SCAI KERN CHAP 35 Carotids and Vertebrals Flashcards by Fady Geha

Q1: What does the natural history of carotid artery stenosis depend on?

Q2: How much higher is the risk of stroke in symptomatic patients compared to asymptomatic patients?

Q3: In a Medicare registry, what is the ratio of asymptomatic to symptomatic patients undergoing carotid revascularization?

Q4: What percentage of patients over age 65 have carotid stenosis >50%?

Q5: What percentage of patients over age 65 have carotid stenosis >75%?

Q6: What percentage of ischemic strokes have no warning symptoms?

Q7: Why is management of asymptomatic carotid atherosclerosis important?

Q8: What is the risk of stroke within 6 months after transient focal neurologic symptoms?

Q9: How is TIA currently defined?

Q10: What does TIA stand for?

Q11: What is stroke defined as?

Q12: What types of evidence are used to define stroke?

Q13: What is the difference between TIA and stroke based on injury?

Q14: Did initial studies on carotid artery disease use the current definitions of TIA and stroke?

Q15: What did initial studies on carotid artery disease primarily use to define infarction?

A1: Presence of symptoms (TIA, stroke, amaurosis fugax)

A2: 5- to 10-fold higher risk

A3: 2.5 to 1 (asymptomatic to symptomatic)

A4: Approximately 5% to 10%

A5: Approximately 1%

A6: More than 80%

A7: Because many ischemic strokes occur without warning symptoms

A8: 30% risk of stroke within 6 months

A9: Transient episode of neurologic dysfunction caused by focal ischemia without acute infarction

A10: Transient ischemic attack

A11: Central nervous system infarction with permanent injury

A12: Neuropathologic, neuroimaging, and/or clinical evidence

A13: TIA has no acute infarction; stroke has permanent injury

A14: No, they predate current definitions

A15: Clinical definition of infarction

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Q1: What two large RCTs in the 1990s studied asymptomatic carotid artery stenosis?

Q2: What procedure was shown to reduce ipsilateral stroke incidence by 50% in these trials?

Q3: In patients with what degree of asymptomatic carotid stenosis did CEA reduce ipsilateral stroke?

Q4: Did CEA reduce overall stroke and death in these trials?

Q5: Did CEA show benefit in women or patients older than 75 years?

Q6: How has medical therapy changed since these trials?

Q7: What is the current risk of progression of asymptomatic carotid stenosis to occlusion with modern medical therapy?

Q8: In a cohort of 3681 patients, what percentage of asymptomatic patients had occlusions during observation?

Q9: What percentage of occlusions occurred before initiation of modern intensive medical therapy?

Q10: What was the mean annual ipsilateral stroke rate in nonrevascularized asymptomatic patients with 70%-99% stenosis under contemporary medical therapy in a retrosective community-based cohort ?

Q11: What percentage of the cohort above progressed from severe to high-grade stenosis over 4 years?

Q12: What percentage progressed from severe stenosis to total occlusion?

Q13: What percentage of patients with baseline high-grade stenosis progressed to total occlusion?

Q14: What medical therapies are included in contemporary medical therapy?

Q15: Over what period was the retrospective community-based cohort study conducted?

A1: Asymptomatic Carotid Atherosclerosis Study (ACAS) and Asymptomatic Carotid Surgery Trial (ACST)

A2: Carotid endarterectomy (CEA) in asymptomtic patients vs. medical therapy ( ASA )

A3: Greater than 60% carotid stenosis

A4: No

A5: No

A6: It has significantly improved

A7: Very low

A8: 8.6%

A9: 80%

A10: 0.9% ( 4.7 % by 5 year )

A11: 21.5%

A12: 8.4%

A13: 28.2%

A14: Modern lipid lowering, antidiabetic, and antihypertensive therapies

A15: 2008-2012

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Q1: How is symptomatic carotid disease defined?

Q2: What trial provided data on the natural history of symptomatic carotid artery stenosis?

Q3: What was the 5-year risk of ipsilateral stroke in patients with <50% stenosis managed medically?

Q4: What was the 5-year risk of ipsilateral stroke in patients with 50%-69% stenosis?

Q5: What was the 2-year risk of ipsilateral stroke in patients with 70%-99% stenosis?

Q6: Which other trial showed similar results to NASCET?

Q7: What was the 3-year risk of ipsilateral stroke in symptomatic patients with stenosis >80%?

Q8: **How does the risk of ipsilateral stroke change as stenosis approaches total occlusion 95%-99%?

Q9: Name three symptoms of carotid artery stenosis.

Q10: What scale is used to quantify neurologic deficit in symptomatic patients?

Q11: How does the NIHSS score correlate with patient outcome?

Q12: How might asymptomatic patients present with carotid stenosis?

Q13: What is a cervical bruit?

Q14: What is a class IIA recommendation related to carotid stenosis screening?

Q15: What risk factors contribute to a class IIB recommendation for carotid screening?

A1: Focal neurologic symptoms of sudden onset in the carotid artery distribution within the previous 6 months

A2: North American Symptomatic Carotid Endarterectomy Trial (NASCET)

A3: 18.7%

A4: 22.2%

A5: 26%

A6: European Carotid Surgery Trial (ECST)

A7: 26.5%

A8:** It decreases to 17.2%

A9: Ipsilateral Amaurosis fugax, contralateral weakness/numbness of face or exteremity , dysarthria and finally aphasia (if the dominant hemisphere is involved )

A10: National Institutes of Health Stroke Scale (NIHSS)

A11: It correlates with outcome

A12: Carotid stenosis noted on duplex or carotid screening

A13: An abnormal sound over the carotid artery indicating turbulent blood flow

A14: Screening in asymptomatic patients with carotid stenosis noted on duplex in presence of a cervical bruit

A15: Symptomatic peripheral artery disease, coronary artery disease, or ≥2 risk factors like HTN, hyperlipidemia, tobacco use, family history of premature atherosclerosis or ischemic stroke

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Q1: What is the gold standard for defining carotid anatomy?

Q2: What is the most widely accepted methodology for stenosis measurement in carotid imaging?

Q3: What is the risk range of iatrogenic cerebral infarction with invasive cerebral catheter-based angiography?

Q4: Why should noninvasive imaging be the initial strategy for carotid evaluation?

Q5: Name four preferred noninvasive methods for carotid assessment.

Q6: Which noninvasive imaging method is optimal for initial screening of carotid disease?

Q7: What are the advantages of carotid duplex imaging?

Q8: What anatomical areas should cerebral and cervical imaging define?

Q9: What does DSA stand for?

Q10: What does CTA stand for?

Q11: What does MRA stand for?

Q12: What is the main risk associated with invasive cerebral catheter-based angiography?

Q13: What imaging method uses the NASCET method for stenosis measurement?

Q14: Why is carotid duplex imaging widely used?

Q15: What is the Circle of Willis?

A1: Digital subtraction angiography (DSA)

A2: NASCET method

A3: 0.5% to 1.2%

A4: To avoid risks associated with invasive procedures

A5: Carotid duplex imaging, transcranial Doppler imaging, computed tomography angiography (CTA), magnetic resonance angiography (MRA)

A6: Carotid duplex imaging

A7: Safety profile, low cost, wide availability

A8: Aortic arch and Circle of Willis

A9: Digital subtraction angiography

A10: Computed tomography angiography

A11: Magnetic resonance angiography

A12: Iatrogenic cerebral infarction

A13: Digital subtraction angiography (DSA)

A14: Because it is safe, affordable, and widely available

A15: A circular network of arteries supplying blood to the brain

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Q1: Name three classes of medications involved in current antiatherosclerotic medical therapy.

Q2: What is the primary focus of medical therapy for carotid atherosclerosis?

Q3: Why is blood pressure control important in stroke prevention?

Q4: Which two medication classes are particularly beneficial in stroke prevention for high-risk cardiovascular patients?

Q5: What effect do statin drugs have on stroke risk in ASCVD patients?

Q6: Besides lipid-lowering, what other effects might statins have to prevent strokes?

Q7: What do current AHA/ASA and ACC/AHA guidelines recommend for high-intensity statin therapy in patients under 75 years with clinical ASCVD?

Q8: What is the recommendation for high-intensity statin therapy in patients 75 years or older?

Q9: What does class I, Level of Evidence A mean in guideline recommendations?

Q10: What is the role of PCSK9 inhibitors in lipid management?

Q11: What LDL-cholesterol level is a threshold for considering PCSK9 inhibitors in high-risk ASCVD patients?

Q12: What additional medication is often combined with PCSK9 inhibitors?

Q13: What is the association between PCSK9 inhibitors and hemorrhagic stroke risk?

Q14: What years do the modern studies and meta-analysis on PCSK9 inhibitors cover?

Q15: Why is PCSK9 inhibitor therapy highlighted in recent guideline updates?

A1: ACE inhibitors (ACE-Is), angiotensin receptor blockers (ARBs), statins, PCSK9 inhibitors, antidiabetic medications, antiplatelet agents

A2: Preventing stroke and stabilizing atherosclerotic lesions to prevent plaque rupture and atheroembolization

A3: Because high blood pressure is a primary risk factor for stroke, atrial fibrillation, and myocardial infarction, which increase stroke risk

A4: ACE inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs)

A5: They lower the risk of stroke in ASCVD patients

A6: Pleiotropic effects on endothelial function and plaque stabilization

A7: Initiate or continue high-intensity statin therapy unless contraindicated (class I, LOE A)

A8: Consider high-intensity statin therapy if benefits outweigh risks (class IIa, LOE B)

A9: Strong recommendation based on high-quality evidence

A10: Lower LDL cholesterol and reduce cardiovascular mortality. Lower risk of total and ischemic stroke without increase in hemorrhagic stroke risk.

A11: LDL-C ≥70 mg/dL ( while on maximally tolerated statin therapy (with ezetimibe) in setting of known/high-risk ASCVD )

A12: Ezetimibe

A13: No increase in hemorrhagic stroke risk

A14: 2015-2020

A15: Because of evidence supporting reduced stroke risk and cardiovascular mortality in high-risk patients

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1- ASCVD and age below 75

2- ASCVD and age above 75

3- LDL above 190

4- Diabetes and age 40-75 with LDL above 70

5- Diabetes and age 40-75 with LDL above 70 and 10 year risk above 7.5 %

6- Diabetes and age 40 -75 with LDL above 70 and 10 year risk below 7.5%

7- Age 40 to 75 without diabetes or ASCVD

8- Age 40 to 75 without diabetes or ASCVD and 10 year risk above 7.5%

1- High intensity statins

2- Moderate intensity statins

3- High intensity statins

4- Check 10-year risk

5- High intensity statins

6- Moderate intensity statins

7- Check 10-year risk

8- Moderate to high intensity statins

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Q1: Which agency has approved statins for stroke prevention in cardiovascular and high-risk hypertensive patients?

Q2: What trial demonstrated the effectiveness of high-dose atorvastatin for secondary stroke prevention?

Q3: In the SPARCL trial, which patients benefited from high-dose atorvastatin?

Q4: What condition did patients in the SPARCL trial have besides ischemic stroke or TIA?

Q5: What did the JUPITER study evaluate?

Q6: What was the key finding of the JUPITER study regarding rosuvastatin?

Q7: In the JUPITER study, what was notable about the cholesterol levels of patients treated?

Q8: Which trial established a target LDL-C <70 mg/dL as superior for preventing major cardiovascular events?

Q9: What was the higher LDL-C target compared against in the TST trial?

Q10: What is the clinical significance of statins in stroke treatment and prevention?

Q11: In which patient population are statins especially important for stroke prevention?

Q12: What does ASCVD stand for?

Q13: What does TIA stand for?

Q14: What is the primary benefit of achieving LDL-C <70 mg/dL according to the TST trial?

Q15: What type of stroke patients does the SPARCL trial focus on?

A1: Food and Drug Administration (FDA)

A2: Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial

A3: Patients with ischemic stroke or TIA without concomitant coronary heart disease

A4: None; they did not have concomitant coronary heart disease

A5: Rosuvastatin treatment in patients with normal cholesterol but elevated C-reactive protein

A6: Rosuvastatin reduced the rate of stroke

A7: They had normal cholesterol levels

A8: Treat Stroke to Target (TST) trial

A9: 90-110 mg/dL

A10: Statins are a cornerstone of stroke treatment and prevention

A11: Patients with known atherosclerotic cardiovascular disease (ASCVD) in any vascular bed

A12: Atherosclerotic cardiovascular disease

A13: Transient ischemic attack

A14: Prevention of major cardiovascular events

A15: Ischemic stroke or TIA patients

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Q1: By approximately what percentage did antiplatelet therapy reduce the occurrence of any vascular event in high-risk patients?

Q2: What dose range of aspirin was found to be as beneficial as higher doses?

Q3: What was the aspirin dosing schedule in the Women’s Health Study?

Q4: How much did aspirin reduce the risk of stroke over 10 years in the Women’s Health Study?

Q5: Did high-dose aspirin provide more benefit than lower doses?

Q6: What was a downside of high-dose aspirin compared to lower doses?

Q7: What did the CAPRIE trial compare?

Q8: What relative risk reduction did clopidogrel provide versus aspirin in the CAPRIE trial?

Q9: Was the benefit of clopidogrel significant in patients who presented with stroke in the CAPRIE trial?

Q10: What did the MATCH trial compare?

Q11: What were the findings of the MATCH trial regarding combination therapy in stroke patients?

Q12: What was the conclusion of the CHARISMA trial regarding aspirin alone vs aspirin plus clopidogrel?

Q13: What aspirin dose was found optimal in the CHARISMA trial?

Q14: What was the primary outcome in the THALES trial?

Q15: What was a significant side effect seen with ticagrelor plus aspirin in the THALES trial?

A1: About 25%

A2: 75 to 150 mg

A3: 100 mg every other day

A4: 17% reduction

A5: No

A6: More side effects

A7: Clopidogrel 75 mg daily vs aspirin 325 mg daily

A8: 8.7% *relative risk reduction in ischemic stroke, MI or vascular death

A9: No, benefit was not significant in stroke patients ( patients presenting with stroke )

A10: Clopidogrel 75 plus aspirin 75 vs clopidogrel alone

A11: Combination did not improve outcomes but increased major bleeding

A12: Aspirin alone was as effective as combination therapy ( 4300 patients with a prior TIA or stroke and found that aspirin (75-162 mg daily) was as eﬀective as aspirin plus clopidogrel in preventing future MI, stroke, or cardiovascular death in patients with multiple risk factors or with clinically evident cardiovascular disease )

A13: 81 mg daily

A14: Composite of stroke or death

A15: Increased severe bleeding

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Q1: What do the AHA and ASA guidelines recommend for all patients with carotid atherosclerosis?

Q2: What is the primary benefit of antiplatelet therapy?

Q3: Has complete benefit for stroke prevention in *asymptomatic patients been established with antiplatelet therapy?

Q4: What is the CREST-2 trial currently enrolling patients to study?

Q5: What are the two parallel arms of the CREST-2 trial ( *asymptomatic ) ?

Q6: What does BMT stand for in the CREST-2 trial?

Q7: What medical management goals are emphasized in CREST-2?

Q8: Name two smaller European trials mentioned that evaluated revascularization versus BMT.

Q9: What were the findings of the ECST-2 and SPACE-2 trials regarding ipsilateral stroke, MI, or death?

Q10: Why are ECST-2 and SPACE-2 considered less robust than CREST-2?

Q11: What procedure is primarily evaluated in the ECST-2 and SPACE-2 trials?

Q12: What lifestyle interventions are emphasized in the CREST-2 trial?

Q13: What is the target systolic blood pressure in CREST-2 for patients without diabetes?

Q14: What is the LDL cholesterol target in CREST-2 medical management?

Q15: When can definitive guideline recommendations be expected for asymptomatic carotid artery disease?

A1: To be placed on antiplatelet medications

A2: Reduction of myocardial infarction (MI) and ischemic cardiovascular events

A3: No, it has not been established

A4: Comparing carotid endarterectomy (CEA) or carotid artery stenting (CAS) plus best medical therapy versus best medical therapy alone

A5: CEA + BMT vs BMT alone, and CAS + BMT vs BMT alone

A6: Best medical therapy

A7: SBP <140 mm Hg (<130 mm Hg for diabetes), LDL <70 mg/dL, HbA1c <7.0%, smoking cessation, weight management, exercise ( 30 minutes moderate exercise 3 times a week )

A8: 2nd European Carotid Surgery Trial (ECST-2) and SPACE-2

A9: No difference in ipsilateral stroke, MI, or death between revascularization + BMT and BMT alone

A10: Due to power, recruitment, and execution issues

A11: Carotid endarterectomy (CEA)

A12: Lifestyle interventions including smoking cessation, weight management, and exercise

A13: Less than 140 mm Hg

A14: Less than 70 mg/dL

A15: After the results of CREST-2 are available

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Q1: What is the purpose of carotid revascularization in asymptomatic patients?

Q2: How many large RCTs have compared CEA to antiplatelet therapy in asymptomatic patients?

Q3: What degree of carotid stenosis was studied in these RCTs?

Q4: Which study randomized 444 men with asymptomatic carotid stenosis >50%?

Q5: What medication and dose were all patients assigned in the Veterans Affairs Cooperative Study?

Q6: What was the 30-day risk of stroke or death in the CEA group?

Q7: After nearly 4 years, what was the ipsilateral neurologic event rate in the surgical arm?

Q8: What was the ipsilateral neurologic event rate in the medical therapy arm?

Q9: Was the difference in ipsilateral neurologic event rates between surgical and medical arms statistically significant?

Q10: How did the risk of ipsilateral stroke alone compare between medical treatment and CEA?

Q11: Was there a difference between surgery and medical therapy for combined stroke or death?

Q12: What types of neurologic events were included in the ipsilateral neurologic event rate?

Q13: What does CEA stand for?

Q14: Why are these RCTs considered less relevant today?

Q15: What is the significance of the P-value < .001 in the study results?

A1: To prevent ischemic stroke

A2: Three

A3: Moderate (>50%-60%) carotid stenosis

A4: Veterans Affairs Cooperative Study

A5: Aspirin 650 mg twice daily

A6: 4.7%

A7: 8%

A8: 20.6%

A9: Yes

A10: Reduced from 9.4% to 4.7% with CEA

A11: No difference

A12: TIA, transient monocular blindness, fatal and nonfatal stroke

A13: Carotid endarterectomy

A14: Due to advances in modern medical therapy

A15: Indicates a highly statistically significant difference

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Q1: The purpose of carotid revascularization is to prevent ________ stroke.

Q2: Three large ________ compared CEA to antiplatelet therapy in moderate *asymptomatic carotid stenosis.

Q3: The degree of carotid stenosis studied was greater than ________%.

Q4: The Veterans Affairs Cooperative Study randomized ________ men with *asymptomatic carotid stenosis to CEA with med therapy vs med therapy alone.

Q5: Patients were assigned aspirin ________ mg twice daily.

Q6: The 30-day risk of stroke or death in the CEA group was ________%.

Q7: At nearly 4 years of follow-up, the ipsilateral neurologic event rate in the surgical arm was ________%.

Q8: The ipsilateral neurologic event rate in the medical arm was ________%.

Q9: The P-value for the difference in ipsilateral neurologic event rate was less than ________.

Q10: The risk of ipsilateral stroke alone was reduced from ________% with medical treatment to 4.7% with CEA.

Q11: The P-value for the reduction in ipsilateral stroke alone was less than ________.

Q12: There was no difference between surgery and medical therapy for combined ________ or death.

Q13: The neurologic events included TIA, transient monocular blindness, and ________ stroke.

Q14: Many patients did not tolerate the assigned aspirin ________.

Q15: Modern medical therapy has made these trials ________.

A1: ischemic

A2: randomized controlled trials (RCTs)

A3: 50-60

A4: 444

A5: 650 mg

A6: 4.7%

A7: 8%

A8: 20.6 %!!

A9: 0.001

A10: 9.4

A11: 0.06

A12: stroke

A13: fatal and nonfatal

A14: dose

A15: less relevant

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Q1: ACAS randomized ________ *asymptomatic patients with carotid stenosis >60% to medical therapy or medical therapy with CEA.

Q2: All patients in ACAS received aspirin ________ mg daily.

Q3: Angiography was performed only in the ________ group in ACAS.

Q4: The risk of stroke associated with angiography in ACAS was ________%.

Q5: The 30-day risk of stroke or death in the surgical group in ACAS was ________%.

Q6: The projected 5-year risk of ipsilateral stroke in the medical arm of ACAS was ________%.

Q7: The projected 5-year risk of ipsilateral stroke with CEA in ACAS was ________%.

Q8: The number of patients needed to treat with surgery to prevent one ipsilateral stroke at 5 years in ACAS was ________.

Q9: The benefit for women in ACAS was a ________% reduction in events.

Q10: The benefit for men in ACAS was a ________% reduction in events.

Q11: ACST evaluated ________ asymptomatic patients with >60% carotid stenosis.

Q12: In ACST, drug treatment was left to the discretion of the patients’ ________.

Q13: Drug treatment in ACST usually included antiplatelet medications, antihypertensive therapy, and ________ agents.

Q14: The 30-day perioperative risk of stroke or death in ACST was ________%.

Q15: The 5-year risk of perioperative death or total stroke was reduced from ________% to 6.4% with CEA in ACST.Nevertheless, CEA did not reduce overall stroke and death and did not show any beneﬁt in women or in patients older than 75 years of age.

A1: 1662

A2: 325

A3: CEA

A4: 1.2

A5: 2.7

A6: 11

A7: 5.1

A8: 19

A9: 17

A10: 66

A11: 3120

A12: primary physicians

A13: lipid-lowering

A14: 3.1

A15: 11.8

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Q1: How many large RCTs have evaluated the benefit of CEA compared to medical therapy in *symptomatic patients?

Q2: What was the patient population in the Veterans Administration 309 trial?

Q3: How many symptomatic men were screened in the Veterans Administration 309 trial?

Q4: What degree of ICA stenosis did patients have in the Veterans Administration 309 trial?

Q5: Why was the Veterans Administration 309 trial ended prematurely?

Q6: What was the absolute reduction in risk of ipsilateral stroke or TIA in the Veterans Administration 309 trial? CEA with BMT vs BMT alone ( BMT = Best medical management )

Q7: In which patients was the benefit of surgery most profound in the Veterans Administration 309 trial?

Q8: What was the patient condition for enrollment in the NASCET trial?

Q9: How were patients stratified in the NASCET trial based on carotid stenosis?

Q10: How many patients with >70% stenosis were randomized to CEA in NASCET?

Q11: What was the absolute risk reduction of ipsilateral stroke at 2 years in NASCET for patients with >70% stenosis?

Q12: How much did CEA lower the 2-year risk of major or fatal stroke in NASCET?

Q13: Was there a benefit of CEA for stroke prevention in patients with <50% stenosis in NASCET?

Q14: What was the 5-year rate of ipsilateral stroke on BMT alone?

Q15: What was the 5-year rate of ipsilateral stroke for patients who received CEA + BMT?

A1: Three

A2: Symptomatic men who presented within 4 months

A3: 5000

A4: ≥50%

A5: Due to early results from NASCET and ECST

A6: 11.7%. At mean follow-up of almost 1 year, there was a reduction in ipsilateral stroke or TIA (9.4% BMT vs 7.7% in the revascularization arm with an absolute reduction in risk of 11.7%).

A7: Patients with stenosis >70%. The beneﬁt of surgery was most profound in patients with stenosis >70% (an absolute risk reduction of 17.7%).

A8: TIA or nondisabling stroke within 180 days

A9: <50%, 50%-69%, and 70%-99% stenosis

A10: About 659

A11: 17% (26% CEA vs 9% BMT) of ipsilateral stroke at 2 years.

A12: From 13.1% to 2.5%

A13: No

A14: 22.2%

A15: 15.7% ( absolute risk reduction of 6.5% for CEA and BMT )

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Q1: How many symptomatic patients were studied in ECST?

Q2: What percentage of ECST patients were randomized to CEA + BMT?

Q3: What percentage of ECST patients were randomized to BMT alone?

Q4: What did BMT consist of in the ECST trial?

Q5: What was the 30-day perioperative risk of major stroke or death with revascularization in ECST?

Q6: Was there benefit to revascularization for stenosis below 70%-80% in ECST?

Q7: Among patients with stenosis >80%, what was the rate of major stroke or death at 3 years with BMT?

Q8: Among patients with stenosis >80%, what was the rate of major stroke or death at 3 years with revascularization?

Q9: What was the absolute risk reduction of major stroke or death with revascularization in patients with stenosis >80%?

Q10: Did patients with near occlusion benefit from revascularization in ECST?

Q11: How does ECST define 80% stenosis compared to NASCET?

Q12: What did the meta-analysis find about surgery for lesions <30% by NASCET criteria?

Q13: What was the absolute risk reduction with CEA in patients with 50%-69% stenosis?

Q14: In which stenosis group was CEA most beneficial according to the meta-analysis?

Q15: What is near occlusion defined as?

A1: 3024

A2: 60%

A3: 40%

A4: Antihypertensive medications, antiplatelet agents, antismoking counseling

A5: 7%

A6: No

A7: 26.5%

A8: 14.9%

A9: 11.6%

A10: No

A11: ECST 80% stenosis ≈ NASCET 60% stenosis

A12: Surgery increased 5-year risk of ipsilateral stroke

A13: 4.6%

A14: >70% stenosis (16% absolute risk reduction)

A15: Stenosis causing reduced flow to distal ICA and/or narrowing of poststenotic ICA

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Current AHA/ASA guidelines recommend CEA in :

1- Symptomatic patients with stenosis of **50% to 99% if the risk of perioperative stroke or death is <6%.

2- The recommended timing for carotid revascularization after a nondisabling stroke or TIA is within the ﬁrst 2 weeks after the event.

3- In asymptomatic patients, guidelines recommend CEA for stenosis of **60% to 99% if the perioperative risk of stroke is <3% and life expectancy is at least 5 years.

Study These Flashcards

Q1: What does TCAR stand for?

Q2: When did TCAR emerge as a carotid revascularization approach?

Q3: Which company developed the Enroute system used in TCAR?

Q4: What components are included in the Enroute system?

Q5: What is the diameter range of the RX balloons used in TCAR?

Q6: What size is the guidewire used in TCAR?

Q7: What type of stent is used in the TCAR transcarotid stent system?

Q8: How long is the delivery system for the TCAR stent?

Q9: Where is the surgical incision made for TCAR access?

Q10: What artery is accessed during the TCAR procedure?

Q11: What standard practices are observed during TCAR regarding blood thinning?

Q12: What is the target activated clotting time (ACT) during TCAR?

Q13: What technique is used to access the CCA in TCAR?

Q14: What is done to the proximal CCA during the procedure?

Q15: How is blood flow managed during TCAR to protect the brain?

Study These Flashcards

A1: Transcarotid artery revascularization

A2: Mid-2010s

A3: Silk Road Medical

A4: Enhance transcarotid access kit, sheath with 10 cm marker, reverse-flow neuroprotection system, RX balloons, guidewire, transcarotid stent system

A5: 4 to 6 mm

A6: 0.014 inches

A7: Open cell Cordis PRECISE nitinol self-expanding stent

A8: 57 cm

A9: 3 cm longitudinal incision over proximal ipsilateral common carotid artery. Stent delivery is directly through this access point, thus avoiding navigation through the aorta and iliofemoral arteries.

A10: Common carotid artery (CCA)

A11: Standard antiplatelet and anticoagulation practices

A12: ACT ≥250 seconds

A13: Standard Seldinger technique

A14: Clamped

A15: Flow reversed through sheath and neuroprotection system to femoral vein

Q1: What is preplaced around the CCA immediately proximal to the puncture site after cutdown?

Q2: What technique is used to access the CCA in TCAR?

Q3: What is introduced after accessing the CCA?

Q4: What happens to the proximal CCA during the procedure?

Q5: Through what system is the CCA flow reversed?

Q6: Where is the retrograde flow eventually delivered?

Q7: What is the purpose of continuous flow reversal in TCAR?

Q8: What procedure is performed after the guidewire crosses the lesion?

Q9: How do the Enroute balloon and stent delivery systems differ from transfemoral equipment?

Q10: What does the Enroute NPS require for embolic protection?

Q11: What happens after stenting is completed in TCAR?

Q12: What is deployed to close the arteriotomy site?

Q13: What flow resumes through the CCA after sheath removal?

Q14: Name two contraindications for TCAR.

Q15: What anatomical measurement is considered a contraindication for TCAR regarding CCA length?

Study These Flashcards

A1: A suture

A2: Standard Seldinger technique

A3: The sheath

A4: It is clamped

A5: The sheath and accompanying neuroprotection system (NPS)

A6: Common femoral vein

A7: To provide embolic protection

A8: Percutaneous transluminal angioplasty (PTA) and carotid artery stenting (CAS)

A9: They have shorter shaft/working lengths (57 cm vs 135 cm)

A10: Contralateral flow crossover through anterior or posterior circulation

A11: Proximal CCA clamp and sheath are removed

A12: The previously placed suture

A13: Antegrade flow

A14: Prior radiation therapy, heavily calcified carotid lesion (others include short/small CCA, tracheal stoma, high medical risk, hostile neck)

A15: Short CCA (<5 cm from arteriotomy to lesion)

Q1: Has the Enroute TCAR system been evaluated through randomized controlled trials (RCTs)?

Q2: Through what type of data has clinical information on TCAR been obtained?

Q3: What is the name of the registry initiative collecting TCAR data?

Q4: For which patient group was TCAR initially reserved?

Q5: To which patient group has TCAR use expanded?

Q6: According to the Vascular Quality Initiative-TSP database, how does TCAR compare to CEA in terms of length of stay?

Q7: How does TCAR compare to CEA regarding rates of myocardial infarction (MI)?

Q8: How does TCAR compare to CEA in operative/procedural time?

Q9: Is nerve injury rates are lower with TCAR compared to CEA?

Q10: How do all-cause mortality and ipsilateral stroke rates compare between TCAR and CEA?

Q11: What factors should be considered when choosing TCAR for patients?

Q12: In what year was TCAR included in the CMS expansion for CAS?

Q13: What is expected as TCAR moves away from regular proctoring?

Q14: How is TCAR similar to CAS and CEA?

Q15: What organization oversees the TCAR Surveillance Project (TSP)?

Study These Flashcards

A1: No

A2: Registries

A3: TCAR Surveillance Project (TSP)

A4: High surgical risk (HSR) patients

A5: Standard surgical risk patients

A6: Shorter length of stay

A7: Lower rates of MI

A8: Shorter operative/procedural time

A9: Lower rates of cranial nerve injury

A10: Comparable rates of all-cause mortality and ipsilateral stroke

A11: Lesion, anatomic, institutional, operator experience, and other variables

A12: 2023

A13: Further data will emerge, especially in real-world use

A14: It is an option for appropriate patients

A15: Society of Vascular Surgery Patient Safety Organization

Q1: What has historically been lacking in the comparison between CEA and CAS?

Q2: What type of study is the second ACST?

Q3: How many patients were randomized in ACST-2?

Q4: Over how many centers was ACST-2 conducted?

Q5: What was the follow-up schedule in ACST-2?

Q6: When did ACST-2 run?

Q7: What was reviewed regarding operators in ACST-2?

Q8: What were the periprocedural rates of serious complications in CAS and CEA in ACST-2?

Q9: What were the long-term annual rates of serious complications in CAS and CEA?

Q10: Which stroke type was statistically higher with CAS compared to CEA?

Q11: What was the percentage of nondisabling stroke in CAS vs CEA?

Q12: What does MRS ≤2 indicate?

Q13: What level of evidence does ACST-2 provide regarding CAS and CEA?

Q14: Are high-risk features for CEA and CAS interchangeable?

Q15: What overall procedural risk does ACST-2 report for stroke in asymptomatic patients?

Study These Flashcards

A1: High-quality direct comparison data

A2: Multicenter international randomized controlled trial ( CAS versus CEA in asymptomatic severe carotid artery stenosis necessitating revascularization )

A3: About 3625 patients

A4: 130 centers

A5: At 1 month postrevascularization and then annually for 5 years

A6: 2008 through 2020

A7: Competency in performing CAS and/or CEA.

A8: Approximately 1% periprocedural for both

A9: Approximately 0.5% per year for both. ACST-2 found that *serious (disabling or fatal stroke) complications were similarly uncommon after competent CAS or CEA

A10: *Nondisabling stroke

A11: 2.7% for CAS vs 1.9% for CEA

A12: Mild or no disability

A13: ACST-2 oﬀers the highest LOE to date that CAS and CEA are *comparable in terms of severe adverse outcomes for *asymptomatic patients who are candidates for either procedure and that the overall procedural risk of stroke is low.

A14: No, high-risk features for CEA and CAS are not necessarily interchangeable or equivalent.

A15: Low procedural risk of stroke

Study These Flashcards

Features that place a patient at increased risk for complications from CEA vs CAS are summarized in this table

Study These Flashcards

Q1: What does the SAPPHIRE trial compare?

Q2: How many symptomatic patients were randomized in the SAPPHIRE trial?

Q3: What were the stenosis criteria for patient inclusion in SAPPHIRE?

Q4: What percentage of patients in SAPPHIRE were symptomatic?

Q5: What was the primary endpoint measured at 30 days and up to 1 year in SAPPHIRE?

Q6: What was the event rate in the stenting group for the primary endpoint?

Q7: What was the event rate in the CEA group for the primary endpoint?

Q8: What was the P-value for noninferiority between stenting and CEA?

Q9: What were the 30-day stroke and death rates among asymptomatic patients for CAS and CEA?

Q10: Were there any differences between CEA and CAS at 3 years?

Q11: How many high surgical risk (HSR) patients are generally included in contemporary registry data?

Q12: What stenosis levels define symptomatic and asymptomatic patients in these registries?

Q13: Which procedure is preferred for stroke prevention in HSR patients with suitable anatomy?

Q14: What is required for a patient to be treated with CAS according to registry data?

Q15: What is the significance of operator experience in CAS for HSR patients?

Study These Flashcards

A1: CEA versus CAS in high surgical risk patients

A2: About 334

A3: >50% stenosis for *symptomatic, >80% for *asymptomatic

A4: Approximately 30%

A5: Death, stroke, or MI at 30 days and ipsilateral stroke or neurologic death up to 1 year

A6: 12.2%

A7: 20.1%

A8: 0.004

A9: 4.6% for CAS, 5.4% for CEA

A10: No differences

A11: Over 10,000

A12: Symptomatic >50%, asymptomatic >70%-80% stenosis

A13: CAS. *It is apparent that in HSR patients who require revascularization for stroke prevention, CAS is the preferred procedure in patients who can be treated by an experienced operator and have suitable anatomy for CAS.

A14: Suitable anatomy and experienced operator

A15: It is critical for successful treatment

Q1: Five large ________ in average- or low surgical risk patients have compared ________ to CEA. Q2: Three of these trials were conducted in ________, although procedural standards were compromised by allowing very inexperienced ________ operators to participate. Q3: The EVA-3S trial randomized *symptomatic patients with carotid stenosis of greater than ________% to either CEA or CAS. Q4: All patients had ipsilateral neurologic symptoms within ________ days of enrollment. Q5: The use of embolic protection devices (EPDs) was ________ in the EVA-3S trial. Q6: The EVA-3S study was ________ early. Q7: The 30-day incidence of stroke or death was ________% in the CAS group and ________% in the CEA group. Q8: The SPACE trial randomized ________ *symptomatic average surgical risk patients to either CEA or CAS. Q9: The use of embolic protection devices was ________ in the SPACE trial. Q10: The 30-day rate of ipsilateral stroke or death was not different between the two groups (______% CAS vs ________% CEA). Q11: The 2-year outcomes demonstrated a statistically significant benefit for CAS over CEA in patients younger than ________ years of age.

A1: RCTs, CAS A2: Europe, CAS A3: 60% A4: 120 days A5: optional A6: terminated A7: 9.6, 3.9 A8: 1214 A9: optional A10: 6.8, 6.3 A11: 68

Q1: The International Carotid Stenting Study (ICSS) enrolled over ________ symptomatic patients. Q2: Patients in ICSS were randomized to either ________ or CEA. Q3: Use of embolic protection devices (EPDs) in ICSS was ________. Q4: To qualify as an experienced center, a surgeon had to have performed ________ CEA procedures. Q5: An interventionalist had to have performed ________ CAS procedures to qualify as experienced. Q6: Less experienced centers were tutored until considered ________ by their proctor. Q7: Centers were upgraded to experienced after randomizing ________ patients with acceptable outcomes. Q8: Patients were assigned to CAS or CEA in a ________ fashion. Q9: Median follow-up duration in ICSS was ________ years. Q10: The 5-year risk of fatal or disabling strokes did not differ significantly between CAS and CEA groups, being ________% vs ________%. Q11: The CREST trial included ________ patients. Q12: CREST included ________ symptomatic and ________ asymptomatic patients. Q13: The primary outcome of periprocedural stroke, death, or MI or follow-up ipsilateral stroke was ________ between CAS and CEA in CREST. Q14: The 30-day risk of all stroke was higher for ________ in CREST. Q15: CAS appeared safer than CEA for patients younger than ________ years of age.

A1: 1700 A2: CAS A3: Optional A4: 50 A5: 10 A6: Proficient A7: 20 A8: 1:1 A9: 4.2 A10: 6.4, 6.5 A11: 2502 A12: 1321, 1181 A13: Not significantly different A14: CAS ( CEA was associated with a higher 30-day risk of MI ) A15: 69 y/o ( CEA yielded better outcomes in those >70 years of age )

Q1: CREST differed from previous trials by requiring more ________ CAS operators. Q2: EVA-3S required operators to perform at least ________ CAS procedures. Q3: ICSS required operators to perform at least ________ CAS procedures. Q4: Which trial had no minimum number of carotid stenting procedures required for operators? Q5: CREST mandated the use of ________, unlike other trials. Q6: What percentage of patients in CREST were symptomatic? Q7: The other trials enrolled patients who were *entirely ________. Q8: The Asymptomatic Carotid Trial enrolled patients with average surgical risk and ________ carotid stenosis. Q9: CAS was ________ to CEA regarding death, stroke, or MI within 30 days or ipsilateral stroke within 1 year in the Asymptomatic Carotid Trial. Q10: What were the rates of stroke or death within 30 days for CAS and CEA in the Asymptomatic Carotid Trial? Q11: Was there a significant difference in stroke or death rates within 30 days between CAS and CEA? Q12: What was the freedom from ipsilateral stroke from 30 days to 5 years in the CAS group? Q13: What was the freedom from ipsilateral stroke from 30 days to 5 years in the CEA group? Q14: Was there a significant difference in freedom from ipsilateral stroke between CAS and CEA groups? Q15: What do the results highlight about the importance of operator experience in carotid stenting?

A1: experienced ( The value of experience cannot be overstated ) A2: five A3: ten A4: SPACE A5: embolic protection devices (EPDs) A6: just over 50% A7: symptomatic A8: asymptomatic A9: noninferior A10: 2.9% for CAS and 1.7% for CEA A11: No (P = .33) A12: 97.8% A13: 97.3% A14: No (P = .51) A15: Critical importance for procedural success and patient outcomes

Q1: What is CAS considered an alternative to in average surgical risk patients? Q2: What is required for CAS to be properly performed? Q3: Name one society that urged CMS to update coverage for CAS. Q4: Which patient groups are now included in CMS coverage for CAS? Q5: When did CMS expand coverage to include FDA-approved carotid stents? Q6: What is the minimum *symptomatic carotid stenosis percentage for CAS coverage? Q7: What is the minimum *asymptomatic carotid stenosis percentage for CAS coverage? Q8: Who must conduct the neurological assessment before and after CAS? Q9: What are the first-line imaging methods for evaluating carotid stenosis? Q10: What imaging is used if noninvasive imaging results are discrepant? Q11: Which surgical risk group was added to CAS coverage by CMS? Q12: What facility requirement did CMS remove for CAS providers? Q13: What must facilities maintain to support a carotid stent program? Q14: What is the role of institutional oversight committees? Q15: Why must facilities ensure appropriately trained staff? Q16: What type of program must facilities maintain to ensure patient safety? Q17: What process is emphasized before offering CAS to patients? Q18: Who has discretion over CAS coverage for non-covered indications? Q19: What is the goal of reducing prior barriers to CAS access? Q20: How do recent data describe CAS compared to CEA in terms of safety and efficacy?

A1: Carotid endarterectomy (CEA) A2: Experienced operators A3: Multispecialty Carotid Alliance (MSCA) A4: Asymptomatic and standard surgical risk patients A5: Late 2023 A6: ≥50% stenosis A7: ≥70% stenosis A8: Neurologist or NIHSS-certified health professional A9: Duplex ultrasonography, computed tomography angiography (CTA), magnetic resonance angiography (MRA) A10: Intra-arterial digital subtraction angiography (DSA) A11: Standard surgical risk individuals A12: Formal facility approval requirement A13: Institutional and physician standards for carotid stent programs A14: Identify minimal case volume and monitor complications A15: To fulfill roles and responsibilities for the program A16: Active quality improvement program A17: Formal shared decision-making A18: Medicare Administrative Contractors A19: To improve access and recognize safety and efficacy of CAS A20: Comparable safety and efficacy to CEA

Q1: What imaging is commonly performed coincident with CTA visualization of extracranial and intracranial vessels? Q2: Why is noninvasive CTA of the aortic arch important before endovascular access? Q3: What is mandatory if noninvasive CTA evaluation is not performed before endovascular therapy? Q4: What anatomical features are identified by aortography at the time of endovascular therapy? Q5: In what projection is an arch aortogram performed to *elongate the arch? Q6: What is the purpose of performing the arch aortogram in the LAO projection? Q7: After determining the aortic arch morphology, what is chosen for selective angiography? Q8: Which arteries are targeted in selective angiography for cerebral vasculature? Q9: What catheters are often used for a type I aortic arch? Q10: Which catheter shapes are used for type II or III arch morphologies? Q11: Why do Shepherd’s crook-shaped catheters require expertise? Q12: Name two examples of Shepherd’s crook-shaped catheters. Q13: What does CTA stand for in vascular imaging? Q14: What is the significance of identifying vertebral artery origin in aortography? Q15: How does arch type influence catheter selection in cerebral angiography?

A1: Noninvasive computed tomography angiography (CTA) A2: To identify high-risk or prohibitive proximal anatomy before endovascular access A3: Aortography at the time of endovascular therapy A4: Arch type, vertebral artery origin, and congenitally aberrant anatomy A5: 30° to 45° left anterior oblique (LAO) projection A6: To elongate the arch and optimize identification of cervical vessel ostia A7: Catheters for selective angiography of cervical arteries A8: Right and left carotid arteries and vertebral arteries (VAs) A9: Berenstein, angled taper, or Judkins Right (JR) catheters A10: Shepherd’s crook-shaped catheters (e.g., Simmons or Vitek) A11: Due to particular mechanisms of use requiring expertise A12: Simmons and Vitek catheters A13: Computed tomography angiography A14: It helps in planning endovascular access and intervention A15: Different arch types require different catheter shapes for optimal vessel selection

Q1: Historically, which vascular access approach has been the choice for most transcatheter interventions including CAS? Q2: Which approach has become increasingly popular for coronary interventions? Q3: What is the primary benefit of the transradial approach compared to transfemoral? Q4: In which patients should transradial CAS be considered? Q5: What imaging modalities are helpful for preprocedure planning of transradial CAS? Q6: Why is the right radial approach technically more difficult in *type I aortic arch? Q7: What percentage of patients in the CREST-2 Registry underwent transradial CAS? Q8: Were there significant differences in major access-related complications between transradial and transfemoral access in CREST-2? Q9: What was transradial CAS associated with regarding general anesthesia use? Q10: What was transradial CAS associated with regarding distal embolic protection device (EPD) use? Q11: What is another access option besides transradial and transfemoral for CAS? Q12: How do vascular access complications compare between transbrachial and transradial access? Q13: When should transradial and transbrachial approaches be avoided? Q14: What artery’s patency is important before considering transradial access? Q15: What anatomical variation can complicate transradial CAS?

A1: Transfemoral A2: Transradial A3: Lower vascular access complications A4: Patients with **“bovine” or type III aortic arches, tortuous, severely stenosed, aneurysmal, calcific, or unfavorable iliofemoral/aortic anatomy A5: Computed tomography angiography (CTA) or magnetic resonance angiography (MRA) A6: Because right radial approach for left CCA cannulation is more difficult A7: 3.8% A8: No significant differences A9: Lower general anesthesia use A10: Higher use of distal EPD A11: Transbrachial A12: Higher vascular access complications with transbrachial A13: Absence of patent ipsilateral ulnar artery or challenging aortic arch variation A14: Ipsilateral ulnar artery A15: Aberrant right subclavian artery

Type I Aortic Arch: The origin of the great vessels (brachiocephalic artery, left common carotid artery, left subclavian artery) is at the same horizontal level or slightly above the top of the aortic arch. This type has a relatively short distance from the arch to the origin of the vessels, making catheter navigation easier. Type II Aortic Arch ( vessels origins are skewed to the middle ) : The origin of the great vessels is between 1 and 2 cm below the top of the aortic arch. The arch is more elongated compared to type I, causing a slightly more challenging catheter path. Type III or bovine Aortic Arch ( vessels origins are skewed to the right ) : The origin of the great vessels is more than 2 cm below the top of the aortic arch. This is the most elongated and tortuous arch type, often making catheterization more difficult due to increased distance and angulation.

Q1: Which catheters can be used from the right radial approach to engage the right common carotid artery (CCA)? Q2: Which catheter is used to engage the left CCA in patients with a *bovine type arch from the right radial approach? Q3: What is the technique to engage the left CCA from the right radial approach in patients without aberrant anatomy? Q4: Where is the 0.035″ guidewire ideally looped during left CCA engagement? Q5: After positioning the guidewire, how is the catheter manipulated to engage the left CCA? Q6: What is the role of LAO angulation aortography and roadmap imaging in transradial CAS? Q7: How should Simmons catheters be manipulated during engagement and disengagement? Q8: How does engagement from the left radial artery compare to the femoral approach? Q9: What types of catheters are used from the left radial artery for CAS? Q10: What is the typical size of the incision for transradial CAS hemostasis? Q11: What is the benefit of the transradial approach in CAS? Q12: How is hemostasis achieved after transradial CAS? Q13: What is the significance of imaging the nontarget CCA and ICA first during transradial CAS? Q14: What is the typical shaft length difference between Enroute balloon/stent delivery systems and transfemoral equipment? Q15: What is the purpose of retracting the guidewire into the Simmons 2 catheter during left CCA cannulation?

A1: JR 4, multipurpose, internal mammary, Kimny, or Simmons 2 catheters A2: Simmons 2 catheter A3: Looping a 0.035″ guidewire in the sinus of Valsalva ( ideally the noncoronary cusp) with the tip of the guidewire extending superiorly toward, or stationed in, the transverse aorta and manipulating the catheter over it. A4: Noncoronary cusp A5: The catheter is brought down over the guidewire until it points superiorly , the guidewire is retracted to allow shaping, then the system is retracted to engage the ostial left CCA. Thereafter, the guidewire is advanced into the CCA, the catheter advanced over it onto the proximal-to-mid CCA. **Alternatively, from the right radial approach, the guidewire can be placed in the descending aorta, a Simmons 2 catheter advanced until the tip is in the proximal distal aorta (pointing toward the transverse aorta), and then the guidewire retracted into the Simmons 2 catheter at which point it will be shaped and can be used to directly canulate the left CCA (often with counter clockwise torque of the catheter). A6: They help in cannulating both CCAs via transradial approach A7: *Pulled back to engage/dive into a vessel and torqued plus *pushed to disengage. Simmons catheters should be manipulated in a similar fashion as Amplatz curve coronary catheters: *pulled back to engage/dive into a vessel and *torqued + pushed to disengage from a vessel. A8: It is similar, using double-curve catheters like Simmons or Newton A9: Double-curve catheters such as Simmons and Newton A10: Hemostasis is achieved in standard transradial fashion, typically with a patent hemostasis technique A11: Reduced vascular complications and improved patient comfort A12: Using patent hemostasis techniques A13: To ensure safe and effective navigation during the procedure A14: Enroute systems have shorter shaft lengths (~57 cm) compared to transfemoral equipment (~135 cm) A15: To shape the catheter for direct cannulation of the left CCA

Q1: Why has demonstrating clinical benefit for any embolic protection device (EPD) in CAS been difficult in randomized controlled trials? Q2: What is the catastrophic potential associated with iatrogenic embolization during CAS? Q3: What do contemporary CAS trials that utilize EPDs show regarding outcomes? Q4: How many meta-analyses support the use of EPDs? Q5: What anecdotal evidence supports the empirical benefits of EPDs? Q6: What is an alternative to distal embolic protection? Q7: What is the name of the only commercially available *proximal protection device in the United States? Q8: What two balloons does the Mo.Ma system consist of? Q9: Where is the proximal balloon of the Mo.Ma system inflated? Q10: Where is the distal balloon of the Mo.Ma system inflated? Q11: What happens to blood flow through the ICA when the Mo.Ma balloons are inflated? Q12: What size wire is used to advance the sheath and deflated ECA balloon into the external carotid artery? Q13: What is done once patient tolerance of balloon occlusion is confirmed in the Mo.Ma procedure? Q14: Can a distal EPD be used in conjunction with the Mo.Ma system? Q15: What were the procedural success rate and 30-day death and stroke rate reported in a registry using the Mo.Ma device?

A1: Because of the very low incidence of stroke complicating CAS A2: Catastrophic potential of iatrogenic embolization A3: Improved outcomes and mandate for EPD use in optimal practice A4: Two ( one has failed to show benefit ) A5: Retrieving a filter full of debris during the procedure A6: Proximal protection A7: Mo.Ma system ( proximal ) A8: A proximal balloon and a distal balloon A9: Common carotid artery (CCA) A10: External carotid artery (ECA) A11: Blood flow through the internal carotid artery (ICA) is arrested A12: 0.035-inch stiff wire A13: The internal carotid lesion is crossed with a 0.014-inch wire, dilated, and stented A14: Yes, typically deployed before Mo.Ma balloons are inflated A15: 99.7% procedural success; 1.38% 30-day death and stroke rate !! Maybe : The distal embolic protection device (EPD) is placed inside the internal carotid artery (ICA), **beyond (distal to) the carotid artery stenosis ( closer to the brain and distal from the access site). The proximal ( more proximal to the access ite ) device usually consists of balloons inflated in the CCA and ECA to temporarily block blood flow **before the lesion. This stops antegrade blood flow through the internal carotid artery (ICA), preventing embolic debris from traveling toward the brain during the procedure. Blood flow is often reversed through the sheath, directing it away from the brain, usually into the venous system.The goal is to provide embolic protection by halting or reversing flow before the lesion, unlike distal devices that capture debris after it passes the lesion.

Q1: What is the standard of care in the United States for carotid artery stenting? Q2: What should be done if the embolic protection device (EPD) cannot cross the lesion? Q3: What size balloon is used for predilation before placing the EPD? Q4: After distal EPD deployment, what size balloon is typically used for predilation? Q5: What type of stent is placed across the lesion after predilation? Q6: The stent covering the origin of the internal carotid artery (ICA) is typically sized to fit which artery? Q7: Is there demonstrated benefit for using tapered stents? Q8: When treating an internal carotid bifurcation lesion, where is the stent typically placed? Q9: What are the three types of self-expanding stents? Q10: Which stent type is more flexible and better for navigating tortuous vessels? Q11: Which stent type is more rigid but offers better plaque coverage? Q12: Is there consistent evidence linking stent design to embolic complications in symptomatic patients? Q13: Name the three leading *dual-layered carotid stents. Q14: What are the two layers in dual-layered stents designed for? Q15: What have studies shown about CAS performed using dual-layered stents?

A1: Embolic protection devices (EPDs) A2: Cross the lesion with a 0.014-in guidewire and predilate with a small balloon A3: 2.5 mm A4: 3 to 4 mm coronary balloon A5: Self-expanding stent A6: Common carotid artery (CCA) A7: No A8: Across the ostium of the external carotid artery A9: Closed cell, open cell, and *dual layered A10: Open-cell stents A11: Closed-cell stents A12: No, findings are inconsistent A13: Scafford (W.L. Gore and Associates), Roadsaver (Microvention), CGuard (Inspire-MD) A14: External self-expanding layer for scaffolding; internal micromesh layer for plaque coverage A15: Encouraging results

Q1: What are the typical stent sizes in diameter and length used in carotid artery stenting? Q2: What size balloon is often used for gentle postdilation to improve stent apposition? Q3: Is aggressive postdilation beneficial in carotid artery stenting? Q4: Why are balloons conservatively sized (<1:1) during postdilation? Q5: What is considered an acceptable poststent carotid diameter stenosis result? Q6: What vagal responses can occur when pressure is applied to the carotid bulb? Q7: When do vagal responses most frequently occur during carotid stenting? Q8: What is the immediate treatment for vagal responses during stent postdilatation? Q9: What additional therapies may be required if vagal responses persist? Q10: What must be done carefully when retrieving a filter-type embolic protection device (EPD)? Q11: What could happen if the EPD basket collapses during retrieval? Q12: What maneuvers may assist in withdrawing the EPD if gentle traction is insufficient? Q13: What imaging is performed after removal of the EPD? Q14: What is done after aspiration and balloon deflation with a proximal protection device? ( aspiration is required by the manufacturer when a proximal EPD is used ) Q15: What neurologic assessments should be performed *prior to equipment removal?

A1: 6 to 10 mm in diameter and 2 to 4 cm in length A2: ≤5 mm balloon A3: No, there is no benefit to aggressive postdilation ( restenosis and late loss are rare with carotid arteries ) A4: To minimize vessel trauma, dissection, plaque embolization, and carotid sinus stimulation A5: <50% diameter stenosis A6: Profound hypotension, bradycardia, and heart block A7: During stent postdilatation A8: Immediate administration of IV atropine A9: Continuous chronotropic therapies or temporary pacemaker placement A10: Ensure the EPD basket is captured sufficiently to avoid collapse A11: Forced embolization of captured debris A12: Manipulation of the sheath or rotation of the neck A13: Final carotid and cerebral angiography A14: Final angiography is performed after balloon deflation and aspiration A15: Speech, movement, and mental status assessment !! It is critical that prior to wiring or manipulation within any supra-aortic vessel that therapeutic anticoagulation (goal ACT >250 seconds) is achieved and maintained throughout the case. Furthermore, meticulous aspiration technique must be utilized, especially since *larger equipment (eg, CAS delivery systems) will *entrain air within the system while being delivered to the target vessel.

Stent partially protruds into the aorta. Postdilation with Ostial flash balloon.

Q1: What physiological structure’s stimulation is common during carotid interventions and can cause hypotension and bradycardia? Q2: How do patients sensitive to predilation typically react? Q3: What can acute hypotension lead to in the brain? Q4: What precaution is advised regarding antihypertensive medications on the morning of intervention? Q5: What medications may be used to treat acute bradycardia during carotid interventions? Q6: When might a prophylactic dose of atropine be considered? Q7: What are two risks associated with prophylactic atropine use? Q8: What should be considered if more than 2 mg of IV atropine has been administered? Q9: What measurement is reasonable to obtain prior to aortography to help guide fluid management? Q10: Why might operators obtain routine venous access during carotid interventions? Q11: What is important in treating hypotension during the procedure? Q12: What vasopressor medication can be given in repeated boluses to treat hypotension? Q13: When might a continuous infusion of vasopressors be required? Q14: How soon can phenylephrine typically be weaned after the procedure? Q15: What medication can support blood pressure in prolonged hypotension and how is it dosed?

A1: Carotid sinus baroreceptor A2: They react negatively, often with hypotension and bradycardia A3: Brain hypoperfusion and neurologic symptoms A4: Holding baseline antihypertensive medications is prudent A5: Atropine (0.4 to 1 mg) or glycopyrrolate A6: Before stent deployment if patient was sensitive to predilation A7: Urinary retention in men and worsening of acute angle glaucoma A8: Alternative parenteral inotropes or vasopressors should be considered A9: Left ventricular end-diastolic pressure A10: To minimize delay when fluid or vasopressor administration is needed A11: Aggressive fluid administration A12: Phenylephrine (25 to 50 µg boluses) A13: If hypotension persists despite boluses ( always keep SBP > 100 mmHg ) A14: Within several hours of the procedure A15: Midodrine 2.5 to 10 mg three times daily, titrated downward as tolerated ! Access site bleeding is a common cause of hypotension and should not be overlooked in the setting of postprocedural hypotension.

Q1: What can the opening of a stenotic carotid artery lead to in terms of cerebral blood flow? Q2: What syndrome occurs in less than 1% of carotid stent patients and is characterized by ipsilateral headache, seizure, or focal neurologic deficit? Q3: Why does a chronically stenotic carotid artery cause cerebral vasculature to remain in a state of maximal vasodilation? Q4: What happens to cerebral autoregulatory mechanisms when stenosis is suddenly alleviated? Q5: What condition exacerbates the failure of cerebral autoregulation after carotid stenosis relief? Q6: What can elevated cerebral perfusion pressure lead to? Q7: Are neurologic symptoms from cerebral edema usually transient or permanent? Q8: What imaging should be obtained if cerebral edema is suspected? Q9: What is critical in managing hyperperfusion syndrome? Q10: Name two medications that should be avoided because they **cause cerebral venous vasodilation. Q11: What medication is preferred for blood pressure control during the procedure if the patient is bradycardic? Q12: What medication is preferred if the patient is not bradycardic? Q13: Which infusion medication is preferred for blood pressure control in this context? Q14: What should be done if intracranial bleeding occurs? Q15: What is the recommended goal systolic blood pressure to reduce the risk of hyperperfusion syndrome and intracranial bleeding?

A1: Significant increases in cerebral blood flow, sometimes more than twice preprocedure flow A2: Hyperperfusion syndrome A3: Because of chronic maximal vasodilation due to stenosis A4: They fail to control blood flow A5: Hypertension (HTN) A6: Cerebral edema or intracranial hemorrhage (ICH) A7: Usually transient A8: Neurology consultation and head CT A9: Strict blood pressure control A10: **Nitroprusside and nitroglycerin A11: Hydralazine IV pushes A12: Labetalol A13: Nicardipine A14: Stop antiplatelet medications and consult neurosurgery A15: 120-140 mm Hg may decrease the risk of hyperperfusion syndrome

Q1: After carotid artery revascularization, what should patients be monitored for? Q2: What type of imaging surveillance is recommended following carotid intervention? Q3: When is the baseline Doppler ultrasound (DUS) recommended to be performed post-intervention? Q4: At what intervals should DUS studies be repeated after the baseline? Q5: How are carotid DUS velocities affected after stenting? Q6: What common **issue occurs with stenosis severity estimation by DUS after stenting? Q7: Why is the baseline DUS within 1 month post-intervention especially important? Q8: How does the baseline DUS ( 1 month ) compare to standard nonrevascularized carotid DUS criteria?

A1: Continuation of best medical therapy and monitoring for focal neurologic symptoms A2: Doppler ultrasound (DUS) surveillance A3: Within 1 month of intervention A4: At 6 months, 12 months, and yearly thereafter A5: They are altered A6: Overestimation of stenosis severity is very common A7: It serves as a comparator for any changes in stenosis severity A8: It is more meaningful compared to standard criteria in nonrevascularized patients

vertebral artery interventions

SCAI KERN CHAP 35 Carotids and Vertebrals Flashcards

(41 cards)