Show Notes
CORE RESOURCES: Rutherford's Vascular and Endovascular Therapy 10th Edition, Chapters 88, 89, 91, and 94
Atlas of Vascular Surgery and Endovascular Therapy 2nd Edition, Chapter 9
ADDITIONAL RESOURCES: Audible Bleeding Episodes Holding Pressure - Carotid Endarterectomy: https://www.audiblebleeding.com/2024/02/27/holding-pressure-carotid-endarterectomy/
Holding Pressure Case Prep - Endovascular Basics: https://www.audiblebleeding.com/2023/04/23/holding-pressure-case-prep-endovascular-basics/
Videos TCAR Technical Video: https://jnis.bmj.com/content/14/8/842
Articles Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovascular disease: https://www.jvascsurg.org/article/S0741-5214%2821%2900893-4/fulltext
Technical aspects of transcarotid artery revascularization using the ENROUTE transcarotid neuroprotection and stent system: https://www.jvascsurg.org/action/showPdf?pii=S0741-5214%2816%2931862-6
Referenced Studies ROADSTER-1
https://pubmed.ncbi.nlm.nih.gov/30611582/
ROADSTER-2
https://pubmed.ncbi.nlm.nih.gov/32811386/
https://pubmed.ncbi.nlm.nih.gov/35381327/
TCAR Surveillance Project
https://pubmed.ncbi.nlm.nih.gov/36172943/
OUTLINE:
CAROTID ARTERY DISEASE 1. Pathophysiology/etiology Carotid artery disease is primarily driven by atherosclerotic plaque deposition.
Risk factors: hypertension, hyperlipidemia, diabetes, smoking, and advanced age.
Nonatherosclerotic etiologies: fibromuscular dysplasia, carotid dissection, vasculitic disease, carotid webs, and trauma.
When the endothelium is damaged, monocytes migrate to the site and differentiate into macrophages that take up oxidized LDL particles to become foam cells. Meanwhile, an inflammatory response occurs where activated platelets release thromboxane A2, platelet derived growth factor, and inflammatory cytokines that promote further platelet aggregation and vascular inflammation. Smooth muscle cells migrate and proliferate, forming the structural framework of the atheroma.
Within the lesion, necrotic debris and lipid accumulate, creating a vulnerable plaque. Plaque rupture exposes this material to the bloodstream, serving as a nidus for thrombus formation which can lead to ischemic events.
Carotid bifurcation is particularly prone to plaque formation due to turbulent blood flow. Embolization of plaque from this area can result in TIA or ischemic stroke.
2. Presentation Patients are often asymptomatic and stenosis is incidentally found on imaging.
Symptomatic patients present with neurologic symptoms including unilateral motor and sensory loss, aphasia (difficulty finding words), dysarthria (difficulty speaking), amaurosis fugax (temporary monocular vision loss due to embolus to the ophthalmic artery), transient ischemic attacks
Physical exam findings may be notable for auscultation of a carotid bruit. Patients may also have evidence of retinal artery embolization on fundoscopic examination (Hollenhorst plaque) or asymptomatic cerebral infarction.
3. Diagnosis USPTF recommends against screening for asymptomatic carotid artery stenosis.
In patients with no risk factors, SVS recommends against screening for asymptomatic carotid artery stenosis. However, they do recommend screening for asymptomatic clinically significant carotid bifurcation in certain groups of patients with multiple risk factors.
These risk factors include patients with clinically significant peripheral vascular disease, patients 65 and older with history of CAD, smoking, hypercholesterolemia, and patients prior to coronary artery bypass.
Relevant findings on physical exam or imaging findings may warrant screening, but screening is not recommended for the presence of neck bruit alone without other risk factors, as this finding has a low sensitivity and specificity for detecting clinically significa
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