Carotid INTRODUCTION

Carotid atherosclerotic disease

byMohammed Salah

Ass .lecturer –vas .surgery departmentAUH-assuit university

anatomyARCH &ICA

Anatomy: Aortic Arch Brachiocephalic trunk or

Innominate Artery (1) R common carotid artery R subclavian artery

Vertebral artery Left common carotid Artery (2) Left subclavian artery(3)

L vertebral artery

True in about 70% Common variant: L CCA

originating from innominate artery

12 3

Anatomy: Common Carotid Artery

Located anterolaterally in the neck and medial to the jugular vein

The carotid artery, jugular vein, and vagus nerve are enclosed in connective tissue - carotid sheath

Terminates as the carotid bifurcation Internal carotid artery (ICA) and External carotid artery (ECA) At the vicinity of the superior

border of the thyroid cartilage or approximately at the level of C4

Bifurcation has been described to be as low as T2 and as high as C1.

External Carotid Artery smaller of the two terminal

branches of the CCA Has 8 branches : the superior

thyroid, ascending pharyngeal, lingual, facial, occipital, posterior auricular, and the terminal branches, the superficial temporal, and the internal maxillary artery.

The abundant number of anatomoses between the branches of the ECA and the intracranial circulation provides important collateral pathway for cerebral perfusion when significant disease is present in the ICA

Internal Carotid Artery

The larger of the CCA terminal branches

Divided into 4 main segments: Cervical

begins at the CCA bifurcation and extends to the base of the skull

normally has a slight dilation, termed the carotid bulb and/or the carotid sinus

usually does not have branches

Petrous - inside the petrous part of the temporal bone

Internal Carotid ArteryCavernous

invested within the cavernous sinus

situated between the layers of the dura mater of the cavernous sinus, but covered by the lining membrane of the sinus

Cerebral – begins after the artery perforates the dura matter, passes between the optic and oculomotor nerves, then proceeds to the terminal bifurcation into

Segments and branches

the artery divided into four parts: "cervical",

"petrous",

"cavernous",

and "cerebral

Bouthillier classification of ICA segments

classification system of the internal carotid artery describing seven anatomical segments of the internal carotid artery.

The segments are subdivided based on anatomical and microsurgical landmarks and surrounding anatomy, more than angiographic appearance of the artery

The segments of the internal carotid artery are as follows:• Cervical segment, or C1, identical to the commonly used Cervical portion• Petrous segment, or C2• Lacerum segment, or C3

• C2 and C3 compose the commonly termed Petrous portion• Cavernous segment, or C4, almost identical to the commonly used 

Cavernous portion• Clinoid segment, or C5. This segment is not identified in some earlier

classifications, and lies between the commonly usedCavernous portion and Cerebral or Supraclinoid portion

• Ophthalmic, or supraclinoid segment, or C6• Communicating, or terminal segment, or C7

• C6 and C7 together constitute the commonly used Cerebral or Supraclinoid portion

Mnemonic for branches in skull: Please Let Children Consume Our Candy (first letter for each branch, in order).

The following are the branches of the internal carotid artery, listed by segment:C1: Branches from the cervical portion - none.

C2: Branches from the petrous portion1.Caroticotympanic arteries2.Artery of pterygoid canal (vidian artery)

C3: Branches from the lacerum portion - none

C4: Branches from the cavernous portion1.Branches of the meningohypophyseal trunk:

Tentorial basal branchTentorial marginal branchMeningeal branch - helps supply blood to the meninges of the anterior cranial fossaClivus branches - tiny branches that supply the clivus2.Inferior hypophyseal artery

Capsular branches - supplies wall of cavernous sinus3.Branches of the inferolateral trunk:

Branches to trigeminal ganglion - provide blood to trigeminal ganglionArtery of the foramen rotundumBranches to nerves

)

C5: Branches from the clinoid portion – none

C6: Branches from the ophthalmic portionOphthalmic arterySuperior hypophyseal artery

C7: Branches from the communicating portionPosterior communicating arteryAnterior choroidal arteryAnterior cerebral artery (a terminal branch)Middle cerebral artery(a terminal branch)

EPIDEMIOLOGY

EPIDEMIOLOGY

Stroke, or cerebral infarction, is the acute development of a focal neurologic deficit caused by the disruption of blood supply to an area of the brain. Strokes can be

I. ischemic, due to occlusion of a blood vessel ( the majority of strokes about 87%, are ischemic in etiology)

II. or hemorrhagic, due to rupture of a blood vessel. Hemorrhagic strokes include both intracerebral hemorrhage, which is bleeding within the brain parenchyma, and subarachnoid hemorrhage, which is bleeding in the subarachnoid space.(13%)

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY OF STROKE RELATED TOEXTRACRANIAL CEREBROVASCULAR DISEASE

Development of AtherosclerosisThe carotid bulb is the major site of involvement

Hemodynamic factors are thought to be involved in the predisposition of this particular location to the development of atherosclerotic plaque. Specifically segments with low wall shear stress and resulting flow stagnation, such as occurs in the carotid bulb, appear to be at increased risk.

Carotid artery plaque can cause TIA or stroke by two mechanisms: 1.embolization and 2.hypoperfusion.

EVALUATION OF CAROTID DISEASE

CLINICAL FINDINGS IN PATIENTS WITH

CEREBROVASCULAR DISEASE

1.TIAoften referred to as a ministroke, is a

neurologic event that manifests as stroke-like symptoms lasting less than 24 hours. In fact, the vast majority of these symptoms last for only a few minutes Symptoms of TIA or stroke resulting from carotid disease are related to the cerebral vascular territory affected.

Because the carotid artery supplies the anterior circulation, carotid disease can cause symptoms associated with injury to brain parenchyma of the anterior cerebral artery or MCA distribution

2.Stroke

stroke is defined as an acute neurologic dysfunction of vascular etiology with corresponding signs and symptoms lasting more than 24 hours and resulting from infarction of focal areas of the brain.

3.Global Ischemia

Global ischemia, or systemic hypoperfusion, represents only a small fraction of all ischemic strokes from carotid occlusive disease. Patients presenting with global ischemia often are brought unconscious to an emergency department or with symptoms resembling near syncope.

Evaluation of Patients with Carotid Disease – Carotid Artery Bruit

Hemodynamically significant stenotic lesions may exist in the absence of an audible bruit.

The absence of CAB may also signify complete occlusion of the carotid artery.

DUPLEX(D.U.S)

INVESTIGATION

Carotid Duplex Ultrasound

The degree of stenosis is determined by the velocity of blood flow through the artery

the higher the velocity, the greater the degree of stenosis

Carotid Duplex Ultrasound

Color doppler can demonstrate the area of stenosis with increased flow ( blue/ yellow flow pattern in this image)

B-mode can demonstrate the walls of the vessel and the area of stenosis

Limitations in Clinical Practice

(1) inability to image high bifurcations

(2) inability to image the proximal common carotid artery ( inflow stenosis)

(3) inability to image distal ICA suggesting a distal (tandem lesion)

D.U.S LIMITATION

4) the presence of a contralateral occlusion or very severe stenosis, because peak systolic velocity values may be increased in the contralateral ICA .

(5) excessive calcification (which prevents accurate velocity measurement because of acoustic shadowing).

(6) suspicion of subocclusion

(7) a patient being considered for CAS.

CT Angiography

MDCTA

CTA is a widely available imaging method and it has the advantage of high resolution and rapid acquisition times. 

Because it is a fast scan, image degradation due to patient motion is less common than with MRA

MDCTA

CTA relies on intraluminal contrast rather than signal changes due to blood flow So discriminate between occlusion from a hairline residual lumen.

CTA also shows surrounding anatomy, such as bony structures, which may be useful for surgical planning.

Digital Subtraction Angiogram

Limitations of CTA

heavy, circumferential calcification, which can cause artifacts that can result in over-estimation of stenosis.

Metal stents can also result in artifacts, although new post-processing techniques can minimize such problems. 

In addition, because CTA requires the administration of iodinated contrast, use in patients with chronic kidney disease is discouraged.

CTAUsed when US is not reliable:-Severe calcific artery-Severe kinking of the vessels-Short neck-High bifurcation-Overview of surgical field

MR Angiogram

LR

MRA

TYPES TOF MRA (time of flight )have limited

advantage over DUS .

CEMRA (contrast enhanced MRA) considered gold standard for carotid stenosis disease.

MR Angiogram 70% to 99% ICA stenoses

Time-of-flight MRA Sensitivity 91.2% Specificity

88.3% Contrast-enhanced MRA Sensitivity 94.6% Specificity 91.9%

ICA occlusion Time-of-flight MRA

Sensitivity 94.5% Specificity 99.3% Contrast-enhanced MRA

Sensitivity 99.4% Specificity 99.6% Moderate (50 to 69%) stenoses

Time-of-flight MRASensitivity 37.9% Specificity 92.1%

Contrast-enhanced MRASensitivity 65.9% Specificity 93.5%

Stroke. 2008;39:2237-2248

MRAMay be more Sensitive and Specific than US

(esp. CEMRA)Contrast-enhanced MRA appears to be the

most accurate non-invasive imaging modality and is regarded by some as the gold standard for visualizing occlusion in the ICA.

MRA also offers the advantage of being able to add concurrent brain imaging to the examination. 

much greater field of view that enables high-resolution imaging from the aortic arch up to the circle of Willis

the ability to also evaluate flow directionality.(STEAL$).

Another advantage of CEMRA is that it can be combined with MR functional brain imaging.

Disadvantage:Cannot be done if patient is

critically ill , or has a pacemaker.Expensive.Claustrophobia

Conventional angiographyGold standardVisualize the entire

cerebrovascular systemInvasive testExpensive testNeurological morbidity/mortality

Carotid trialsAsymptomatic/symptomatic carotid

atherosclerotic disease trials

Asymptomatic Carotid trials

ACAS Asymptomatic Carotid Atherosclerosis Study .

ACST European Asymptomatic Carotid Surgery Trial.

Both the ACAS and the ACST demonstrated a benefit of CEA with medical therapy over medical therapy alone for patients with carotid stenosis in the 60% to 99% range.

Both ACAS and ACST used duplex ultrasound criteria for determining the degree of carotid stenosis

Symptomatic carotid trialsNorth American Symptomatic Carotid

Endarterectomy Trial (NASCET).

European Carotid Surgery Trial (ECST).

Both using angiography to determine degree of

stenosis .

Carotid symptomatic trialNASCET and ECST also differed in the

angiographic determination of stenosis. In NASCET (as well as ACAS), the degree of

stenosis on angiography was determined by comparing the residual lumen at the narrowest point of stenosis with the lumen of the internal carotid artery (ICA) distal to the carotid bulb (i.e., distal to the point where the walls of the ICA first become parallel).

ECST used estimated bulb diameter as the denominator for determination of stenosis, which will overestimate the degree of stenosis relative to the ACAS/NASCET .

Management of carotid artery

stenosis

• Decision making

SUMMARY

All guidelines agree with the following recommendations:1. Symptomatic patients with angiographic

stenosis of less than 50% and asymptomatic patients with stenosis of less than 60% should not undergo intervention and are best treated by BMT.

In symptomatic patients with stenosis of more than 50 %are candidate for revascularization.

SUMMARY

In good risk patients with asymptomatic stenosis of more than 60%, revascularization may be recommended in addition to BMT for reduction of stroke risk as long as the combined stroke and death rates are less than 3%.

In asymptomatic patients at high risk for intervention, neither CAS nor CEA has been proven superior to BMT.

Recently, there has been an increasing argument to favor BMT as sole treatment in all neurologically asymptomatic patients regardless of the degree of carotid stenosis

Medical treatmentRisk factor modification

Smoking

.. Nicotine inhalation has been demonstrated to1- reduce high density lipoprotein (HDL) levels,

2- increase platelet aggregation,

3- decrease prostacyclin, increase levels of thromboxane, and promote vasoconstriction.

Each of these effects contributes to the development and progression of atherosclerotic process.

SMOKING CESSATION therapy

NRT buccal mucosa spray patch

1ST LINE DRUGS bupropion varenicline

2ND LINE nortriptyline clonidine

EMERGING THERAPY nicotine vaccine NICVAX

Diabetes Mellitus

The association between DM and atherosclerotic vascular disease is well documented.

Diabetes is an independent predictor of recurrent stroke and is associated with up to 9% of recurrent stroke.

Mechanism by which DM accelerate atherosclerosis

1- Alterations in nitric oxide availability to endothelial cells .

2- stimulation of proatherogenic activity in vascular smooth muscle cells by the reduction of phosphatidylinositol-3 kinase. 3- enhanced platelet aggregation.

4- increased blood viscosity, and elevation of fibrinogen levels .

DM

No benefit in stroke reduction or overall reduction in the rates of adverse cardiovascular events was seen with tight control; however, there was an increased mortality rate in the tight control group.

recommended levels of HgbA1c of less than 7.

Effect of hypertension on atheroscelorsis

BP control

Control of blood pressure has been shown to reduce the overall risk of stroke and risk of recurrent stroke in a number of studies.

in the first 24 hours after an acute stroke, where aggressive reduction of blood pressure should be avoided to optimize cerebral perfusion pressure.

There is no definitive benefit of one class of antihypertensive agents over another for stroke reduction.

HYPERLIPIDEMIAElevated cholesterol levels have been shown

to be related to increased risk of stroke

Total serum cholesterol levels greater than 200 mg/dL are associated with an increased risk of cardiac-related events, especially in combination with a low HDL fraction (<40 mg/Dl) .

Lipid lowering agents, specifically 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (“statins”), have been shown to decrease the risk of MI-related death in high-risk patients.

Statins

Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) have been found to be highly effective in preventing stroke in both male and female patients with cardiovascular disease.

Hepatic injury from statin therapy is rare and likely idiosyncratic., liver enzyme monitoring should be performed before initiating statin therapy and as clinically indicated thereafter.

reversible and generally nonserious cognitive effects from statins. (memory impairment)

myopathy (0.1%), which if strongly suspected, warrants measurement of total creatine phosphokinase markdly elevated.

Statins

The beneficial effects of statin therapy are:-pleotropic , independent of their lipid lowering properties;

altering the lipid content of platelets, thereby decreasing platelet aggregability

stabilizing existing atherosclerotic plaques,

decreasing oxidative stress,

reducing vascular inflammation.

statinsanti-inflammatory,

antithrombogenic, antiproliferative

antileukocyte adhesion properties

Homocystenemia There is important influence of homocysteine metabolism on

premature atherosclerosis . young patients with advanced atherosclerosis and no other

established risk factors was homocystenemia must be suspected.

Plasma levels of homocysteine are regulated in part by B vitamins, and vitamin supplementation lowers plasma homocysteine levels.

Thus, low levels of folate and vitamin B are also associated with the risk of PAD,stroke perhaps through the modulation of homocysteine levels.

Early studies found elevated homocysteine to be an independent risk factor for coronary artery disease and stroke.

Homocysteinemia

Elevated circulating homocysteine results in

1- endothelial dysfunction and injury2-followed by platelet activation and thrombus formation.3- production of hydrogen peroxide (which mediates endothelial injury), 4- increases in factors XII and V, decreases in protein C. 5- inhibition of thrombomodulin and heparin sulfate.

Homocystenemiaserologic evaluation for elevated homocysteine levels is still recommended for patients with:

1- family histories of multiple thrombotic events, 2- premature cardiovascular symptoms in the absence of conventional risk factors, and 3- coronary artery disease, PAD, stroke, deep venous thrombosis, and pulmonary embolism.

- Supplemental B vitamins or folic acid therapy may be worthwhile.

Alcohol consumptionAlcohol seems to have a bimodal

effect.

with mild alcohol consumption (<2 drinks/day) associated with a reduced risk of stroke in several studies.

Excessive alcohol consumption (>2 drinks/day) should be discouraged. There are no data that support encouraging consumption of alcohol for stroke prevention.

BEST MEDICAL TREATMENT

(BMT)medication

Antiplatelet TherapyAspirin is the most common antiplatelet

agent used and the best studied.

The benefit of stroke reduction is seen over a wide range of aspirin doses (50-1500 mg); however, the gastrointestinal side effects of aspirin increase with increasing dosage.

recent evidence that enteric-coated aspirin is more frequently associated with aspirin resistance, and therefore, low-dose, nonenteric-coated aspirin may be preferred.

Antiplatelet TherapyDipyridamole has been combined with

aspirin for stroke reduction in patients with a history of stroke or TIA.

Mechanism of Action By inhibiting phosphodiesterase.

low-dose aspirin (25 mg twice daily), extended release dipyridamole (200 mg daily)and a combination called Aggrenox, is used mainly for prevention of stroke in patients .

Antiplatelet TherapyThe combination of these two

drugs reduced the risk of subsequent neurologic events compared with placebo, and the combination therapy was superior to either drug alone for reduction of stroke.

headache and gastrointestinal symptoms were more common with combination therapy

Antiplatelet TherapyTiclopidine (250 mg twice daily) has been

shown to be effective in preventing recurrent cardiovascular events.

inhibit ADP-induced platelet aggregation.

is similar to aspirin in its effectiveness.

However, the side effects of neutropenia, and rarely, thrombotic thrombocytopenic purpura, associated with its administration have limited its clinical use.

Antiplatelet TherapyClopidogrel has emerged as an

alternative antiplatelet agent.

Used alone or with combination with aspirin or dipyridamole.

no clear benefit of combining aspirin and clopidogrel therapy over either agent alone.

conclusionThe ease and cost savings of

aspirin therapy have made it the preferred treatment for most patients with atherosclerotic disease and stroke.

there is consensus that patients undergoing CAS should receive dual antiplatelet treatment.(aspirin +clopidogrel)

STATINS & beta blockadeUsed routinely apart from it lipid

lowering effect. (used even without hyperlipidemia).

Beta blocker used as indicated .(individalized)as indicated

EXERCISE THERAPY Regular aerobic exercise reduces cardiovascular Risk By

Lowering Cholesterol And Blood Pressure And By Improving glycemic control.

structured exercise The guidelines suggest that exercise training, In The Form Of walking, Should Be Performed For a minimum of 30 to 45 minutes per session, three to four times per week, for a period not less than 12 weeks.

During each session, the patient should be encouraged to

walk until the limit of lower extremity pain tolerance is reached, followed By A short period of rest until pain relief is obtained, then a return to exercise

EXERCISE THERAPYThis cycle should be followed for the duration of the

session.

Although exercise therapy appears to be easy to implement, Effectiveness Is often limited by poor patient compliance. Studies have shown the superiority of clinic-based exercise programs over home-based programs.

Treatment Strategy #1 stabilize or halt the progression of the carotid plaque

Risk Factor Target CommentHypertension SBP <140 and DBP <90.

For patients with diabetes, SBP<130 and DBP <85

Use of ACEIs should be encouraged

Diabetes FBS < 126 mg/Dl,glycated hb less than 7 Diet and oral hypoglycemic agents or insulin as needed

Elevated lipid levels LDL <100 mg/dL AHA step II diet (<30% fat, <7% saturated fat, < 200mg chol/d) Statin therapy

Cigarette smoking Stop smoking Counseling, specific therapies

Alcohol use Eliminate excessive use Mild to moderate use (1-2 drinks per day)

Physical activity 30-60 minutes of exercise at least 3x per week