify predictors of increased retrograde aortic blood flow indicating an elevated risk of brain embolization from the DAo. Methods: A total of 485 patients with acute ischemic stroke were prospectively included and underwent transesophageal echocardiography. Blood flow velocities in the proximal DAo were studied using 2D pulse-wave Doppler ultrasound. Velocity-time integrals (VTI) were calculated for antegrade and retrograde velocity directions. The ratio (VTI_retrograde/VTI_antegrade) was used to estimate retrograde flow extent. Associations between patient demographics, cardiovascular risk factors, echocardiographic parameters, and VTI_ratio were analyzed using multivariate linear regression. Results: Retrograde blood flow in the DAo occurred in all patients. Velocity profiles in the proximal DAo were as follows (mean ± SD): VTI_antegrade = 21.1 ± 6.5, VTI_retrograde = 11.0 ± 3.6, and VTI_ratio = 0.54 ± 0.16. Diameter (r = 0.25, p < 0.001), presence of complex plaques (r = 0.12, p = 0.007), and reduced strain of the DAo (r = -0.23, p < 0.001) had significant partial effects in a predictor model based on predefined variables, which predicted 26% (adjusted R² = 0.26) of the variance in VTI_ratio. A unit increase in the DAo diameter was associated with a 2% increase in VTI_ratio (95% CI 1-2.8%, p < 0.001). Presence of complex plaques increased VTI_ratio by 7% (95% CI 2-13%, p = 0.007) and an increase in strain by 0.1 indicated a decrease in VTI_ratio by about 11% (95% CI 6.2-15.5%, p < 0.001). Complex atheroma was found in the proximal DAo of 79 subjects, of which 40 (50.6%) had a VTI_ratio above average (VTI_ratio ≥0.54) compared to 87 of 261 (33.3%) patients without any complex plaques (p < 0.001). Twenty-five of 79 (31.7%) patients with complex DAo plaques had a VTI_ratio ≥0.60, which indicates a high likelihood of retrograde pathline length of ≥3 cm and thus increased risk of retrograde cerebral embolization. Stroke etiology of those 25 patients was determined in 13 and cryptogenic in 12 cases. Conclusions: Retrograde blood flow in the DAo was found in all stroke patients. However, it increased further in patients with concomitant complex plaques, low strain, and/or large aortic diameter, that is, in those with atherosclerosis of the DAo. Accordingly, such patients may be predisposed to retrograde embolization in case of occurrence of a complex plaque in proximity to a brain-supplying artery.

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Section: Discussionmentioning

confidence: 99%

Aortic Atherosclerosis Determines Increased Retrograde Blood Flow as a Potential Mechanism of Retrograde Embolic Stroke

Wehrum

Guenther²,

Vach³

et al. 2017

Cerebrovasc Dis

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“…None of the patients with a score of 0 or 1 had ischemic events, whereas all 3 patients with a score of 7 had ischemic events. When the USR score was classified as low [0, 1], medium [2,3], high [4,5] and very high [6,7] categories, a linear increase in ischemic event risk was observed (P<0.001 for trend; Table 4; Figure 3B). The ischemic event risk was 0% (0/9…”

Section: Usr Score Scalementioning

confidence: 99%

“…Currently, guidelines for prevention on stroke in patients with carotid atherosclerosis are based on quantification of carotid stenosis degree (3,4). However, a growing amount of evidence has shown that vulnerable carotid plaques play an important role in the occurrence of stroke, independent of the severity of carotid stenosis (5,6). This paradigm shift of assessment of the occurrence of ischemic events provides a new strategy for primary and secondary stroke prevention (7).…”

Section: Introductionmentioning

confidence: 99%

An ultrasound-derived stroke risk score to identify patients at high risk of stroke

Li¹,

Zheng²,

Zhang³

et al. 2021

Ann Transl Med

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Background: To develop an ultrasound-derived stroke risk (USR) score combining plaque stiffness, surface morphology and lumen narrowing to evaluate the risk of stroke in patients with asymptotic carotid stenosis. Methods:We developed the USR score in a prospective study of symptomatic and asymptomatic patients with ipsilateral carotid lumen narrowing. Multivariable analysis was performed to identify parameters associated with ischemic events, and a USR score was constructed based on the observed β coefficient. The discrimination performance of the USR score was assessed using receiver operating characteristic (ROC) curves. Twenty iterations of 5-fold cross-validation were used for internal validation.Results: We derived the USR score (range, 0-7) by incorporating plaque stiffness (≥80 kPa, 0 points; 60-79 kPa, 1 point; 40-59 kPa, 2 points; <40 kPa, 3 points), plaque surface (smooth, 0 points; irregular, 1 point; ulcer, 2 points) and carotid stenosis (<50%, 0 points; 50-69%, 1 point; ≥70%, 2 points). After adjusting for age and sex, the odds ratio (OR) for every 1-point increase in the USR score increase was 3.3 (P<0.001). The risk of ischemic events increased with increasing USR score (P for trend <0.001). The C statistic of the USR score was 0.84 in the derivation sample and 0.82 in the validation sample. Conclusions:The USR score to assess the risk of ischemic events in patients with carotid stenosis showed preferable discrimination ability and robustness. While external validation is warranted to prove the predictive value, this risk score could help accelerate triage decisions in similar patient populations.

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“…These two groups of plaques in typical, routinely performed imaging studies are difficult to distinguish. Currently, there are numerous novel imaging techniques that can detect potentially unstable plaques: magnetic resonance imaging, high-resolution computed tomography, positron emission tomography and contrast-enhanced ultrasound (7)(8)(9)(10)(11). Processes indicating plaque activity (molecular imaging) such as: glucose absorption, protein degradation, exposure of adhesive molecules or content of markers for apoptosis are tested for use in the diagnosis of plaques at risk of destabilization (12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

New insight into biology, molecular diagnostics and treatment options of unstable carotid atherosclerotic plaque: a narrative review

Migdalski¹,

Jawień²

2021

Ann Transl Med

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Indications for intervention in hemodynamically relevant carotid artery stenosis (carotid endarterectomy or stenting) are primarily based on a degree of stenosis and symptomatology. To date the plaque vulnerability is rarely taken into account in clinical decision making although development of molecular imaging allows a better understanding of plaque biology and provides new techniques detecting potentially vulnerable plaque at risk. A significant number of reports describing the mechanisms of unstable plaque formation suggest that it is a multifactorial process. Inflammation, lipid accumulation, apoptosis, proteolysis, the thrombotic process and angiogenesis are among the main factors of carotid plaque destabilization. Although inflammation is a key process in development of plaque vulnerability, the hemostasis and neoangiogenesis should be regarded as equally important. Only a small group of asymptomatic patients may benefit from the invasive treatment and it remains a challenge to determine whether initially asymptomatic carotid plaque become unstable or vulnerable. Currently, the main task of research on atherosclerotic lesion imaging is focused on functional state of the plaque. The presence of one or more features such as stenosis progression, large plaque area, large juxta-luminal black area, plaque echolucency, intra-plaque hemorrhage, impaired cerebral vascular reserve and spontaneous embolization may indicate patients at higher risk for stroke suitable for revascularization. Treatment of carotid stenosis as one of the manifestations of generalized atherosclerosis requires a broad approach. Nowadays pharmacological treatment options for the atherosclerotic process are largely aimed at stimulating the plaque stabilization, but in symptomatic patients and selected asymptomatic patients, carotid plaque should be removed as a potential source of embolism.

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High-Intensity Signal in Carotid Plaque on Routine 3D-TOF-MRA Is a Risk Factor of Ischemic Stroke

Cited by 29 publications

References 38 publications

Aortic Atherosclerosis Determines Increased Retrograde Blood Flow as a Potential Mechanism of Retrograde Embolic Stroke

Aortic Atherosclerosis Determines Increased Retrograde Blood Flow as a Potential Mechanism of Retrograde Embolic Stroke

An ultrasound-derived stroke risk score to identify patients at high risk of stroke

New insight into biology, molecular diagnostics and treatment options of unstable carotid atherosclerotic plaque: a narrative review

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