Carotid Artery Disease After Stroke (CADAS). (CADAS)
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|ClinicalTrials.gov Identifier: NCT03721523|
Recruitment Status : Not yet recruiting
First Posted : October 26, 2018
Last Update Posted : October 30, 2018
Stroke is a significant medical problem with 150,000 events occurring per year in the UK and incurring healthcare costs of £4 billion per year. Fifty percent of strokes will leave a lasting disability on first manifestation and 10-15% (roughly 16,500 per year) are unheralded ischaemic events in previously asymptomatic Carotid artery disease.
Carotid Artery Disease is caused by the formation of an atherosclerotic plaque in the vessel. Stroke or TIA occurs when plaque or adherent thrombus breaks off and embolises to the brain, blocking off its blood supply. Hence, a carotid plaque is said to be symptomatic if it has caused a Stroke or TIA in the territory of the brain supplied by that vessel in the previous six months.
Currently, the degree of stenosis (narrowing) of the artery by doppler ultrasound is the main assessment performed. Doppler ultrasound measures stenosis and elevation of blood flow velocity in the artery prior to surgical intervention. However, it has been shown that the degree of stenosis is a poor predictor of stroke as many asymptomatic patients have severe stenosis and many symptomatic patients have moderate stenosis. Stenosis is a two dimensional assessment of a 3-D structure.
Other features of the plaque should be considered including the volume of the carotid plaque and its constituents. Carotid Plaque Volume has been measured in 339 individuals, with plaque volume being higher in symptomatic than asymptomatic individuals. In this study, plaque volume did not correlate with stenosis degree. No studies have been conducted measuring the change in carotid plaque volume and morphology following a stroke. This pilot study will perform serial duplex scans on recently symptomatic individuals over a 12 week period and observe the changes in Plaque Volume and morphology. This will attempt to prove that carotid plaque volume is a better predictor of stroke than stenosis. The investigators will also aim to identify other plaque features that may have an important role in predicting stroke risk. Documenting the timescale of change in plaque volume will aid us in defining appropriate timescales for treating the symptomatic population and when those having medical management's risk has returned to baseline. Observing the change in plaque immediately after stroke will improve our knowledge of the changes in plaques that lead to symptoms and may in the future help us predict which patients with asymptomatic carotid stenosis need operation.
|Condition or disease||Intervention/treatment|
|Carotid Artery Diseases Stroke Transient Ischemic Attack||Diagnostic Test: 3 Dimensional tomographic Ultrasound Diagnostic Test: Platelet Aggregometry|
Show Detailed Description
|Study Type :||Observational|
|Estimated Enrollment :||15 participants|
|Official Title:||Observational Cohort Study of Changes in Carotid Plaque Volume After Stroke.|
|Estimated Study Start Date :||November 1, 2018|
|Estimated Primary Completion Date :||November 1, 2020|
|Estimated Study Completion Date :||November 1, 2021|
- Diagnostic Test: 3 Dimensional tomographic Ultrasound
3-D tUS at five timepoints following acute ipsilateral stroke or Transient Ischaemic attack (TIA) to document carotid plaque volume and presence or absence of adverse plaque features.
- Diagnostic Test: Platelet Aggregometry
Blood test to test for platelet resistance to aspirin or clopidogrel and to measure effect of acute inflammatory response post event.
- Changes in Carotid Plaque Volume using 3-D tomographic Ultrasound over time following acute cerebral event. [ Time Frame: Measured at 5 separate timepoints up to 12 weeks following acute cerebral event. ]Measured by 3-D tUS with contrast administration
- Identify adverse morphological features within the carotid plaque by 3-D tomographic Ultrasound. [ Time Frame: At five timepoints over 12 weeks. ]Duplex ultrasound to identify intraplaque haemorrhage, fibrous cap thickness, ulceration, juxtaluminal black area.
- Assess the acute inflammatory response to stroke on platelet aggregation and resistance to antiplatelet agents. [ Time Frame: Twice during study period ]Platelet aggregometry blood test.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03721523
|Contact: Alison S Phair, MBBS||07793004089 ext email@example.com|
|Contact: Charles McCollum, Prof.||firstname.lastname@example.org|
|Manchester Foundation Trust, Wythenshawe site.||Not yet recruiting|
|Manchester, United Kingdom|
|Contact: Alison Phair, MBBS 07793004089 ext 07793004089 email@example.com|
|Principal Investigator: Charles McCollum, Professor of Surgery|