Relation of Carotid Artery Plaque Inflammation, Covert Stroke and White Matter Disease

This study is currently recruiting participants. (see Contacts and Locations)
Verified March 2014 by University of Ottawa Heart Institute
Sponsor:
Collaborator:
The Ottawa Hospital
Information provided by (Responsible Party):
Terrence Ruddy, University of Ottawa Heart Institute
ClinicalTrials.gov Identifier:
NCT01236508
First received: November 5, 2010
Last updated: March 14, 2014
Last verified: March 2014

November 5, 2010
March 14, 2014
November 2010
November 2014   (final data collection date for primary outcome measure)
Plaque Inflammation [ Time Frame: 30 days ] [ Designated as safety issue: No ]
The extent to which plaque inflammation, as measured by the extent of FDG uptake, contributes to the number of covert infarcts and the magnitude of white matter hyperintensity.
Same as current
Complete list of historical versions of study NCT01236508 on ClinicalTrials.gov Archive Site
Not Provided
Not Provided
Not Provided
Not Provided
 
Relation of Carotid Artery Plaque Inflammation, Covert Stroke and White Matter Disease
Relation of Carotid Artery Plaque Inflammation, Covert Stroke and White Matter Disease

The investigators hypothesize that inflammation in carotid plaque is predictive of the extent of ischemic lesion burden on the brain and will add to risk stratification for individuals with carotid disease.

Objectives:

  1. To investigate the relationship of carotid inflammation, as measured by FDG positron emission tomography (PET) to standardized uptake value in atherosclerotic plaque, with the number of covert brain infarcts.
  2. To investigate the relationship of FDG PET standardized uptake value with the relative volume of white matter hyperintensity.
  3. To correlate vascular inflammation in the entire aorta and aortoiliac vessels to carotid inflammation and cerebral infarcts and white matter disease.
Interventional
Phase 4
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Screening
  • TIA
  • Stroke
  • Carotid Artery Stenosis
Radiation: PET/CT imaging with F-18 fluorodeoxyglucose
Dose of 5 MBq/kg F-18-FDG given to fasting participant. Nuclear whole body imaging starting at 3 hours post-injection. The relation of the PET/CT image results and both the number of covert brain infarcts and the extent of white matter MRI hyperintensity will be investigated.
Experimental: Nuclear imaging
PET/CT imaging with F-18 fluorodeoxyglucose
Intervention: Radiation: PET/CT imaging with F-18 fluorodeoxyglucose
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
50
February 2015
November 2014   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Age 60 or greater at time of enrollment
  • Written informed consent from patient or legal representative
  • Diagnosis of stroke or TIA made by a stroke specialist within 90 days and fulfilling the following criteria:
  • A TIA must involve a focal speech/language, motor or visual deficit (transient monocular blindness, amaurosis fugax) referable to the distribution of a carotid artery and lasting less than 24 hours.
  • A stroke consisting of deficits as noted above with duration greater than 24 hours and/or confirmed on cerebral imaging. Post event Modified Rankin Score of 2 or less.
  • Stroke meets the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria for large artery atherosclerosis
  • Carotid Doppler, CTA or MRA confirming the presence of bilateral atherosclerotic disease resulting in carotid stenosis of any degree. Stenosis will be measured following the method used in NASCET for CTA and MRA. Carotid Doppler measurements will follow the criteria defined by the Society for Ultrasound consensus conference.
  • 12 lead ECG or Holter monitor confirming the absence of atrial fibrillation.

Exclusion Criteria:

  • TIA or stroke in the vertebrobasilar system
  • Index event was primary hemorrhage
  • History of intermittent atrial fibrillation
  • Cardiac source of embolus suspected as cause of index event (artificial valve, segmental or global LV dysfunction, congenital cardiac defect)
  • Diagnosis of vasculitis, dissection, or non-atherosclerotic carotid disease (Ehlers-Danlos, Marfans)
  • Sinovenous thrombosis, endocarditis or hypercoagulable state
  • Pacemaker, ICD or other contraindications to MRI
  • Diminished Kidney Function
  • Contraindication to radiation exposure (eg: pregnancy)
  • Severe Claustrophobia
Both
60 Years and older
No
Contact: Marlie A. Poirier, BScN, CCRP 613-761-5103 mpoirier@ottawaheart.ca
Canada
 
NCT01236508
20100606-01H
No
Terrence Ruddy, University of Ottawa Heart Institute
University of Ottawa Heart Institute
The Ottawa Hospital
Principal Investigator: Terrence Ruddy, MD The Ottawa Hospital
University of Ottawa Heart Institute
March 2014

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP