Holding Pressure - TransCarotid Artery Revascularization (TCAR)

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

1. Carotid artery disease is primarily driven by atherosclerotic plaque deposition.

2. Risk factors: hypertension, hyperlipidemia, diabetes, smoking, and advanced age.

3. Nonatherosclerotic etiologies: fibromuscular dysplasia, carotid dissection, vasculitic disease, carotid webs, and trauma.

4. 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.

5. 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.

6. 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

1. Patients are often asymptomatic and stenosis is incidentally found on imaging.

2. 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

3. 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

1. USPTF recommends against screening for asymptomatic carotid artery stenosis.

2. 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.

3. 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.

4. 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.

5. Carotid duplex ultrasound: first-line imaging modality for both screening and initial evaluation of stenosis, noninvasive, low-cost

6. CTA: rapid, high-resolution, three-dimensional imaging of vascular anatomy, risk of contrast and radiation exposure

7. MRA: high-quality, three-dimensional imaging without radiation or contrast, expensive with longer acquisition time, can overestimate stenosis in severe disease

8. DSA/angiography: gold standard, expensive, invasive, not generally recommended for routine diagnostic evaluation or screening

4. Classification

1. Carotid artery stenosis is classified by degree of luminal narrowing.

2. 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.

3. Classification of stenosis:

   1. Mild: <50% narrowing

   2. Moderate: 50-69% narrowing

   3. Severe: ≥70% narrowing

TRANSCAROTID ARTERY REVASCULARIZATION (TCAR)

5. Relevant Trials

1. 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.

   1. 30-day stroke rate of 1.4% and a combined stroke/death/MI rate of 3.5%, with technical success in 99% of cases

   2. At 1 year, the ipsilateral stroke rate was 0.6%, indicating excellent durability in a high-risk population

   3. 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.

2. 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.

   1. 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.

3. TCAR Surveillance Project: ongoing study that provides real-world, comparative data using the VQI registry.

   1. 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%).

   2. 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).

   3. 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

1. All patients with carotid artery stenosis benefit from best medical therapy (BMT): antiplatelet, high-intensity statin, aggressive risk factor control, and lifestyle modification.

2. Asymptomatic patients: ≥70% stenosis, provided the anticipated perioperative risk for stroke, MI, or death is <3%. The decision to intervene in asymptomatic patients is more nuanced due to advances in medical therapy and lower contemporary stroke rates. Life expectancy should also be taken into consideration.

3. Symptomatic patients: >50% stenosis, benefit of revascularization increases with higher degrees of stenosis.

   1. Carotid intervention for symptomatic patients should be performed 2-14 days after stroke.

4. TCAR anatomic criteria:

   1. Internal carotid artery diameter 4-9mm

   2. Clavicle-carotid bifurcation distance ≥ 5cm

   3. Common carotid artery (CCA) diameter ≥ 6mm

   4. No or mild puncture site plaque

5. 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)

6. Contraindications: 100% occlusion, or patients with severe comorbidities or life expectancy <1 year, recent MI, recent stroke, or modified Rankin Scale >3, unsuitable anatomy or an inability to tolerate flow reversal

7. Surgery

1. Preop

   1. DAPT at least 3 days and statin for 5 days to reduce periprocedural risk of stroke and mortality.

   2. Anesthesia: general anesthesia or MAC

   3. 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.

2. Steps to the procedure and relevant anatomy

Common carotid artery exposure

1. Identify the triangle created by the sternal and clavicular heads of the sternocleidomastoid muscle (SCM) and the superior edge of the clavicle.

2. Create a 2- to 4-cm longitudinal or transverse incision between the two heads.

3. Electrocautery is used to divide through the subcutaneous tissue and platysma.

4. The SCM is retracted laterally to access the carotid sheath.

5. The carotid sheath contains three critical structures. From medial to lateral we have the common carotid artery, vagus nerve, and internal jugular vein.

6. The internal jugular vein is dissected and retracted.

7. A branch off of the internal jugular vein that we commonly encounter is the facial vein. This can be safely ligated when encountered.

8. 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.

9. Other critical structures:

   1. Hypoglossal nerve: crosses the carotid artery transversely approximately 2-3 cm above the carotid bifurcation

   2. Ansa cervicalis: encountered in the carotid sheath as it branches from the hypoglossal nerve as it crosses the internal carotid artery

   3. Carotid body: at the base of the carotid bifurcation

   4. Marginal mandibular branch of the facial nerve: encountered at higher incisions, though this is not as common as with carotid endarterectomies

10. Once the common carotid artery is dissected and exposed, a vessel loop or umbilical tape is placed to facilitate manipulation of the vessel during carotid artery access.

11. A purse string or U-stitch 5-0 polyproline suture is placed on the common carotid for the closure of the arterial puncture site at the end of the procedure.

Femoral vein access

1. Femoral triangle anatomy:

   1. Borders

      1. Superior: inguinal ligament

      2. Lateral: medial border of the sartorius muscle

      3. Medial: lateral border of the adductor longus muscle

   2. Contents

      1. Lateral to medial: femoral nerve, femoral artery, femoral vein, empty space/femoral canal, and lymphatics

      2. Mnemonic - NAVEL: nerve, artery, vein, empty space, lymphatics

2. Using ultrasound guidance, the femoral vein contralateral to the common carotid artery we just exposed is visualized.

3. The common femoral vein is typically accessed 1-2 cm below the inguinal ligament and is around 2-4 cm deep to the skin in most adults. We access the vein with a micropuncture system via Seldinger technique.

4. The TCAR venous return sheath is advanced over a 0.035-inch guidewire. Blood is aspirated from the flow line and the sheath is flushed with heparinized saline to ensure proper access.

5. Secure the venous return sheath with suture.

6. The contralateral femoral vein is accessed to facilitate optimal circuit setup and minimize interference with arterial access and other steps.

Common carotid artery access and sheath placement

1. Heparin should be given prior to obtaining arterial access. An activated clotting time, also known as ACT, between 250-300 should be achieved.

2. Obtain micropuncture access of the common carotid at the site where we previously placed the suture. A 21-gauge micropuncture needle is slowly advanced into the anterior wall of the common carotid artery and a 0.018-inch micropuncture wire is advanced 3 cm into the common carotid artery. A micropuncture sheath and dilator are advanced 2-3 cm into the common carotid.

3. After removal of the dilator and micropuncture wire, brisk and pulsatile backbleeding confirms correct positioning.

4. Angiogram is obtained to delineate the carotid bifurcation and where the lesion is located.

5. A 0.035-inch ENROUTE J wire is positioned in the CCA, the micropuncture sheath is removed, and the arterial sheath and dilator are inserted (stop short technique).

6. The arterial access sheath is advanced to the 2.5-cm marker, predetermined by the sheath stopper.

7. The sheath position should be checked using angiography in two projections after removal of the dilator to ensure the sheath tip is placed coaxially within the common carotid.

8. Secure the sheath to the patient at 3 points using 2-0 silk stitches. The side ports are burped and a control run confirms no evidence of dissection or vessel injury.

Initiation of dynamic flow reversal

1. The flow controller is connected to the arterial access sheath. The column should be held upward and arterial blood should fill the column.

2. Once it fills to the line on the controller, connect the system to the venous return sheath. You have now established an extracorporeal AV shunt.

3. The integrity of the circuit is verified by flushing the venous sheath with hep saline and confirming rapid blood flow through the circuit.

4. Perform a TCAR time out, confirming systolic blood pressure 140–160 mmHg, heart rate >70 bpm, and ACT >250 seconds to optimize cerebral perfusion and minimize thrombotic risk.

5. Clamp the carotid artery just proximal to the arterial sheath to establish active flow reversal.

6. Flow controller settings:

   1. Low setting

   2. High setting

   3. Flow-stop button: allows for temporary cessation of flow (used when we inject contrast).

7. Confirm flow reversal via two different ways:

1. The first way is to stop flow to the venous return sheath with the stopcock, clearing the line with hep saline injection, and then opening the stopcock and seeing the blood returning to the controller in a reverse fashion.

2. The second way is to perform an angiogram with a small amount of contrast injection while holding the flow-stop button. Using the angio we want to make sure that contrast is flowing retrograde in the cervical ICA thereby confirming flow reversal.

Carotid artery stenting, balloon angioplasty, and completion angiogram

1. At this point, a standard carotid angioplasty and stenting procedure is performed.

2. ENROUTE transcarotid Neuroprotection System device:

   1. inner diameter of 8F and an outer diameter of 10F

   2. Has its own carotid artery stent system but is also compatible with all FDA-approved carotid stents.

3. Final angiogram is performed to confirm stent position, vessel patency, and absence of complications including vasospasm at the distal end of the stent and filling defects from protrusion of atheromatous material through the stent

Cessation of flow reversal and sheath removal

1. Allow the flow reversal to run for a few minutes after the final balloon angioplasty to clear any debris.

2. Antegrade flow is restored by releasing the carotid clamp and closing the stopcocks on the neuroprotection system.

3. The patient is auto-transfused the blood from the flow line back to the venous system.

4. As the arterial access system is removed and the puncture site is closed with the U-stitch.

5. IV protamine is administered to reverse the heparin.

6. Standard closure is performed at the incision site. Meanwhile, hemostasis is achieved after removal of the femoral vein sheath with brief manual compression.

1. Postop care/complications

   1. Postop care

      1. All patients after a TCAR should be monitored in the ICU setting for 24 hours, as an embolic stroke, hypotension with or without bradycardia, or hypertension can occur.

         1. Should a TIA or stroke be observed, a carotid duplex scan and CT angiogram should be immediately obtained to assess the stent site and the presence of an embolic or thrombotic filling defect, dissection, or occlusion.

      2. Dual antiplatelet therapy: continue for 45 days to 12 months

      3. Aspirin and statin therapy: continued indefinitely

      4. Surveillance duplex imaging: 4 weeks, 6 months, and 12 months, and annually thereafter.

   2. Postop complications

      1. Hematoma

      2. Stroke

      3. Myocardial infarction

      4. Cerebral hyperperfusion syndrome

         1. Sudden and excessive increase in cerebral blood flow to previously hypoperfused brain tissue is met with vasculature that cannot constrict appropriately from chronic vasodilation

         2. Leads to breakthrough hyperperfusion. This results in cerebral edema, intracerebral hemorrhage, and neurological symptoms.

      5. Cranial nerve injury

         1. Hypoglossal nerve (CN XII) injury: ipsilateral tongue deviation. It is the most commonly injured cranial nerve.

         2. Vagus nerve (CN X) injury: hoarseness and possible vocal cord paralysis.

         3. Glossopharyngeal nerve (CN IX) injury: soft palate dysfunction.

         4. Recurrent laryngeal nerve injury: voice hoarseness and inability to cough as it innervates all of the voice box muscles except for the cricothyroid muscle

         5. Marginal mandibular nerve injury: ipsilateral lip droop, injury is rare in TCAR.

      6. Stent restenosis

      7. Pseudoaneurysm

      8. Access site infection