Study to Investigate the Sensitivity and Specificity of 3.0 Tesla MRI for Carotid Artery Plaque
The aim of this study is to develop non-invasive MRI, and MRS approaches that will quantify the plaque composition and lipid content of plaques and will have the potential for repeated in vivo measurements. To investigate sensitivity and specificity of 3.0 Tesla MRI and MRS for dimension and composition assessment of carotid artery plaques, in particularly those plaques with lipid rich necrotic cores. This non-invasive cross-sectional study, compares carotid parameters of in-vivo 3.0 Tesla MRI, MRS and B-mode ultrasound with histology specimens collected at endarterectomy.
|Study Design:||Time Perspective: Cross-Sectional|
|Official Title:||Study to Investigate the Sensitivity and Specificity of 3.0 Tesla MRI, MRS and Ultrasound Imaging for Carotid Artery Plaque Dimension and Composition Assessment|
- Plaque characteristics as assessed by 3.0 Tesla MRI. [ Time Frame: 1 month ] [ Designated as safety issue: No ]Total plaque volume, plaque calcification volume, plaque haemorrhage volume, lipid rich necrotic core volume, fibrous cap thickness, as assessed by 3.0 Tesla MRI
- Water and lipid content of the plaque as assessed by MRS/3.0T MRI [ Time Frame: 1 month ] [ Designated as safety issue: No ]The ratio of the integrated lipid peak versus the unsuppressed water peak (expressed as a percentage), as assessed by MRS.
- Plaque composition and size as assessed by histological analysis [ Time Frame: 1 month ] [ Designated as safety issue: No ]Plaque size, morphology and phenotype (presence of collagen, smooth muscle cells, calcifications, macrophages, thrombus and fat), as assessed by histology analysis.
|Study Start Date:||July 2009|
|Estimated Study Completion Date:||June 2015|
|Estimated Primary Completion Date:||June 2015 (Final data collection date for primary outcome measure)|
|Patients with ≥70% carotid artery stenosis|
Atherosclerosis is a protracted and in fact lifelong progressive disease. Over time, lipids accumulate in the artery wall forming fatty streaks, which eventually can develop into atherosclerotic plaques (1). The later stages of the process, from quiescent atherosclerotic plaque to an active plaque, have a high risk of triggering acute vascular events, such as myocardial infarction and stroke (1).
Much effort has been put in the development of novel drugs aimed to prevent cardiovascular disease. Low Density Lipoprotein cholesterol (LDL-C) lowering drugs, in particularly statins, play a pivotal role. The hypothesis that serum lipid lowering results in decrease of lipid accumulation in the arterial wall and thus atherogenesis, has formed the basis for successful drug developing strategies (1;2).
To draw valid conclusions on determinants of disease and effectiveness of lipid modifying therapeutic intervention, imaging of atherosclerosis can be used as a validated tool to assess efficacy of novel compounds (3;4).
Although imaging arterial wall dimensions by B-mode ultrasound and intra-vascular ultrasound have proven their value, longitudinal data of the effects of cardiovascular drugs on arterial wall and plaque composition, in particular of vulnerable plaques with lipid rich necrotic cores (LRNC), are scarce.
Magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) are non-invasive imaging modalities that can potentially image plaque composition in-vivo in human carotid arteries. MRI image acquisition at various weightings enables visualisation of plaque composition. Calcification, haemorrhage, fibrous cap and lipid rich necrotic cores can readily be distinguished, providing information on plaque vulnerability. MRS gives a spectrum of resonances, affording detection of specific chemical components through their inherent frequency shift relative to water (5). In image guided MRS, an MR image can be utilized to image and localize a plaque. Proton spectra can then be collected from these plaques, such that the specific proton resonances of lipid components in a mobile state, including cholesterol ester (CE), can be identified (6).
Please refer to this study by its ClinicalTrials.gov identifier: NCT01632254
|Contact: Erik Stroes, MD PhDemail@example.com|
|Contact: Diederik van Wijk, MD||+31205662377||D.F.vanWijk@amc.nl|
|Academic Medical Center||Recruiting|
|Amsterdam, Netherlands, 1105AZ|
|Contact: Erik Stroes, MD PhD +31205666612 firstname.lastname@example.org|
|Contact: Diederik van Wijk, MD +31205662377 D.F.vanWijk@amc.nl|
|Principal Investigator: Erik Stroes, MD PhD|