Structural Stability of Carotid Plaque and Symptomatology

NCT ID: NCT02476396

Last Updated: 2024-08-16

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

176 participants

Study Classification

OBSERVATIONAL

Study Start Date

2015-11-09

Study Completion Date

2024-07-14

Brief Summary

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The purpose of the research is to understand structural plaque abnormalities that make a carotid plaque unstable and brake off (embolize) which would help to predict and treat individuals who are likely to suffer not only classic episodic major strokes but also cognitive impairment.

Detailed Description

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This study examines the relationship between the structural stability of carotid atherosclerotic plaque forming at the bifurcation of the common internal/external carotids and the ability of such lesions to cause disease. The theory behind this work is the hypothesis that carotid atherosclerotic stroke presents not only as a classical episodic clinical condition, but may also involve elements of a continuous process involving large and small vessel circulations, microcirculatory changes, cellular metabolic resistance to ischemia and micro embolic events. Recent studies suggest for every recognized clinical stroke, 5 silent strokes take place.

The patient implications are enormous as imaging suggests 11 million "silent strokes" occur yearly in the US with poor understanding of the pathophysiology or cognitive consequences for our patients. Within this framework, the investigators choose to study the hypothesis that carotid artery atherosclerosis is likely to cause microemboli, as well as classic macroemboli, which may result in more subtle disturbances than those ordinarily detected by more obvious clinical events such as stroke and transient ischemia attacks.

Understanding the structural plaque abnormalities that render a carotid plaque unstable and at risk of embolization would help to predict and treat individuals who are likely to suffer not only classic episodic major strokes, but also cognitive impairment from the contribution of microemboli to this overall disease process. The investigators have previously described a non-invasive ultrasound-based measure of plaque structural stability which will be further studied in this proposal. This study will expand on previous work performed at the University of Wisconsin-Madison, and will include patients with carotid artery stenosis, both with and without classic stroke symptoms, as well as a control group of patients without known atherosclerotic disease. Current treatments for carotid artery stenosis include either carotid endarterectomy to remove plaque or carotid stenting using a expandable metal coil to prevent the artery from narrowing.

In the previous version of this protocol, the investigators have enrolled 95 -subjects (75 patient-subjects and 20 control-subjects) with no safety concerns. Findings include new understanding of the relatively of atherosclerosis and cognition as well as the basic pathophysiology of atherosclerotic large to small vessel disease.

The study will run for 5 years from IRB approval with potential to further expand it. All patient-subjects will have a baseline and 1-year follow-up, ultrasound, TCD, blood collection and cognitive study to see if endarterectomy or stenting (endovascular) affected pre-op change. Change in cognition will be compared to report studies in the normal control group. In past, carotid patients have been recruited at a greater pace. Given the complexity of these studies the investigators anticipate recruitment and complete analysis of 20 patients/year. During this time initial psychological testing will be done pre-operatively. During the final year of the study, the data analysis of the plaque ultrasounds, and histopathology and 1-year follow-up the patient received in the last year of recruitment will take place. The investigators can recruit additional patients to fill any missing data points if these results identify a subset of classically asymptomatic patients with significant carotid plaques and microemboli causing vascular cognitive decline.

* Specific Aim 1: Atherosclerosis, plaque elasticity, strain defects and histopathology of plaque. This aim will study the relationship of structural instability in the carotid plaques with histopathologic evidence for fissuring of the plaques that may represent a micro-emboli source. The determination of a structural defect causing abnormal strain measurements in a carotid atherosclerotic plaque will be important in understanding the pathophysiology of this disorder, as well as, addressing future treatment strategies, which could include preventing angiogenesis, thrombosis, or abnormal cholesterol deposit within the plaque.
* Specific Aim 2: Plaque strain deficits and microemboli. In this aim, the investigators will preoperatively measure the structural stability of each plaque ultrasonically while simultaneously recording distally for the presence of microemboli over time within the carotid system. Statistical analysis will establish the structural instability signature that predicts ongoing subclinical microemboli.
* Specific Aim 3: Plaque strain deficits, microemboli, and cognition. This aim will analyze increased elasticity strain within carotid plaques as measured preoperatively with ultrasound and correlate these parameters with cognition
* Specific Aim 4: Blood RNA expression profiles can be used as biomarkers to identify the patients with a higher risk of plaque instability. This aim will analyze the mRNA and microRNA expression profiles of the blood and the excised plaque samples from patients with stable and ruptured carotid atherosclerotic plaques. The RNA analysis will be conducted with the microarrays.

Conditions

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Carotid Stenosis Stroke Carotid Artery Plaque Transient Ischemic Attack Cerebrovascular Accident Carotid Artery Stenosis

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

PROSPECTIVE

Study Groups

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patient-subject

Patients will be recruited from the population of patients scheduled to undergo carotid endarterectomy or stenting (endovascular) for established clinical indications. These indications include patients scheduled to have a carotid endarterectomy or stenting due to the presence of a high-grade atherosclerotic cervical internal carotid artery stenosis with or without clinical symptoms, following the ACAS or NASCET criteria (carotid artery stenosis of 60% or greater without clinical symptoms; stenosis 70% or greater with clinical symptoms).

Carotid Endarterectomy or Stenting

Intervention Type PROCEDURE

Carotid endarterectomy is a procedure to treat carotid artery disease. This disease occurs when fatty, waxy deposits build up in one of the carotid arteries. The carotid arteries are blood vessels located on each side of your neck (carotid arteries).

This buildup of plaques (atherosclerosis) may restrict blood flow to your brain. Removing plaques causing the narrowing in the artery can improve blood flow in your carotid artery and reduce your risk of stroke.

In carotid endarterectomy, you an anesthetic. Your surgeon makes an incision along the front of your neck, opens your carotid artery and removes the plaques that are clogging your artery. Your surgeon then repairs the artery with stitches or a patch made with a vein or artificial material (patch graft).

Source: Mayo Clinic

Carotid stenting uses a expandable metal coil to prevent the artery from narrowing.

patient-control

The controls will be recruited by the patient-subjects. The investigators will ask their patient-subjects to speak to a spouse or family member to see if they are interested in participating. If they do have an interest they will contact the research team/study coordinator(s). In case, a spouse or a family member is accompanying the patient-subject, they will be recruited at the same time as the patient-subject.

No interventions assigned to this group

Interventions

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Carotid Endarterectomy or Stenting

Carotid endarterectomy is a procedure to treat carotid artery disease. This disease occurs when fatty, waxy deposits build up in one of the carotid arteries. The carotid arteries are blood vessels located on each side of your neck (carotid arteries).

This buildup of plaques (atherosclerosis) may restrict blood flow to your brain. Removing plaques causing the narrowing in the artery can improve blood flow in your carotid artery and reduce your risk of stroke.

In carotid endarterectomy, you an anesthetic. Your surgeon makes an incision along the front of your neck, opens your carotid artery and removes the plaques that are clogging your artery. Your surgeon then repairs the artery with stitches or a patch made with a vein or artificial material (patch graft).

Source: Mayo Clinic

Carotid stenting uses a expandable metal coil to prevent the artery from narrowing.

Intervention Type PROCEDURE

Eligibility Criteria

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Inclusion Criteria

* Patients undergoing carotid endarterectomy or stenting (endovascular) for established clinical criteria
* Age \> 18 years
* Male or Female
* English speaking
* Patients must sign written informed consent form


* A spouse or sibling of a Patient Subject
* Age \> 18 years
* Male or Female
* English speaking
* Control-Subject must sign a written informed consent form

Exclusion Criteria

* Previous history of carotid artery surgery (endovascular or open) on the same side
* Previous cervical radiation
* Patients not felt be suitable for carotid endarterectomy or stenting (endovascular)
* Patients with impaired consent capacity
* Contraindication to MRI scans (impaired renal function, need for sedative medication during scans, inability to lie in scanner for 60 minutes)
* Prisoner status


* Control-Subjects with impaired consent capacity
* Prisoner status
* Previous history of Stroke or TIAs
* Previous history of carotid artery surgery (endovascular or open)
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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National Heart, Lung, and Blood Institute (NHLBI)

NIH

Sponsor Role collaborator

National Institute of Neurological Disorders and Stroke (NINDS)

NIH

Sponsor Role collaborator

University of Wisconsin, Madison

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Robert J Dempsey, MD

Role: PRINCIPAL_INVESTIGATOR

University of Wisconsin, Madison

Locations

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University of Wisconsin-Madison

Madison, Wisconsin, United States

Site Status

Countries

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United States

References

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Wang X, Jackson DC, Mitchell CC, Varghese T, Hermann BP, Kliewer MA, Dempsey RJ. Estimation of ultrasound strain indices in carotid plaque and correlation to cognitive dysfunction. Annu Int Conf IEEE Eng Med Biol Soc. 2014;2014:5627-30. doi: 10.1109/EMBC.2014.6944903.

Reference Type BACKGROUND
PMID: 25571271 (View on PubMed)

Wang X, Jackson DC, Varghese T, Mitchell CC, Hermann BP, Kliewer MA, Dempsey RJ. Correlation of cognitive function with ultrasound strain indices in carotid plaque. Ultrasound Med Biol. 2014 Jan;40(1):78-89. doi: 10.1016/j.ultrasmedbio.2013.08.001. Epub 2013 Oct 11.

Reference Type BACKGROUND
PMID: 24120415 (View on PubMed)

Wesley UV, Vemuganti R, Ayvaci ER, Dempsey RJ. Galectin-3 enhances angiogenic and migratory potential of microglial cells via modulation of integrin linked kinase signaling. Brain Res. 2013 Feb 16;1496:1-9. doi: 10.1016/j.brainres.2012.12.008. Epub 2012 Dec 14.

Reference Type BACKGROUND
PMID: 23246924 (View on PubMed)

McCormick M, Varghese T, Wang X, Mitchell C, Kliewer MA, Dempsey RJ. Methods for robust in vivo strain estimation in the carotid artery. Phys Med Biol. 2012 Nov 21;57(22):7329-53. doi: 10.1088/0031-9155/57/22/7329. Epub 2012 Oct 18.

Reference Type BACKGROUND
PMID: 23079725 (View on PubMed)

Rocque BG, Jackson D, Varghese T, Hermann B, McCormick M, Kliewer M, Mitchell C, Dempsey RJ. Impaired cognitive function in patients with atherosclerotic carotid stenosis and correlation with ultrasound strain measurements. J Neurol Sci. 2012 Nov 15;322(1-2):20-4. doi: 10.1016/j.jns.2012.05.020. Epub 2012 Jun 1.

Reference Type BACKGROUND
PMID: 22658531 (View on PubMed)

Dempsey RJ, Vemuganti R, Varghese T, Hermann BP. A review of carotid atherosclerosis and vascular cognitive decline: a new understanding of the keys to symptomology. Neurosurgery. 2010 Aug;67(2):484-93; discussion 493-4. doi: 10.1227/01.NEU.0000371730.11404.36.

Reference Type BACKGROUND
PMID: 20644437 (View on PubMed)

Shi H, Varghese T, Mitchell CC, McCormick M, Dempsey RJ, Kliewer MA. In vivo attenuation and equivalent scatterer size parameters for atherosclerotic carotid plaque: preliminary results. Ultrasonics. 2009 Dec;49(8):779-85. doi: 10.1016/j.ultras.2009.06.004. Epub 2009 Jul 3.

Reference Type BACKGROUND
PMID: 19640556 (View on PubMed)

Shi H, Varghese T, Dempsey RJ, Salamat MS, Zagzebski JA. Relationship between ultrasonic attenuation, size and axial strain parameters for ex vivo atherosclerotic carotid plaque. Ultrasound Med Biol. 2008 Oct;34(10):1666-77. doi: 10.1016/j.ultrasmedbio.2008.02.014. Epub 2008 May 19.

Reference Type BACKGROUND
PMID: 18490099 (View on PubMed)

Shi H, Tu H, Dempsey RJ, Varghese T. Ultrasonic attenuation estimation in small plaque samples using a power difference method. Ultrason Imaging. 2007 Jan;29(1):15-30. doi: 10.1177/016173460702900102.

Reference Type BACKGROUND
PMID: 17491296 (View on PubMed)

Tureyen K, Vemuganti R, Salamat MS, Dempsey RJ. Increased angiogenesis and angiogenic gene expression in carotid artery plaques from symptomatic stroke patients. Neurosurgery. 2006 May;58(5):971-7; discussion 971-7. doi: 10.1227/01.NEU.0000210246.61817.FE.

Reference Type BACKGROUND
PMID: 16639334 (View on PubMed)

Vemuganti R, Dempsey RJ. Increased expression of genes that control ionic homeostasis, second messenger signaling and metabolism in the carotid plaques from patients with symptomatic stroke. J Neurochem. 2006 Apr;97 Suppl 1:92-6. doi: 10.1111/j.1471-4159.2005.03516.x.

Reference Type BACKGROUND
PMID: 16635256 (View on PubMed)

Vemuganti R, Dempsey RJ. Carotid atherosclerotic plaques from symptomatic stroke patients share the molecular fingerprints to develop in a neoplastic fashion: a microarray analysis study. Neuroscience. 2005;131(2):359-74. doi: 10.1016/j.neuroscience.2004.08.058.

Reference Type BACKGROUND
PMID: 15708479 (View on PubMed)

Shi H, Mitchell CC, McCormick M, Kliewer MA, Dempsey RJ, Varghese T. Preliminary in vivo atherosclerotic carotid plaque characterization using the accumulated axial strain and relative lateral shift strain indices. Phys Med Biol. 2008 Nov 21;53(22):6377-94. doi: 10.1088/0031-9155/53/22/008. Epub 2008 Oct 21.

Reference Type BACKGROUND
PMID: 18941278 (View on PubMed)

Dempsey RJ, Varghese T, Jackson DC, Wang X, Meshram NH, Mitchell CC, Hermann BP, Johnson SC, Berman SE, Wilbrand SM. Carotid atherosclerotic plaque instability and cognition determined by ultrasound-measured plaque strain in asymptomatic patients with significant stenosis. J Neurosurg. 2018 Jan;128(1):111-119. doi: 10.3171/2016.10.JNS161299. Epub 2017 Mar 10.

Reference Type DERIVED
PMID: 28298048 (View on PubMed)

Mitchell CC, Stein JH, Cook TD, Salamat S, Wang X, Varghese T, Jackson DC, Sandoval Garcia C, Wilbrand SM, Dempsey RJ. Histopathologic Validation of Grayscale Carotid Plaque Characteristics Related to Plaque Vulnerability. Ultrasound Med Biol. 2017 Jan;43(1):129-137. doi: 10.1016/j.ultrasmedbio.2016.08.011. Epub 2016 Oct 5.

Reference Type DERIVED
PMID: 27720278 (View on PubMed)

Other Identifiers

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A535700

Identifier Type: OTHER

Identifier Source: secondary_id

SMPH\NEURO SURG\NEURO SURG

Identifier Type: OTHER

Identifier Source: secondary_id

1F31HL141008-01A1

Identifier Type: NIH

Identifier Source: secondary_id

View Link

1R01HL147866-01A1

Identifier Type: NIH

Identifier Source: secondary_id

View Link

R01NS064034

Identifier Type: NIH

Identifier Source: secondary_id

View Link

Protocol Version Aug 2023

Identifier Type: OTHER

Identifier Source: secondary_id

2015-0289

Identifier Type: -

Identifier Source: org_study_id

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