CAROTID DISEASE

1. Carotid atherosclerotic
disease
by
Mohammed Salah
Ass .lecturer –vas .surgery department
AUH-assuit university

2. anatomy
ARCH &ICA

3. 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
1
2 3

4. 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.

5. 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

6. 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

7. Internal Carotid Artery
Cavernous
 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

8. Segments and branches
the artery divided into four parts:
 "cervical",
 "petrous",
"cavernous",
and "cerebral

10. 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

11.  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).

13. 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 portion
1.Caroticotympanic arteries
2.Artery of pterygoid canal (vidian artery)
C3: Branches from the lacerum portion - none

14. C4: Branches from the cavernous portion
1.Branches of the meningohypophyseal trunk:
Tentorial basal branch
Tentorial marginal branch
Meningeal branch - helps supply blood to the meninges
of the anterior cranial fossa
Clivus branches - tiny branches that supply the clivus
2.Inferior hypophyseal artery
Capsular branches - supplies wall of cavernous sinus
3.Branches of the inferolateral trunk:
Branches to trigeminal ganglion - provide blood
to trigeminal ganglion
Artery of the foramen rotundum
Branches to nerves
)

15. C5: Branches from the clinoid portion – none
C6: Branches from the ophthalmic portion
Ophthalmic artery
Superior hypophyseal artery
C7: Branches from the communicating portion
Posterior communicating artery
Anterior choroidal artery
Anterior cerebral artery (a terminal branch)
Middle cerebral artery(a terminal branch)

16. EPIDEMIOLOGY

17. 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%)

19. PATHOPHYSIOLOGY

20. PATHOPHYSIOLOGY OF STROKE RELATED TO
EXTRACRANIAL CEREBROVASCULAR DISEASE
Development of Atherosclerosis
 The 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.

22. EVALUATION OF CAROTID
DISEASE

24. CLINICAL FINDINGS IN
PATIENTS WITH
CEREBROVASCULAR
DISEASE

25. 1.TIA
 often 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

27. 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.

28. 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.

29. 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.

30. DUPLEX
(D.U.S)
INVESTIGATION

31. 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

32. 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

34. 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)

35. 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.

36. CT Angiography

37. 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

38. 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.

39. Digital Subtraction Angiogram

40. 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.

41. CTA
 Used when US is not reliable:
-Severe calcific artery
-Severe kinking of the vessels
-Short neck
-High bifurcation
-Overview of surgical field

42. MR Angiogram
LR

43. MRA
TYPES
 TOF MRA (time of flight )have limited
advantage over DUS .
CEMRA (contrast enhanced MRA)
considered gold standard for carotid
stenosis disease.

44. 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 MRA
Sensitivity 37.9% Specificity 92.1%
 Contrast-enhanced MRA
Sensitivity 65.9% Specificity 93.5%
Stroke. 2008;39:2237-2248

45. MRA
 May 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$).

46.  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

47. Conventional angiography
 Gold standard
 Visualize the entire cerebrovascular
system
 Invasive test
 Expensive test
 Neurological morbidity/mortality

48. Carotid trials
Asymptomatic/symptomatic carotid
atherosclerotic disease trials

49. 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

50. Symptomatic carotid trials
 North American Symptomatic Carotid
Endarterectomy Trial (NASCET).
 European Carotid Surgery Trial (ECST).
 Both using angiography to determine degree of
stenosis .

51. Carotid symptomatic trial
 NASCET 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 .

53. Management of
carotid artery
stenosis

54. • Decision making

55. 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.

56. 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

57. Medical treatment
Risk factor modification

58. Smoking
.. Nicotine inhalation has been demonstrated to
1- 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.

59. SMOKING CESSATION therapy
NRT buccal mucosa spray patch
1ST LINE DRUGS bupropion varenicline
2ND LINE nortriptyline clonidine
EMERGING THERAPY nicotine vaccine
NICVAX

60. 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.

61. 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 .

63. 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.

65. Effect of hypertension on
atheroscelorsis

66. 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.

67. HYPERLIPIDEMIA
 Elevated 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.

68. 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.

69. 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.

70. statins
 anti-inflammatory, antithrombogenic,
antiproliferative
 antileukocyte adhesion properties

71. 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.

72. Homocysteinemia
 Elevated circulating homocysteine results
in
1- endothelial dysfunction and injury
2-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.

73. Homocystenemia
serologic 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.

74. Alcohol consumption
 Alcohol 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.

75. BEST MEDICAL
TREATMENT
(BMT)
medication

76. Antiplatelet Therapy
 Aspirin 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.

77. Antiplatelet Therapy
 Dipyridamole 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 .

78. Antiplatelet Therapy
 The 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

79. Antiplatelet Therapy
 Ticlopidine (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.

80. Antiplatelet Therapy
 Clopidogrel 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.

81. conclusion
 The 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)

82. STATINS & beta blockade
 Used routinely apart from it lipid
lowering effect. (used even without
hyperlipidemia).
 Beta blocker used as indicated
.(individalized)as indicated

83. 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

84. EXERCISE THERAPY
 This 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.

85. Treatment Strategy #1
stabilize or halt the progression of the carotid plaque
Risk Factor Target Comment
Hypertension 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