Carotid MRI Research Articles

Effects of inverted photoperiods on the blood pressure and carotid artery of spontaneously hypertensive rats and Wistar-Kyoto rats.

The objective of this study was to investigate the effects of inverted photoperiods on the blood pressure and carotid arteries in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats (homologous control group). This study used two inverted photoperiods [inverted light:dark (ILD)16 : 8 and ILD12 : 12] to create the model. A total of 27 male SHR and 27 male WKY rats were randomly divided into six groups (nine rats per group): SHR (LD12 : 12), SHR (ILD16 : 8), SHR (ILD12 : 12), WKY (LD12 : 12), WKY (ILD16 : 8) and WKY (ILD12 : 12). We recorded the trajectory of the activity rhythm of the rats and performed carotid vascular ultrasound examination, MRI (arterial spin labelling) analysis and carotid biopsy. The results showed that inverted photoperiods increased the blood pressure, carotid intima-media thickness, resistance index and blood flow velocity. In addition, inverted photoperiods led to the development of carotid arterial thrombosis, significantly reduced cerebral blood flow and increased the number of collagen fibres. Moreover, it increased the expression of angiotensin receptor and low-density lipoprotein receptor in the carotid arteries, leading to decreased expression of 3-hydroxy-3-methylglutaryl-Coenzyme A reductase and nitric oxide synthase. Inverted photoperiods induced the formation of atherosclerotic plaque. Multiple results of SHR were worse than those of WKY rats. Taken together, inverted photoperiods can produce a series of adverse consequences on blood pressure and carotid arteries. Hypertension can aggravate the adverse effects of inverted photoperiods.

Management of Cardiovascular Disease in Kidney Disease Study: Rationale and Design

Introduction: Atherosclerosis, inflammation, and vascular stiffness are prominent interrelated risk factors contributing to the high incidence of cardiovascular disease (CVD) in patients with CKD. Conventional CVD management strategies in CKD largely target atherosclerotic CVD and have had a limited impact on the cardiovascular mortality in this population. Multiple in vivo and in vitro studies and epidemiological evidence from the rheumatologic cohorts have shown that low-dose hydroxychloroquine has beneficial effects on inflammation, endothelial function, insulin sensitivity, and metabolic syndrome. Our recent proof-of-concept animal study showed that hydroxychloroquine has marked protection against atherosclerosis and vascular stiffness. We hypothesize that hydroxychloroquine has the potential to provide significant cardiovascular benefits in patients with CKD. Methods: The Management of Cardiovascular disease in Kidney disease study (NCT 03636152) is a phase 2B, randomized, double-blind, placebo-controlled trial evaluating the effects of low-dose hydroxychloroquine therapy on the parameters of atherosclerosis, inflammation, and vascular stiffness in patients with CKD. The study plans to enroll 100 CKD patients estimated to be at high cardiovascular risk by a combination of low estimated glomerular filtration rate and albuminuria and treat them for 18 months with hydroxychloroquine or placebo in 1:1 allocation. Results: The study will assess the change in the total carotid plaque volume as measured by serial noncontrast carotid MRI as the primary outcome and the serial changes in plasma inflammation markers, vascular stiffness, renal function, and the composition characteristics of the carotid plaque as secondary outcome measures. Discussion/Conclusion: The results of this trial will provide the proof-of-applicability for hydroxychloroquine in the CVD in CKD. If positive, this trial should lead to phase-3 trials with clinical end points for this potentially transformative, novel, and inexpensive therapy for CVD in CKD.

Serial magnetic resonance imaging detects a rapid reduction in plaque lipid content under PCSK9 inhibition with alirocumab.

PCSK9 inhibitors lower low-density lipoprotein cholesterol (LDL-C) and reduce cardiovascular events. The clinical benefits presumably result from favorable effects on atherosclerotic plaques. Lipid-core and plaque inflammation have been recognized as main determinants of risk for plaque rupture and cardiovascular events. Both can be noninvasively assessed with carotid MRI. We studied if PCSK9 inhibition with alirocumab induces regression in lipid-core or plaque inflammation within 6months as measured by MRI. Patients with non-calcified carotid plaque(s) and baseline LDL-C ≥ 70mg/dl, who were statin-intolerant or taking a low-dose statin (≤ 10mg per day of atorvastatin or an equivalent), received subcutaneous alirocumab 150mg every 2weeks. Carotid MRI was performed at baseline and 6months after treatment, including pre- and post-contrast images for measuring percent lipid-core volume (%LC) and dynamic contrast-enhanced images for measuring microvessel leakiness (Ktrans), a marker of inflammation. Twenty-eight patients completed the study (69 ± 9years; 64% male). Alirocumab led to significant changes in LDL-C (p < 0.001) and high-density lipoprotein cholesterol (HDL-C) (p = 0.003). At 6months, there was a significant reduction in %LC (mean: - 2.1% [- 3.5, - 0.7], p = 0.005; a 17% reduction from baseline of 9.9%) without significant changes in lumen/wall area or in the inflammatory index Ktrans. Carotid plaque lipid content was reduced by 17% after 6months of PCSK9 inhibition with alirocumab. This was seen before observable changes in lumen or wall areas, which supports pursing plaque lipid content as a more sensitive marker of therapeutic response compared to lumen or wall areas in future technical developments and serial studies.

Identification of high-risk carotid plaque with MRI-based radiomics and machine learning.

We sought to build a high-risk plaque MRI-based model (HRPMM) using radiomics features and machine learning for differentiating symptomatic from asymptomatic carotid plaques. One hundred sixty-two patients with carotid stenosis were randomly divided into training and test cohorts. Multi-contrast MRI including time of flight (TOF), T1- and T2-weighted imaging, and contrast-enhanced imaging was done. Radiological characteristics of the carotid plaques were recorded and calculated to build a traditional model. After extracting the radiomics features on these images, we constructed HRPMM with least absolute shrinkage and selection operator algorithm in the training cohort and evaluated its performance in the test cohort. A combined model was also built using both the traditional and radiomics features. The performance of all the models in the identification of high-risk carotid plaque was compared. Intraplaque hemorrhage and lipid-rich necrotic core were independently associated with clinical symptoms and were used to build the traditional model, which achieved an area under the curve (AUC) of 0.825 versus 0.804 in the training and test cohorts. The HRPMM and the combined model achieved an AUC of 0.988 versus 0.984 and of 0.989 versus 0.986 respectively in the two cohorts. Both the radiomics model and combined model outperformed the traditional model, whereas the combined model showed no significant difference with the HRPMM. Our MRI-based radiomics model can accurately distinguish symptomatic from asymptomatic carotid plaques. It is superior to the traditional model in the identification of high-risk plaques. • Carotid plaque multi-contrast MRI stores other valuable information to be further exploited by radiomics analysis. • Radiomics analysis can accurately distinguish symptomatic from asymptomatic carotid plaques. • The radiomics model is superior to the traditional model in the identification of high-risk plaques.

Comparison of carotid atherosclerotic plaques between subjects in Northern and Southern China: a Chinese atherosclerosis risk evaluation study

Background and purposeTo investigate differences in the characteristics of carotid atherosclerotic plaques of symptomatic subjects in northern and southern China using MRI.MethodsSixty-three subjects in northern China (mean age: 59.1±8.6 years,...

Clinical Value of the Carotid Ultrasound in Evaluation of Plaque Composition as Compared to the Carotid MRI

Abstract Background: The main aim of carotid imaging studies is the assessment of the carotid plaque morphology with the detection of vulnerable plaques which is associated with increased risk of cerebrovascular insult, hence proper deline-ation of plaque composition is a crucial step for further management of brain ischemic insult. Aim of Study: To define the inter method agreement between the carotid ultrasound and carotid MRI for charac-terization of vulnerable plaques with further assessment of carotid ultrasound sensitivity and specificity. Material and Methods: The study was conducted over 60 patients. The modified G-W classification was used to assess the sonographic features of the carotid plaques, and compared with the plaque composition using carotid MRI. Results: Our study included 60 patients, their ages ranged between 53 and 78 years with a mean age of 60.3±9.8 years. 56.7% of patients was male. The agreement between carotid ultrasound and carotid MRI was good with k=0.734, sensitivity of the carotid ultrasound to detect the vulnerable plaque was 88.1% with an overall accuracy of 88.3%. Conclusion: The carotid ultrasound examination is con-sidered the first-line modality for assessment of the carotid plaque composition, with good agreement with carotid MRI and acceptable sensitivity and accuracy for characterization of vulnerable plaques.

Abstract WP181: Preprocedual Carotid Plaque Characterization by Duplex Ultrasonography as a Predictor of in-Stent Intimal Restenosis 6 months After Carotid Stenting

Background and Purpose: In-stent intimal restenosis (ISR) caused by neo-intimal hyperplasia generally occurs &lt;24 months after carotid stenting (CAS). Although the real clinical impact of ISR are still unclear, several studies suggested the development of ISR significantly correlated with ipsilateral stroke and death. Also differences in the rate of ISR between open-cell and closed-cell stents have yet to be well evaluated. We aimed to investigate predictors of ISR 6 months after CAS. Methods: We examined 133 patients (mean age of 72.1±8.4 years old) received CAS in a single hospital during 2014 and 2018. Preoperative carotid plaque evaluation was performed by carotid angiography, duplex carotid ultrasonography (CUS), and black-blood carotid artery MRI (BB-MRI). Mean stenosis rate (NASCET) was 71.0±12.3% (44%-100%). Follow-up carotid angiography was performed six months after CAS in all patients according to a predefined protocol. ISR was defined as in-stent intimal hyperplasia more than 50% stenosis based on the NASCET method. Selection of stent type was at the discretion of the treating physician. Predictors of ISR were determined by multivariate logistic regression analysis. Results: Follow-up angiography demonstrated ISR in 33 patients (24.8%). In 44 patients, more than 2 stents were deployed. Univariate analyses demonstrated hypoechoic plaque, 1 mobile plaque with jerry fish sign, complete occlusive or pseudo occlusive lesion, closed-cell stent are significantly associated with ISR (&gt;50%), however no association was observed in traditional risk factors, MRI plaque characterization, and implantation of multiple stents. Multivariate analysis demonstrated low echoic plaque in preoperative CUS (OR4.67; 95%CI, 1.85-11.78) and closed-cell stent (OR 0.378; 95%CI, 0.15-0.97) as significant predictors of ISR. Conclusions: Preprocedual plaque characterization by CUS but not MRI appeared to be useful to predict ISR 6 months after CAS even after adjustment of stent type.

Coronary CT Angiography and Carotid MRI Improve Phenotyping of Disease Extent Compared with ACC/AHA Risk Score Alone.

To determine the relationship between the American College of Cardiology/American Heart Association (ACC/AHA) risk score and plaque phenotype of the coronary and carotid arteries assessed directly using CT angiography and MRI. Asymptomatic subjects eligible for statin therapy by risk score were enrolled in a prospective study of disease burden using coronary artery calcium (CAC) scoring, coronary CT angiography, and MRI of the carotid arteries. Quartiles were calculated for noncalcified plaque, CAC, and average carotid wall volume and were compared with ACC/AHA risk quartiles. Two hundred three subjects were studied (60% men; mean age, 65 years). There were weak correlations between risk and carotid wall volume (Kendall tau = 0.29), noncalcified plaque (tau = 0.16), and CAC (tau = 0.33). ACC/AHA risk alone misclassified plaque extent compared with measurement by carotid wall volume, CAC, and noncalcified plaque in 22.1%, 24.1%, and 29.6% of subjects, respectively. On average, 13% of the subjects were underclassified, and 12.5% were overclassified. Approximately 25% of subjects had large discrepancies between ACC/AHA risk and plaque burden at imaging. These results suggest that clinical risk score models alone do not fully reflect the amount of atherosclerotic disease present.© RSNA, 2020See also the commentary by Truong and Villines in this issue.

Serum insulin levels are associated with vulnerable plaque components in the carotid artery: the Rotterdam Study.

BackgroundTo investigate the association between fasting serum insulin and glucose levels with atherosclerotic plaque composition in the carotid artery. Impaired insulin and glucose levels are implicated in the etiology of cardiovascular disease; however, their influence on the formation and composition of atherosclerotic plaque remains unclear.MethodsIn 1740 participants (mean age 72.9 years, 46% women, 14.4% diabetes mellitus) from the population-based Rotterdam Study, we performed carotid MRI to evaluate the presence of calcification, lipid core, and intraplaque hemorrhage in carotid atherosclerosis. All participants also underwent blood sampling to obtain information on serum insulin and glucose levels. Using logistic regression models, we assessed the association of serum insulin and glucose levels (per s.d. and in tertiles) with the different plaque components, while adjusting for sex, age, intima-media thickness, and cardiovascular risk factors.ResultsSerum insulin levels were associated with the presence of intraplaque hemorrhage (adjusted odds ratio (OR): 1.42 (95% CI: 1.12–1.7)) We found no association with the presence of calcification or lipid core. Sensitivity analyses restricted to individuals without diabetes mellitus yielded similar results. No associations were found between serum glucose levels and any of the plaque components.ConclusionsSerum insulin levels are associated with the presence of vulnerable components of carotid plaque, specifically with intraplaque hemorrhage. These findings suggest a complex role for serum insulin in the pathophysiology of carotid atherosclerosis and in plaque vulnerability.

Start of Antiplatelet Therapy Increases the Prevalence of Intraplaque Hemorrhage in Patients With Advanced Carotid Artery Lesions: A Longitudinal MR Imaging Study

Introduction: Intraplaque hemorrhage (IPH) is an important feature of plaque vulnerability. Patients with a history of transient ischemic attack or stroke are treated with platelet aggregation inhibitors to prevent secondary myocardial infarction or ischemic stroke. Although antiplatelet medication is effective in reduction of clot formation, it also has adverse effects. It has therefore been hypothesized that platelet aggregation inhibitors could also initiate the onset or progression of IPH. A histopathological study on 154 carotid endarterectomy plaques found that preoperative antiplatelet therapy was associated with an increase in the prevalence of repeated IPH in symptomatic carotid plaques. This longitudinal study investigates the effect of antiplatelet agents on the prevalence of IPH. Methods: 63 symptomatic patients underwent carotid MRI at baseline and after two years of follow-up. Presence of IPH in both carotid arteries was scored. Medication prescription before and after the index event and after follow-up was collected.The presence of IPH was determined using MP-RAGE images and analysed blinded for the clinical data using dedicated vessel wall analysis software (VesselMass). IPH was considered present when a hyperintense signal, compared to the sternocleidomastoid muscle, was visible in the bulk of the plaque. Results: A significant higher prevalence of any IPH was found two years after the index event (42.9% vs. 55.6%; p = 0.008) (Figure 1) Patients already using antiplatelet agents before the index event (n=19) did not show significantly more IPH (52.6% vs. 63.2%, p = 0.50) at follow-up. Patients who did not use platelet aggregation inhibitors before the index event (n=44) and were prescribed medication after the event, showed a significantly higher prevalence of IPH (38.6% vs. 52.3%, p=0.031) at follow-up (Figure 2) Conclusion: Patients who started antiplatelet therapy after the index event show a significant increase in bilateral IPH two years after inclusion, while no significant changes in IPH status were found in the patients that already use antiplatelet therapy before the index event. Future studies are warranted to investigate causal relationships. Disclosure: JE Wildberger reports institutional grants from AGFA, Bard, Bayer, GE, Optimed, Philips, Siemens outside the submitted work; and speakers Bureau: Bayer, Siemens outside the submitted work. This research was performed within the framework of the Center for Translational Molecular Medicine (www.ctmm.nl), project PARISk (grant 01C-202), and supported by the Dutch Heart Foundation. This project has received funding from the European Union Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement No 722609. ME Kooi and JE Wildberger are supported by Stichting de Weijerhorst. ME Kooi is supported by an Aspasia Grant 2018/SGw/00460457 from NWO. J Hendrikse has received funding from the European Research Council under the European Union's Horizon 2020 Programme (H2020) / ERC grant agreement n°637024. FHBM Schreuder is supported by the Dutch Heart Foundation (2012T077).

HYPERGLYCEMIA-ASSOCIATED LACTIC ACIDOSIS IN SEPSIS

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Lactate is a nonspecific lab test widely used as a marker for tissue hypoperfusion in management of sepsis. Elevated blood lactate has been shown to be associated with higher mortality in sepsis. Lactate is frequently trended to assess improvement of sepsis and need for further resuscitative fluids. This case highlights the elevation of lactic acid due to nonischemic mechanisms in a patient with sepsis, which can lead to unnecessary administration of IV fluids and lab testing. CASE PRESENTATION: A 75-year-old female with past medical history including CAD, HTN, HLD, poorly controlled DM2, GERD, and remote history of small bowel resection (secondary to fibroid tumor) presented to the ED with several days of progressively worsening fatigue, dyspnea, productive cough, and wheezing. Patient was recently discharged from the hospital three days prior after treatment of AKI and cystitis. On presentation patient met SIRS criteria with WBC 14.1 and pulse 97. Other vitals were within normal limits. Due to lactate of 4.7 with clinical evidence of pulmonary infection, she was treated for septic shock. In the ED she was treated with 30cc/kg IV fluids, ceftriaxone, azithromycin, and IV solumedrol. The morning after admission patient felt significantly improved. Her repeat lactic acid originally improved from 4.7 to 4.3 after completion of 30cc/kg fluids. Repeat lactate the following morning increased to 5.4, then 5.7. Glucose levels were also elevated concomitantly with the increasing lactic acid levels, likely secondary to IV solumedrol. There was no hypotension, elevated troponins, AKI, or other evidence of tissue hypoperfusion. Metformin and glipizide had been held prior to admission. Abdominal exam was benign. Her insulin regimen was adjusted and as blood glucose levels improved lactic acidosis improved as well. DISCUSSION: In the Cori cycle pyruvate combines with NADH using lactate dehydrogenase to produce lactate and NAD. Lactate is then used by the liver, kidneys, and heart for gluconeogenesis. Lactic acidosis is defined by lactate levels >4 mmol/L and is divided into types A, B, and D. Type A lactic acidosis is related to sepsis, shock, tissue hypoperfusion and ischemia. Type B lactic acidosis is associated with diabetes, malignancy, ethanol, certain drugs, and toxins. Type D lactic acidosis is associated with short bowel syndrome, DKA, and propylene glycol. In this patient elevated lactic acid was likely secondary to nonoxidative glycolysis from diabetes. The mechanism for lactic acidosis in diabetes is not fully understood, but may involve inhibition of pyruvate dehydrogenase or deficiencies in pathway for oxidative glycolysis. CONCLUSIONS: Lactate is a nonspecific marker used in management of septic patients. Due to the numerous processes that can cause elevated lactic acid, it should be used judiciously in septic patients to avoid unnecessary testing and administration of IV fluids. Reference #1: Causes of Lactic Acidosis . www.uptodate.com. https://www.uptodate.com/contents/causes-of-lactic-acidosis. Published September 19, 2017. Accessed March 15, 2019. Reference #2: Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. Int J Epidemiol. December 2010. Reference #3: Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. Int J Epidemiol. December 2010. DISCLOSURES: No relevant relationships by Niloufar Gharib, source=Web Response

Associations between carotid intraplaque hemorrhage and new ipsilateral ischemic lesions after carotid artery stenting: a quantitative study with conventional multi-contrast MRI.

The risk of cerebral embolism after CAS in patients with carotid IPH is still controversial. This study was to further investigate the relationship between IPH and new ipsilateral ischemic lesion (NIIL) after CAS, and to perform a volumetric analysis of IPH for predicting the risk of NIIL following CAS. One hundred and seventeen patients with carotid stenosis undergoing CAS were prospectively enrolled. Preprocedural multi-contrast carotid MRI was performed. NIIL was evaluated by brain DWI before and after CAS. IPH volume, wall volume at the plaque (WVplaque) and relative IPH volume were calculated. Associations between IPH and postprocedural NIIL were studied. NIILs were shown in 52 patients. IPH were identified in 53 patients. NIILs were found more frequently in IPH-positive (33/53, 62.3%) than in IPH-negative patients (19/64, 29.7%, p < 0.001). There was no significant difference of WVplaque between NIIL-positive and NIIL-negative patients (1166.6 ± 432.0 mm3 vs 1124.6 ± 410.4mm3, p = 0.592). The IPH volume from NIIL-positive group was significantly larger than that of NIIL-negative group (252.8 ± 264.9 mm3 vs 59.3 ± 131.1mm3, p < 0.001), with also higher relative IPH volume (20.4 ± 19.1% vs 5.7 ± 12.2%, p < 0.001). ROC curve showed that 183.45mm3 of the IPH volume was the most reliable cutoff value for predicting NIIL with a specificity of 92.3% and a positive predictive value of 86.1%. Larger IPH volume is associated with increased risk of NIIL after CAS procedure. Quantification of IPH volume may be useful for predicting cerebral ischemic events after CAS.

Study of MRI brain findings and carotid US features in systemic sclerosis patients, relationship with disease parameters

Background/objectivesSystemic sclerosis (SSc) is an autoimmune disease associated with immune abnormalities and widespread vascular lesions, including increased intimal and medial thickness. These changes may be reflected in early atherosclerosis and cardiovascular risks. We aimed in this study to examine the carotid artery intima-media thickness and MRI brain findings in SSc patients and compared them to a group of normal controls. A relationship between these parameters and clinical measures in SSc was also sought.MethodsSeventy-two SSc patients with no central nervous system (CNS) symptoms and 42 healthy controls were included. Clinical and laboratory measures, Medsger’s severity scale, and Doppler ultrasound common carotid artery intima-media thickness (CCA-IMT) were measured. Brain fluid-attenuated inversion recovery (FLAIR)-MRI and diffusion-weighted MRI (DWI) were also done.ResultsSSc patients had more CCA-IMT, higher CRP, and more brain MRI hyperintense lesions than controls (P < 0.05). Significant positive correlations existed between CCA-IMT and Medsger vascular (r = 0.7, P = 0.02). The FLAIR-MRI showed multiple hyperintense lesions in 24 patients (33%), ranging 0–36 lesions. SSc patients with more lesions (positive MRI) had longer disease duration (P = 0.001) and left and right carotid artery atheromata (P = 0.001, and 0.013, respectively) than SSc patients with negative MRIs; Medsger vascular score did not separate the SSc groups (P = 0.08).ConclusionsIn systemic sclerosis patients without central nervous system symptoms, MRI lesion numbers correlated with CCA-IMT. MRI abnormalities were found more frequently if CRP was elevated, if the Medsger SSc Severity Scale was increased, or if there was thickened carotid IMT.

Abstract WP248: Cortical Microinfarcts on 3T MRI in Patients With Carotid Artery Stenosis

Background and Purpose: There is still uncertainty about the underlying mechanism of cortical microinfarcts in patients with carotid artery stenosis. We assessed the association between cortical microinfarcts (CMIs) on 3T MRI and imaging features of carotid and brain MRI. Methods: Eighty-nine patients with &gt;50% carotid artery stenosis on carotid ultrasound were prospectively included, and underwent both carotid and brain MRI. CMIs were rated according to pre-determined criteria based on double inversion recovery and 3D FLAIR images. Results: We identified 69 CMIs in 26 (29%) patients. Multivariate-adjusted models showed CMIs were associated with intraplaque hemorrhage, and cortical infarct but not with severe stenosis (&gt;70%) or markers of small vessel disease (SVD) such as white matter hyperintensities and cerebral microbleeds. Among 81 patients with unilateral carotid artery stenosis, 18 patients (22%) had 52 CMIs in ipsilateral hemisphere, while 6 patients (6%) had 9 CMIs in contralateral hemisphere. The number of CMIs were significantly higher in the ipsilateral side than in the contralateral side ( P = 0.005). Conclusions: CMIs were associated with intraplaque hemorrhage, cortical infarct, and carotid artery stenosis. These findings suggest artery-to-artery emboli might be the underlying cause of CMIs in patients with carotid artery stenosis.

Abstract TMP115: Carotid Atherosclerosis Progression and Hippocampal Volume

Background: Carotid atherosclerosis is a known risk factor for stroke and dementia. Carotid atherosclerosis may play a role in neurodegeneration and be a potential target for treatment and preventive efforts for stroke and dementia in asymptomatic individuals. We studied the association of carotid intima media thickness (CIMT) with hippocampal volume (HV) in community-dwelling individuals, and hypothesize that persons with carotid atherosclerosis progression would have a lower HV. Methods: We studied 1,376 Framingham Offspring participants (age 67±8.7 years; 53% women) with two carotid ultrasound measurements (1995-1998 and 2005-2008) and brain MRI scans at or near the second ultrasound, who were stroke, dementia, or other neurological illnesses-free at MRI. We used multivariable linear regression analyses to relate annualized carotid IMT change at internal [ICA] and common carotid [CCA] to HV volume (as a percentage of total cranial volume). Models were adjusted for age, sex, time interval between second carotid duplex and MRI, systolic blood pressure, hypertension treatment (HRx), diabetes, total cholesterol level, smoking, cardiovascular disease and baseline CIMT. We additionally assessed effect modification by HRx and statin use. Results: Mean (±SD) carotid IMT change per year was 0.064±0.082mm in ICA and 0.008±0.008 mm in CCA. Participants with higher ICA IMT progression had significantly lower HV after adjustment for vascular risk factors and baseline IMT (β±SE [standardized beta±standard error]: -0.067±0.027, p= 0.01), but not CCA IMT progression (β±SE: 0.01± 0.0276 p= 0.72). In subgroup analyses, we observed weaker association between ICA IMT change and HV among subjects with HRx (β = -0.047, p=0.19 vs. β =-0.096, p=0.026 in untreated individuals), but HRx by IMT change interaction was not statistically significant (p-interaction=0.39). Effects were similar in statin subgroups and statistically non-significant for CCA IMT progression. Conclusions: Cumulative vascular risk factor exposure, as reflected by ICA IMT progression, are associated with neurodegeneration represented by lower hippocampal volumes. Such changes occur prior to onset of clinical dementia, suggesting that carotid IMT may be a target for preventive efforts.

Abstract TP241: Correlation of Mri Cerebral Perfusion Parameters and Carotid Plaque Characteristics

Purpose: Recent evidence suggests that MRI-detected intraplaque hemorrhage (IPH) improves stroke prediction in all carotid stenosis categories, placing the role of stenosis and impaired perfusion in question. The goal of this study was to determine if carotid stenosis or IPH are associated with baseline perfusion impairment measured by dynamic susceptibility contrast (DSC) and cellular diffusion and perfusion measured by intravoxel incoherent motion (IVIM). Method and Materials: After IRB approval and informed consent, we recruited 25 patients with &gt;=50% stenosis in at least one carotid. Carotid MRI and brain IVIM and DSC were performed at 3T. IVIM was acquired with b-values of 20, 40, 50, 100, 250, 500, and 2000. Post-processing was performed (IVIM with Osirix, and DSC with Olea Sphere). Bilateral regions of interest were drawn in the centrum semiovale with the following measurements obtained for IVIM: percent perfusion fraction (f), tissue diffusion (D), pseudodiffusion (D*) and blood flow related parameter (fD*). DSC parameters included cerebral blood flow (CBF), blood volume (corrected CBV), mean transit time (MTT), and time to peak (TTP). Generalized estimating equations (GEE) and multivariable linear regression was performed accounting for two carotid arteries per patient, to determine the association of each IVIM and DSC perfusion parameter with carotid imaging factors including stenosis, occlusion, near-occlusion, and IPH. Results: Near-occlusion was rare (2/50 carotids) but was the only factor associated with DSC parameters (CBF: coefficient=-9.7, p=0.016, corrected CBV: coefficient=-0.36,p=0.042, MTT: coefficient=1.1,p=0.010, and TTP: coefficient=2.2,p=0.008). Near occlusion was also the only factor associated with the IVIM parameters f (coefficient=1.7, p=0.057) and fD* (coefficient=44, p=0.045). Carotid IPH was the only factor associated with D (coefficient=45, p=0.002). None of the factors were significantly associated with D*. Conclusion: These results suggest that carotid stenosis does not result in decreased baseline cerebral perfusion except in the rare setting of near-occlusion. While these patients may benefit from flow restoration, most patients may primarily benefit from embolic protection.

Aortic pulse wave velocity in children with Cushing syndrome: A window into a marker of early cardiovascular disease.

SummaryObjectiveTo investigate early signs of cardiovascular arterial remodelling in paediatric patients with Cushing syndrome (CS) in comparison with normative values from healthy children.Study DesignThe metrics used to assess cardiac health were from thoracic aorta and carotid MRI. Scans were performed on 18 children with CS (mean: 12.5 ± 3.1 years, range: 6.0‐16.8 years, 10 female). Pulse wave velocity (PWV), aortic distensibility (AD) and carotid intima‐media thickness (cIMT), well‐validated measurements of cardiac compromise, were measured from the images and compared to normative age‐matched values where available.ResultsPatients with CS had significantly higher PWV compared to age‐adjusted normal median control values (4.0 ± 0.7 m/s vs. 3.4 ± 0.2 m/s, respectively, P = 0.0115). PWV was positively correlated with midnight plasma cortisol (r = 0.56, P = 0.02). Internal and common cIMT were negatively correlated with ascending AD (r = −0.75, P = 0.0022, r = −0.69, P = 0.0068, respectively).ConclusionPulse wave velocity data indicate that paediatric patients with CS have early evidence of cardiovascular remodelling. The results suggest the opportunity for monitoring as these changes begin in childhood.

Abstract 17357: Magnetic Resonance Imaging Detected Intraplaque Hemorrhage and Expansive Remodeling in Superficial Femoral Artery

Introduction: Compared to coronary and carotid arteries, there is much less knowledge on atherosclerotic plaque characteristics and their clinical relevance in lower-extremity arteries. Magnetic resonance (MR) vessel wall imaging allows for in vivo detection of intraplaque hemorrhage (IPH), which has been consistently associated with increased risks for clinical events in coronary and carotid artery disease. Objective: In a pilot study, we sought to estimate the prevalence of IPH in peripheral artery disease and examine plaque progression in the presence of IPH. Methods: Ten patients with ankle brachial index &lt;0.90 in one or both legs were recruited. A 3D MR imaging protocol with a large coverage (30 or 45 cm in the head-feet direction) and isotropic resolution (voxel size: 0.8x0.8x0.8 mm 3 ) was used to scan bilateral legs in the coronal plane from the common femoral artery bifurcation to the popliteal artery at baseline and 6 months later. Images were reformatted into axial slices for detailed visualization of vessel wall. Following previous publications on carotid MRI, IPH was detected as hyperintense signals on heavily T1-weighted images. Superficial femoral artery (SFA) segments (3 cm in length) with IPH were identified, of which lumen and outer wall were segmented on black-blood images (motion-sensitized flow suppression for improved vessel wall delineation) to measure plaque progression and remodeling. Image analysis was performed in a blinded fashion without knowing time relationship between serial images. Results: Twenty SFAs were analyzed. After excluding 4 arteries with total occlusion, 5 out of the 16 arteries (31%) or 50% of the subjects showed IPH in 1 or more SFA segments. After 6 months, there was significant progression in vessel wall area in SFA segments with IPH (mean ± standard deviation: 43.5 ± 13.9 mm 2 versus 47.3 ± 17.3 mm 2 , p=0.045), which resulted in outer wall expansion (mean [95% confidence intervals]: +3.9 mm 2 [+0.4, +7.4], p=0.035) rather than lumen reduction (-0.02 mm 2 [-2.6, +2.5], p=0.99). Conclusions: MR vessel wall imaging revealed that IPH is likely a common feature in femoral atherosclerosis. SFA segments with IPH showed expansive remodeling in 6 months, of which the clinical significance needs to be further studied.

Management of velopharyngeal dysfunction in patients with 22q11.2 deletion syndrome: A survey of practice patterns

ObjectiveTo determine demographics and practice patterns of surgeons treating velopharyngeal dysfunction (VPD) in patients with 22q11.2 deletion syndrome (22q11.2DS). MethodsAn anonymous electronic survey study was administered to the surgical membership of the American Cleft Palate-Craniofacial Association and the Society for Ear Nose and Throat Advances in Children. The survey queried surgeon demographics and differences in management practices for submucous cleft palate (SMCP), pharyngoplasty algorithms, and self-reported complications for nonsyndromic versus 22q11.2DS patients. Results126 surveys were returned from 9 international regions with the majority from the United States (73%), followed by Western Europe (9.5%) and Canada (7.9%). Plastic surgery was the most common specialty (61.9%), followed by otolaryngology (27.8%). 88.1% reported fellowship training, and 33% completed multiple fellowships. Prior to proceeding with pharyngoplasty in 22q11.2DS patients, surgeons required the following assessments: speech evaluation (79.4%), velopharyngeal imaging (51.6%), cardiac evaluation (50.0%), carotid artery MRI (29.4%), and cervical spine x-rays (11.1%). Nasoendoscopy was the most common modality used for imaging the velopharynx. Overall, providers managed patients with 22q11.2DS similarly to nonsyndromic patients, with several significant exceptions including that they were more likely to perform SMCP repair alone as a first approach in nonsyndromic patients (p = 0.031) and posterior pharyngeal flap without SMCP repair in those with 22q11.2DS (p = 0.017). ConclusionsPractice patterns for the management of VPD in patients with 22q11.2DS vary across providers. Further collaborative studies are needed to develop optimal treatment paradigms for VPD in patients with 22q11.2 DS.

T2 mapping MRI technique quantifies carotid plaque lipid, and its depletion after statin initiation, following acute myocardial infarction

Background & aimsA recently-validated, highly-sensitive T2 mapping magnetic resonance (MRI) technique accurately quantifies carotid plaque lipid. The aims of this study were to determine: (i) the extent of carotid plaque lipid in patients with acute coronary syndromes (ACS); (ii) the effects of initiation of high-intensity statin on plaque lipid content and (iii) whether plaque lipid content is related to standard or ‘functional’ blood lipid measurements. MethodsStatin naïve subjects presenting with ACS underwent carotid artery MRI at 3 T scanner to quantify plaque lipid. Patients were subsequently commenced on high dose statin as part of clinical care and underwent a second MRI after three months. Plaque composition was measured using objective semi-automated techniques. Results23 out of 24 patients had measurable lipid. Three months after statin initiation there was a significant reduction in carotid lipid percentage [from 10.3% (7.2–14.2) to 7.4% (5.4–10.0), p = 0.002] and a significant increase in fibrous percentage [from 83.3% ± 6.6–85.5% ± 4.8, p = 0.039]. None of the studied functional blood biomarkers were related to either baseline carotid plaque lipid content or its propensity to change with statin treatment. ConclusionsT2-mapping demonstrated depleted carotid plaque lipid following the initiation of high-intensity statin treatment. Standard or ‘functional’ blood biomarkers were dissociated from plaque lipid content or changes with treatment. These findings further reinforce the importance of disease characterisation over risk factor assessment. Subject to clinical trial findings, quantification of plaque lipid may provide the basis for an approach to identify patients suitable for intensive lipid reduction regimes.