Background and Purpose: Internal carotid artery stenosis (ICAS)≥70% is a leading cause of ischemic cerebrovascular events (ICVEs). However, a considerable percentage of stroke survivors with symptomatic ICAS (sICAS) have <70% stenosis with a vulnerable plaque. Whether the length of ICAS is associated with high risk of ICVEs is poorly investigated. Our main aim was to investigate the relation between the length of ICAS and the development of ICVEs. Methods: In a retrospective cross-sectional study, we identified 95 arteries with sICAS and another 64 with asymptomatic internal carotid artery stenosis (aICAS) among 121 patients with ICVEs. The degree and length of ICAS as well as plaque echolucency were assessed on ultrasound scans. Results: A statistically significant inverse correlation between the ultrasound-measured length and degree of ICAS was detected for sICAS≥70% (Spearman correlation coefficient ρ = –0.57, p < 0.001, n = 51) but neither for sICAS<70% (ρ = 0.15, p = 0.45, n = 27) nor for aICAS (ρ = 0.07, p = 0.64, n = 54). The median (IQR) length for sICAS<70% and ≥70% was 17 (15–20) and 15 (12–19) mm ( p = 0.06), respectively, while that for sICAS<90% and sICAS 90% was 18 (15–21) and 13 (10–16) mm, respectively ( p < 0.001). Among patients with ICAS <70%, a cut-off length of ≥16 mm was found for sICAS rather than aICAS with a sensitivity and specificity of 74.1% and 51.1%, respectively. Irrespective of the stenotic degree, plaques of the sICAS compared to aICAS were significantly more often echolucent (43.2 vs. 24.6%, p = 0.02). Conclusion: We found a statistically insignificant tendency for the ultrasound-measured length of sICAS<70% to be longer than that of sICAS≥70%. Moreover, the ultrasound-measured length of sICAS<90% was significantly longer than that of sICAS 90%. Among patients with sICAS≥70%, the degree and length of stenosis were inversely correlated. Larger studies are needed before a clinical implication can be drawn from these results.
Background: Around 9–15% of ischemic strokes are related to internal carotid artery (ICA)-stenosis ≥50%. However, the extent to which ICA-stenosis <50% causes ischemic cerebrovascular events is uncertain. We examined the relation between plaque cross-sectional area and length and the risk of ischemic stroke or TIA among patients with ICA-stenosis of 20–40%.Methods: We retrospectively identified patients admitted to the Department of Neurology, University Hospital of Würzburg, from January 2011 until September 2016 with ischemic stroke or TIA and concomitant ICA-stenosis of 20–40%, either symptomatic or asymptomatic. Plaque length and cross-sectional area were assessed on ultrasound scans.Results: We identified 41 patients with ischemic stroke or TIA and ICA-stenosis of 20–40%; 14 symptomatic and 27 asymptomatic. The plaque cross-sectional area was significantly larger among symptomatic than asymptomatic ICA-stenosis; median values (IQR) were 0.45 (0.21–0.69) cm2 and 0.27 (0.21–0.38) cm2, p = 0.03, respectively. A plaque cross-sectional area ≥0.36 cm2 had a sensitivity of 71% and a specificity of 76% for symptomatic compared with asymptomatic ICA-stenosis. In a sex-adjusted multivariate logistic regression, a plaque cross-sectional area ≥0.36 cm2 and a plaque length ≥1.65 cm were associated with an OR (95% CI) of 5.54 (1.2–25.6), p = 0.028 and 1.78 (0.36–8.73), p = 0.48, respectively, for symptomatic ICA-stenosis.Conclusion: Large plaques might increase the risk of ischemic stroke or TIA among patients with low-grade ICA-stenosis of 20–40%. Sufficiently powered prospective longitudinal cohort studies are needed to definitively test the stroke risk stratification value of carotid plaque length and cross-sectional area in the setting of current optimal medical treatment.
Rationale: Giant cell arteritis (GCA) is known to present with typical manifestations like temporal headache and visual abnormalities. However, several cases with atypical manifestations were reported. Stroke occurs in 3% to 7% of patients with GCA. Patient concerns: A 67-year-old male patient with known hypertension presented with somnolence, disorientation and mild bilateral limb ataxia. The magnetic resonance imaging showed multiple acute infarctions in the territory of the vertebrobasilar system with occlusion of the left vertebral artery. Diagnosis: Ten months later, during a routine neurovascular follow-up, recanalization of the left vertebral artery was observed and a hypoechoic concentric “halo” sign around both vertebral arteries, mainly on the left side was evident. On further examination of the superficial temporal artery, a hypoechoic concentric “halo” sign was also found, which—along with increased inflammatory markers—raised suspicion about GCA. Classical GCA features like headache, temporal tenderness or amaurosis fugax were not present. Repeated in-depth diagnostic work-up including 48 hours Holter-ECG did not reveal another stroke etiology. Interventions: Intravenous Methylprednisolone 250 mg/d was immediately started and after 6 days the dose was tapered to 80 mg/d. The patient was discharged on a tapering scheme with the recommendation to start azathioprine. Additionally, we placed the patient on acetylsalicylic acid 100 mg/d and clopidogrel 75 mg/d. However, the patient was not compliant to treatment; he stopped prednisolone early and did not start azathioprine. Outcomes: The inflammatory markers were markedly reduced at the beginning of the treatment. After stopping the immunosuppressive medications, the inflammatory markers were once again increased. Three months later, the patient developed bilateral middle cerebral artery and right occipital lobe infarctions. Lessons: In patients with cryptogenic vertebrobasilar strokes, GCA may be considered in the differential diagnosis, especially if the inflammatory markers are increased.
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