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://jamanetwork.com/journals/jama/fullarticle/2757579?utm_source=openevidence&utm_medium=referral 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 significant carotid artery stenosis. Carotid duplex ultrasound: first-line imaging modality for both screening and initial evaluation of stenosis, noninvasive, low-cost CTA: rapid, high-resolution, three-dimensional imaging of vascular anatomy, risk of contrast and radiation exposure MRA: high-quality, three-dimensional imaging without radiation or contrast, expensive with longer acquisition time, can overestimate stenosis in severe disease DSA/angiography: gold standard, expensive, invasive, not generally recommended for routine diagnostic evaluation or screening 4. Classification Carotid artery stenosis is classified by degree of luminal narrowing. NASCET method: standard in current practice. Compares the minimal residual lumen at the point of greatest stenosis to the diameter of the normal distal internal carotid artery. Classification of stenosis: Mild: Moderate: 50-69% narrowing Severe: ≥70% narrowing TRANSCAROTID ARTERY REVASCULARIZATION (TCAR) 5. Relevant Trials ROADSTER-1 trial: prospective, multicenter, single-arm study evaluating TCAR with dynamic flow reversal in patients at high risk for carotid endarterectomy (CEA), including both symptomatic (≥50% stenosis) and asymptomatic (≥80% stenosis) patients. 30-day stroke rate of 1.4% and a combined stroke/death/MI rate of 3.5%, with technical success in 99% of cases At 1 year, the ipsilateral stroke rate was 0.6%, indicating excellent durability in a high-risk population Limitations: highly controlled environment with a select group of experienced operators, which raised concerns about the generalizability, especially among physicians new to TCAR. Additionally, ROADSTER-1 was a single-arm study without a comparison group. ROADSTER-2: prospective, multicenter, post-approval registry format. Addressed limitations of ROADSTER-1 by enrolling a larger and more diverse group of operators, the majority of whom were TCAR-naïve. The per-protocol population had a 30-day stroke rate of 0.6% and a combined stroke/death rate of 0.6%, with technical success in 99.7% of cases. These results confirmed the low perioperative stroke and death rates seen in ROADSTER-1, even with less experienced operators. TCAR Surveillance Project: ongoing study that provides real-world, comparative data using the VQI registry. In propensity-matched analyses, TCAR had similar in-hospital stroke/death rates to CEA (1.6% vs 1.6%) and significantly lower rates than transfemoral carotid artery stenting (TF-CAS, 2.9%). TCAR was also associated with significantly lower cranial nerve injury and myocardial infarction rates compared to CEA (0.7 vs 2.4%, and 0.5 vs 0.9%, respectively). At 1 year, stroke/death rates remained similar between TCAR and CEA (5.1-6.4% vs 5.2-6.6%, respectively), but TCAR outperformed TF-CAS (5.1-6.4% vs 9.6-9.7%). 6. Indications for Surgery All patients with carotid artery stenosis benefit from best medical therapy (BMT): antiplatelet, high-intensity statin, aggressive risk factor control, and lifestyle modification. Asymptomatic patients: ≥70% stenosis, provided the anticipated perioperative risk for stroke, MI, or death is Symptomatic patients: >50% stenosis, benefit of revascularization increases with higher degrees of stenosis. Carotid intervention for symptomatic patients should be performed 2-14 days after stroke. TCAR anatomic criteria: Internal carotid artery diameter 4-9mm Clavicle-carotid bifurcation distance ≥ 5cm Common carotid artery (CCA) diameter ≥ 6mm No or mild puncture site plaque TCAR may be more favorable than CEA in patients who have a high lesion at or above C2 vertebral level, high carotid bifurcation, "hostile neck" (restenosis post-CEA, cervical spine immobility, history of neck irradiation or radical neck dissection) Contraindications: 100% occlusion, or patients with severe comorbidities or life expectancy 3, unsuitable anatomy or an inability to tolerate flow reversal 7. Surgery Preop DAPT at least 3 days and statin for 5 days to reduce periprocedural risk of stroke and mortality. Anesthesia: general anesthesia or MAC Positioning: supine position with the head extended and turned to the contralateral side. The neck and contralateral groin are prepped and draped in sterile fashion. Steps to the procedure and relevant anatomy Common carotid artery exposure Identify the triangle created by the sternal and clavicular heads of the sternocleidomastoid muscle (SCM) and the superior edge of the clavicle. Create a 2- to 4-cm longitudinal or transverse incision between the two heads. Electrocautery is used to divide through the subcutaneous tissue and platysma. The SCM is retracted laterally to access the carotid sheath. The carotid sheath contains three critical structures. From medial to lateral we have the common carotid artery, vagus nerve, and internal jugular vein. The internal jugular vein is dissected and retracted. A branch off of the internal jugular vein that we commonly encounter is the facial vein. This can be safely ligated when encountered. In most patients, the vagus nerve lies lateral and posterior to the common carotid artery and care should be taken to avoid injury to it, especially in the later steps when we get to clamping the artery. Other critical structures: Hypoglossal nerve: crosses the carotid artery transversely approximately 2-3 cm above the carotid bifurcation Ansa cervicalis: encountered in the carotid sheath as it branches from the hypoglossal nerve as it crosses the internal carotid artery Carotid body: at the base of the carotid bifurcation Marginal mandibular branch of the facial nerve: encountered at higher incisions, though this is not as common as with carotid endarterectomies Once the co
