Now showing 1 - 3 of 3
  • Publication
    High-resolution MRI (HR-MRI) of atherosclerotic plaque in symptomatic carotid stenosis – relationship with risk factors, treatment, and CT angiographic features
    Purpose: Traditional imaging techniques rely on arterial lumen stenosis as an indirect measure of mural plaque. HR-MRI allows direct imaging of mural plaque burden and composition. However, few data exist on the relationship of these parameters to clinical factors in patients with symptomatic carotid stenosis. We investigated the relationship between MR plaque features, clinical characteristics, and plaque morphology on CT angiography. Methods: A sub-group of patients included in the prospective BIOVASC plaque imaging study were included. Inclusion criteria were: (1) Speech/motor TIA or non-severe stroke (Rankin≤3) <72hours (2) Ipsilateral carotid stenosis ≥50% (3) Age≥50 (4) Carotid HR-MRI and CTA performed. Exclusions were pregnancy, malignancy, dementia, renal impairment, cervical irradiation/endarterectomy/stent. Semi-automated analysis of HR-MRI axial plaque images was done using PlaqueView and manual analysis of co-registered CTA performed. Results: 27 patients met inclusion criteria (78% men, mean age 66 years, 36% stroke/64%TIA, 39% current smoking). By HR-MRI, maximum plaque wall area was greater in patients with index stroke compared with TIA (p=0.007). Plaque maximum wall thickness was greater in diabetes (p=0.016) and statin-untreated patients (p=0.003). Volume of lipid-rich necrotic core was less (p=0.018) and fibrous cap thickness (p=0.05) greater in aspirin-treated patients. When HR-MRI was compared with CTA, high correlations were observed for lumen area (rho=0.976, p<0.001), maximum wall thickness (rho=0.878, p<0.001), and maximum wall area (Pearson r=0.981, p<0.001). Conclusion: If replicated, our findings may inform the application of plaque HR-MRI and CTA as surrogate markers in future clinical practice and randomised trials for stroke prevention.
  • Publication
    A Risk Score Including Carotid Plaque Inflammation and Stenosis Severity Improves Identification of Recurrent Stroke
    Background and Purpose— In randomized trials of symptomatic carotid endarterectomy, only modest benefit occurred in patients with moderate stenosis and important subgroups experienced no benefit. Carotid plaque 18F-fluorodeoxyglucose uptake on positron emission tomography, reflecting inflammation, independently predicts recurrent stroke. We investigated if a risk score combining stenosis and plaque 18F-fluorodeoxyglucose would improve the identification of early recurrent stroke. Methods— We derived the score in a prospective cohort study of recent (<30 days) non-severe (modified Rankin Scale score ≤3) stroke/transient ischemic attack. We derived the SCAIL (symptomatic carotid atheroma inflammation lumen-stenosis) score (range, 0–5) including 18F-fluorodeoxyglucose standardized uptake values (SUVmax <2 g/mL, 0 points; SUVmax 2–2.99 g/mL, 1 point; SUVmax 3–3.99 g/mL, 2 points; SUVmax ≥4 g/mL, 3 points) and stenosis (<50%, 0 points; 50%–69%, 1 point; ≥70%, 2 points). We validated the score in an independent pooled cohort of 2 studies. In the pooled cohorts, we investigated the SCAIL score to discriminate recurrent stroke after the index stroke/transient ischemic attack, after positron emission tomography-imaging, and in mild or moderate stenosis. Results— In the derivation cohort (109 patients), recurrent stroke risk increased with increasing SCAIL score (P=0.002, C statistic 0.71 [95% CI, 0.56–0.86]). The adjusted (age, sex, smoking, hypertension, diabetes mellitus, antiplatelets, and statins) hazard ratio per 1-point SCAIL increase was 2.4 (95% CI, 1.2–4.5, P=0.01). Findings were confirmed in the validation cohort (87 patients, adjusted hazard ratio, 2.9 [95% CI, 1.9–5], P<0.001; C statistic 0.77 [95% CI, 0.67–0.87]). The SCAIL score independently predicted recurrent stroke after positron emission tomography-imaging (adjusted hazard ratio, 4.52 [95% CI, 1.58–12.93], P=0.005). Compared with stenosis severity (C statistic, 0.63 [95% CI, 0.46–0.80]), prediction of post-positron emission tomography stroke recurrence was improved with the SCAIL score (C statistic, 0.82 [95% CI, 0.66–0.97], P=0.04). Findings were confirmed in mild or moderate stenosis (adjusted hazard ratio, 2.74 [95% CI, 1.39–5.39], P=0.004). Conclusions— The SCAIL score improved the identification of early recurrent stroke. Randomized trials are needed to test if a combined stenosis-inflammation strategy improves selection for carotid revascularization where benefit is currently uncertain.
      194Scopus© Citations 25
  • Publication
    Association Between 18-FDG Positron Emission Tomography and MRI Biomarkers of Plaque Vulnerability in Patients With Symptomatic Carotid Stenosis
    Purpose: Pathologic studies suggest that unstable plaque morphology and inflammation are associated with cerebrovascular events. 18F-fluorodeoxyglucose positron emission tomography (18FDG-PET) is a validated technique for non-invasive imaging of inflammation-related plaque metabolism, and MRI can identify morphologic features of plaque instability. The aim of this study was to investigate the association of selected imaging characteristics of plaque vulnerability measured with MRI and PET in patients with symptomatic carotid stenosis. Methods: Patients from the BIOVASC study were selected based on the following inclusion criteria: (1) age ≥ 50 years; (2) recent (<30 days) ischaemic stroke (modified Rankin scale ≤3) or motor/speech/vision TIA; (3) ipsilateral internal carotid artery stenosis (≥5 0% lumen-narrowing); (4) carotid PET/CTA and MRI completed. Semi-automated plaque analysis of MRI images was performed to quantify morphologic features of plaque instability. PET images were co-registered with CTA and inflammation-related metabolism expressed as maximum standardised uptake value (SUVmax). Results: Twenty-five patients met inclusion criteria (72% men, mean age 65 years). MRI-measured plaque volume was greater in men (1,708–1,286 mm3, p = 0.03), patients who qualified with stroke (1,856–1,440 mm3, p = 0.05), and non-statin users (1,325–1,797 mm3, p = 0.03). SUVmax was associated with MRI-measured plaque lipid-rich necrotic core (LRNC) in the corresponding axial slice (rs = 0.64, p < 0.001) and was inversely associated with whole-plaque fibrous cap thickness (rs = −0.4, p = 0.02) and calcium volume (rs = −0.4, p = 0.03). Conclusion: This study demonstrated novel correlations of non-invasive imaging biomarkers of inflammation-related plaque metabolism with morphological MRI markers of plaque instability. If replicated, our findings may support the application of combined MRI and PET to detect vulnerable plaque in future clinical practise and randomised trials.
      78Scopus© Citations 1