Carotid Artery Disease Flashcards

1
Q

What are the pathologies that can be found on a Duplex scan ?

A
  1. Stenosis.
  2. Carotid Body tumor
  3. Dissection
  4. aneurysma
  5. reversal of flow in the vertebral artery
  6. Arteritis
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2
Q

What are the elements of the work up for a patient with asymptomatic carotid stenosis ?

A
  1. History should be directed at identifying risk factors and prior ischemic events.
  2. Physical examination should note signs of cardiac and systemic vascular disease, including assessment of peripheral pulses, signs of prior clinical stroke.
  3. Carotid duplex
  4. CTA or MRA
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3
Q

Why do we not use Angiographie for diagnosis anymore ?

A

In the ACAS study, diagnostic Angios were associated with 1.2% risk of stroke.

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4
Q

What are the indications for CTA, MRA or Angio ?

A
  1. Symptoms dont correlate with the extent of carotid disease.
  2. The top of the plaque is not visualised.
  3. the vessel is extremely tortuous.
  4. The ipsilateral carotid is occluded.
  5. high carotid bifurcation
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5
Q

What is the Evidence for CEA ?

A
  1. VA trail (444 Patients)
    significantly lower incidence of stroke and TIA in the surgery group 8% vs 20.6%
  2. ACAS trial (1662 Patients) Surgery vs BMT (mit Aspirin)
    significantly lower incidence of ipsilateral stroke and any perioperative stroke or death in the surgery group (5% vs 11%)
  3. ACST (3120 Patients) immediate surgery vs deferral group
    5 year risk reduction of all stroke or perioperative death in immediate CEA group vs deferral group (6.4 % vs. 11.8)
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6
Q

When is CEA indicated in asymptomatic patients ?

A

Stenosis of at least 60 % in arteriography or greater than 70% by carotid duplex.

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7
Q

What is the evidence about CEA vs. CAS ?

A

The Carotid Revascularization Endarterectomy vs. Stenting Trial (CREST) 2502 Patients
The CEA group had a higher incidence of periprocedural MI (2.3 vs 1.1)
The CAS group had a higher incidence of periprocedural stroke (4.1 vs. 2.3%)

There is lack of level I evidence comparing either CEA or CAS versus current best medical therapy.

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8
Q

What does BMT in asymptomatic Carotid stenosis include ?

A

Antiplatelets and agressive risk factor modification (Hypertension, Diabetes, Smoking cessation, Hyperlipidemia)

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9
Q

When is Dual anitplatelet therapy recommended ?

A

It is only reserved for patients with other reasons to be on them, such as recently placed coronary stents, who also additionally have asymptomatic carotid stenosis.

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10
Q

When is anticoagulation with warfarin or NOAKs recommended ?

A

Only if patients have other indications for anticoagulation.

Evidence : WARSS investigators performed a subgroup analysis on patients with stroke and large artery stenosis/occlusion and found no beneficial effect seen with warfarin over anti platelet agents.

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11
Q

Whats the benefit of statins ? Where is the evidence ?

A
  1. decreasing the incidence of ischemic stroke by 22% (SPARCL trial)
  2. Two separate meta-analysis showed a 20 to 22% ischemic stroke risk reduction with use of statin therapy.
  3. In diabetic patients 37% reduction in cardiovascular ischemic events and a 48% reduction in ischemic stroke (CARDS trial)
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12
Q

Whats the benefit of ACEIs and ARBs ? Where is the evidence ?

A
  1. Ramipril significantly lowered ischemic stroke, cardiovascular events, and death in high risk cardiovascular patients (HOPE trial).
  2. Losartan significantly reduced cardiovascular events (LIFE trial)
  3. Candesartan significantly reduced non fatal strokes (SCOPE trial)
  4. When ARBs were compared to Ca channel blockers, there was significant reduction in cardiovascular events especially ischemic stroke although both drugs equally lowered Blood pressure. (MOSES trial).
  5. 9% greater reduction in primary stroke in patients on ARBs compared to those on ACEIs (ONTARGET trial)
  6. Meta-analysis from six controlled trials comparing ARBs with ACEIs showed that ARBs are even superior in stroke reduction.
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13
Q

Whats the effect of controlling hypertension ?

A
  1. Decreasing BP by 10 mm Hg can decrease stroke incidence up to 33%.
  2. A meta-analysis of 7 RCTs showed a 24% reduction in stroke with the use of an antihypertensive.
  3. Systolic hypertension in elderly Program (SHEP) and Framingham heart study (FHS) showed that BP is directly related to the progression of carotid stenosis.
  4. Patients with ischemic stroke who received a combination of perindopril and indapamide showed a 28% risk reduction in recurrence ischemic events. (PROGRESS trial).
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14
Q

How do we protect diabetes patients with carotid atherosclerosis ?

A
  1. All patients should receive education on exercise, diet and glucose-lowering medication.
  2. All patients should be treated with statin regardless of baseline lipid levels as the CARDS trial has shown to reduce overall cardiovascular risk by 37% and stroke risk by 48%.
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15
Q

How do we help smokers ?

A
  1. current guidelines recommend that at every visit, the vascular physicians should ask his or her patients about history of smoking and their current smoking status.
  2. Smokers should be assisted with counselling and developing a plan for quitting that may include pharmacotherapy and/or referral to a smoking cessation program.
  3. In absence of contraindications pharmacologic therapies are strongly recommended.
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16
Q

What are medications that help smokers to quit ?

A
  1. Vareniclin.
  2. Bupropion.
  3. Nicotine Replacement Therapie
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17
Q

Whats the current guidelines take on statins and a target LDL ?

A

Previous guidelines recommended treating target LDL levels, however, this is no longer recommended, and statins are recommended for all patients with clinical atherosclerotic vascular disease.

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18
Q

How does smoking and diabetes affect the risk of ischemic stroke

A

The risk of ischemic stroke is increased 2-5 fold among patients with diabetes.

Smoking increases the risk of ischemic stroke by 25-50%

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19
Q

What are causes of TIA ?

A
  1. Embolisation from a stenotic ICA (Most common cause)
  2. Embolisation from a a cardiac source (atrial thrombus, valvular vegetative disease, atrial fibrillation)
  3. Carotid dissection, carotid kink or coils.
  4. aneurysms of extra cranial carotid arteries
  5. Paroxysmal arterial embolie.
20
Q

What are types of TIA ?

A
  1. TMB : Temporary monocular blindness (amaurosis fugax)
  2. Lateralizing TIAs : weakness or parasthesia that affect the contralateral body.
21
Q

When is an emergent operation indicated ?

A
  1. Crescendo TIA: when a patient experiences frequent repetitive neurologic attacks without complete resolution of the deficit between episodes, producing the same deficit but no progressive deterioration in neurologic function.
  2. Stroke in evolution : If a progressive deterioration in neurologic function is seen.
22
Q

When do we prefer angiography to duplex ?

A
  1. proximal common carotid or aortic arch lesions.
  2. contralateral carotid occlusion
  3. high bifurcation of the carotid
  4. discrepancy in symptoms compared to the duplex findings.
23
Q

What is the benefit of CEA in symptomatic patients ?

A
  1. 17% absolute risk reduction of stroke.
  2. 71 % relative risk reduction of at 18 months for surgery and antiplatelet therapy compared to antiplatelet therapy alone.
24
Q

What are the risks in CEA in symptomatic patients ?

A
  1. Death 0,6 %
  2. Stroke 1 %
  3. Cranial nerve injury less than 1 %
  4. wound complications less than 0,01 %
  5. Bleeding less than 0,01 %
  6. Restenosis 5 %
25
Q

Whats the initial mortality of an ischemic stroke ?
Whats the risk for recurrent stroke ?

A

intial mortality of an ischemic stroke is 15-30%.

Survivors have a high risk of recurrent stroke 5-15 % per year, 50 % will suffer a second ischemic incident within 5 years.

26
Q

What did NASCET do ? What were the results ?

A

compared CEA + BMT to BMT alone.

30-day operative morbidity and mortality for patients managed with CEA of 5 %.

At 18 months, 7% incidence of major stroke occurred in the surgical arm of the trial, compared to a 24 % incidence of major stroke in the medical arm.

27
Q

CEA vs CAS in symptomatic stenosis what does the evidence tell us ?

A

CREST showed more devastating strokes in CAS patients than in CEA patients.

28
Q

When is the best time to operate patients with permanent stroke ?

A

In a patient whose neurological deficit has stabilised, as soon as possible within the first week after stroke.

29
Q

Whats the differential for the cause of an ipsilateral acute stroke after CEA ?

A
  1. Intracerebral hemorrhage
  2. Watershed infarction
  3. hypoperfusion intraoperatively or postoperatively.
  4. Hyperperfusion
  5. Embolisation of atheromatous plaque or thrombus occurring intraoperatively.
  6. Embolisation occurring postoperatively with or without a technical defect at the endarterectomy site.
  7. Thrombosis of the endarterectomy site with or without a technical defect.
  8. HIT
  9. Kink in the artery resulting in low flow.
  10. Embolisation from a site other than the carotid bifurcation.
30
Q

Whats the first step to take in case of Stroke after CEA ?

A

Obtain a Duplex-Scan to determine the patency of the artery. If the duplex shows a patent artery with no defects, exploration could be harmful. Then obtain a head CT with Angio.

31
Q

How do we place the clamps in case of thrombosis of the ICA ?

A

The Clamps are only placed on ECA and CCA. The ICA should be allowed to back bleed into the field. If it doesn’t then you use an embolectomy catheter (Fogarty).

32
Q

What to do if there is no technical defect in the endarterectomy site at exploration ?

A

The presumed ethology of the thrombosis is fibrin and platelet aggregation and adhesion to the endarterctomized surface. If this is not replaced, the chance of rethrombosis is high. Thats why we recommend to interposition a saphenous vein graft. And postoperative antiplatelet therapy.

33
Q

How to treat patient with stroke after CEA medically?

A

Dual platelet with Aspirin and Clopidogrel for example.

34
Q

How often does acute stroke after CEA happen ?

A

1-2 %

35
Q

What to do when the patient wakes up after CEA under GA with a neurological deficit ?

A
  • The cause is likely an intraoperative hypoperfusion injury or an embolic event secondary to clamping or shunt placement.
  • Carotid Duplex should be undertaken to assess the patency of the ICA.
  • Reoperation is not recommended due to the potential of extending the ischemic are in the brain with any further clamping of the carotid artery.
  • The patient should be considered for a head CT and CT Angio with lytic salvage of any thromboses intracerebral vessels.
36
Q

What to do when the patient develops neurological deficit 1-2 days after CEA ?

A
  • The probable cause is a cerebral haemorrhage and/or edema secondary to hyperperfusion.
  • Hyperperfusion occurs in patients after repair of a high carotid artery stenosis or in patients who present with severe bilateral stenosis.
  • The symptom complex consists of hypertension, headache and seizures.
  • Diagnosis : CT or MRI of the head
  • Treatment: blood pressure and seizure control
37
Q

What to do when the patient after CEA has a lucid period than develops a neurological deficit ?

A
  • the most common cause is related to technical error that results in postoperative thromboembolism.
  • The cause of the neurologic deficit is usually not due to obstruction of blood flow or ischemia by the thrombus, but rather from embolisation of thrombus material as it was forming within the artery from embolisation originating at the distal extent of the thrombus.
  • Technical errors can and should be corrected; there is conclusive evidence to recommend decisive management in the treatment of post-CEA thrombosis.
  • if corrected in a timely fashion (1-2 hours), there is a high likelihood of significant neurologic recovery. Repair after this time, however, may convert a bland ischemic infarction into a hemorrhagic infarct.
  • Any decision not to perform a reoperation in the presence of delayed neurologic event should be supported by a study demonstrating a patent ICA without technical defects.
38
Q

What are the Secondary to errors or defect at the operative site that may lead to thromboembolism after CEA ?

A
  1. intimal flap
  2. irregularities at the suture lines
  3. kink caused by elongation after endarterectomy
  4. intramural hematoma
  5. constricting suture line
  6. clamp injury
  7. ledges at the end of the endarterectomy
  8. rough endarterectomy surface.
39
Q

Whats the rate of Recurrent carotid stenosis ?
How many of which are symptomatic ?

A

Recurrent carotid stenosis occurs in 8-19% of the cases of which 3 % are symptomatic.

40
Q

What are the factors that dictate the management of Carotid Restenosis ?

A
  1. length of time from index procedure to diagnosis of restonsis.
  2. presence/absence of clinical symptoms
41
Q

What are the causes of carotid restenosis ?

A
  1. within the immediate postoperative period : residual disease/technical failure.
  2. with the first 36 months : neointimal hyperplasia
  3. after 36 months : progressive or new atherosclerotic disease
42
Q

What are risk factors for carotid restenosis ?

A
  1. age less than 60
  2. female sex
  3. smoking
  4. diabetes
  5. hypertension
43
Q

Which cases of post-CEA restenosis should be treated surgically ?

A
  1. asymptomatic greater than 80%
  2. symptomatic 50 % or more
44
Q

When is CAS recommended ?

A
  1. high risk patients with prior neck external beam irradiation
  2. prior neck dissections/tracheosotmies
  3. inaccessible lesions unnameable to CEA (above C2 level)
  4. limited cervical spine mobility
45
Q

How high is the risk of cranial nerve injury with redo CEA ?

A

18 %

46
Q

How many patients undergoing CEA have clinically relevant CAD and what is the most common cause of mortality ?

A

About 50 % of patients undergoing CEA have clinically relevant CAD

The most common cause of Death in these patients is myocardial death.

47
Q

Why is CTA or MRA essential to before doing CAS ?

A

To assess the anatomy and patency of the aortic arch, the supra-aortic vessels and circle of Willis.