Combined carotid and coronary disease the strategy should be

1. Combined Carotid and Coronary Disease:
The strategy should be.
Dr. Majed Othman
Damascus, Syria
Al Bassel Heart Instituteinstitute

2. This for dealing with severe carotid artery
stenosis that may occur in patients
presenting for coronary artery bypass
grafting(CABG)

4. Definition of severe carotid artery stenosis
 One that reduced residual diameter to less than
1.5mm
OR
Reduced residual diameter by more than 70%

5. 1-Definition
Since the mid 1990s, CNC injury after cardiac
surgery has been broadly classified into two
categories:
TYPE I : injury is defined as death due to stroke or
hypoxic encephalopathy ,nonfatal stroke ,transient
ischemic attack, or stupor or coma
TYPE II :a new deterioration in intellectual function,
confusion ,agitation, disorientation, memory deficit
or seizure without evidence of focal injury .

8. 0
1
2
3
4
5
6
7
8
9
10
CABG
AV
CABG+VR
MV
Aortic R.
multiple Vs
Stroke rate according to type of surgery
stroke 2006,37(2):562-571

9. INCIDENCE OF PERIOPERATIVE STROKE
 1986 Gradner et al :
 Pts > 45 Y perioperative risk 0,2%
 Pts = 60 Y perioperative risk 3%
 Pts = 75 Y perioperative risk 8%
 1992 Tuman et al : investigated the effect of AGE on
- low cardiac output .
-myocardial infarction .
- neurologic injury.
Pts> 65 y 0.9%
Pts> 75 y 8.9%

10. Incidence of Carotid Stenosis in
Coronary Artery Bypass patients
 Noninvasive testing prior to myocardial
revascularization revealed:
6% incidence of significant
extracraniel cerebro vascular disease
 The incidence rise from:
3.8% for pts younger than 60 years to
11.3% for pts over 60 years

11. From study of 2108 patients under going elective
(CABG) from a 24 institutions in USA (Roach &
colleagues )the results was:
 6.1% CNS injury
 3.1% Type I (with 0.4 % death )
 3% Type II

12. From our study at Al Bassel Heart Institute of 1615
patients undergoing elective (CABG) the results was:
 2.6% CNS injury
 1.36% Type I (with 0.6 % death )
 1.23% Type II

13. CNS injury after elective CABG
2108 patients in
24 centers in
USA
(Roach et al)
1615 patients in Al
Bassel institute
Damascus-SYRIA
(khalifa,Othman)
CNS injury 6.1% 2.6%
Type I 3.1%(0.4%death) 1.36%(0.6%)
Type II 3% 1.23%

14. CABG & Extracranial Carotid Disease
 Coexist in 9% with stenosis, and 2% occlusion
 NASCETbenefit of surgical treatment for symptomatic
high-grade carotid stenosis
 Standard policy in US centers : of CABG with prophylactic
endarterectomy or carotid angioplasty/stenting(staged or
synchronous)in patients with symptomatic carotid disease.
Chaturvedi et al,2005

15. CABG & Extracranial Carotid Disease
 Risk of stroke after CABG: 2%
 +asymptomatic significant C stenosis: 3-5%
 +coexistent carotid occlusion: 5-11%
Naylor et al,2002

17. Thrombo-emboli of carotid

19. Multivariable predictors of stroke
 Include:
 Aortic calcification
 Renal failure
 Prior stroke
 Smoking
 Carotid vascular disease
 Age
 Peripheral vascular disease
 Diabetes

20. 3-Risk factors

22. Incidence of Stroke in Males and Females
2200
2000
200
1200
1000
800
600
400
0
25–34 35–44 45–54 55–64 65–74 75–84 85
Age Groups
IncidenceofStrokeper100,000
Women
2600
2400
200
1200
1000
800
600
400
0
25–34 35–44 45–54 55–64 65–74 75–84 85
Age Groups
1400
Men
* Incidence per 100,000 persons (cumulative Incidence)
+ Incidence per 100,000 years of persons (density of Incidence)
Berger et al. Dtsch Med Wochenschr 2000; 125 (1–2): 21–25.
Stroke Registry Erlangen *
MONICA Project Eastern Germany *
Senior Study Augsburg +
PROCAM Study +

23. Stroke
 In young Pts 0.5%
 At age 65Ys 5%
 At age 75Ys 8%
 In closed chamber cardiac procedure 2-6%
 In upper chamber procedure 4.2-13%
 Combined procedures 16%
 Valve + CABG 18%

24. Relationship of carotid stenosis to
perioperative stroke
 Carotid bruit(murmer) Present
3.9 fold increase in the ratio for stroke
(poor correlation between auscultatory finding and the degree of carotid stenosis)
 Better definition of the degree of carotid stenosis is obtained with non
invasive carotid testing using doppler ultrasound techniques.
 Brener et al: studied 4047 cardiac surgical pts and found: 9.2% rate of
stroke or transient ischemic attack in pts with asymptomatic carotid
stenosis which was significantly greater than 1.3% in pts with no carotid
stenosis.
 1992 Berner et al carotid duplex scanning for all cardiac surgical pts
 65years of age or older:
Risk 2.5% for lesion> 50%
Risk 7.6% for Stenosis> 50%
Risk 10.9% for Stenosis> 80%

25. Mechanism of Perioperative Stroke
with Carotid Stenosis
 Not well understood
 Loss of pulsetile perfusion or failure to maintain an
adequate perfusion pressure on bypass may lead to
diminshed flow distal to the significant stenosis
resulting in a watershed stroke = 50%
 Delayed strokes in pts with uncorrected carotid
stenosis may relate to the prothrombotic milieu.

26. The causes of a stroke during surgery are many, but
they can be grouped under three general headings:
 1. Problems with Blood Flow to the Brain: Although cardiopulmonary
bypass with the heart-lung machine rarely causes poor blood flow to the brain, certain unusual
circumstances can occur. Each time the left ventricle contracts, it ejects blood from the heart and
causes a pulse in the arteries throughout the body. The brain, however, is sensitive to the loss of
regular pulse, and the heart-lung machine provides a more continuous flow than the normal pulsing
flow from the heart. Because there is a lack of pulsation, it is particularly important that an adequate
blood pressure be maintained when the patient is receiving assistance from the heart-lung machine
to ensure the brain gets enough blood. Partial or complete obstruction of one or both carotid arteries,
which supply blood to the brain, can lead to compromised blood flow to the brain while the heart-
lung machine is working.
 2. Bleeding into the Brain: despite the high doses of very potent blood thinners
(anticoagulants) required when the heart-lung machine is used for coronary artery bypass grafting,
bleeding into the brain is extremely rare. In fact, it almost never occurs during the operation and thus
can be discounted as a cause of stroke during the operation.
 3. Embolus to the Brain: An abnormal clump of material traveling through the blood
vessels is called an embolus. The possible sources of material traveling to the brain include blood
clots from inside the heart, debris from plaque in the aorta or the carotid arteries, and particles of
material or air from the heart-lung machine.

27. Pathophysiology of perioperative stroke

30. Relationship of uncorrected carotid
stenosis to late stroke
Late noninvasive carotid testing
reveals progression of the
carotid artery disease in half of
the pts within four years.

31. Predictor of Severe Carotid disease
 Female gender
 Peripheral vascular disease
 History of transient ischemic attacks
 Smoking history
 Left main coronary artery disease
 Age

32. Clinical Syndromes of Stroke
L.MCA infarction
L.ACA infarction
L.Internal capsule lacunar infarction
L.PCA infarction
L.Cerebellar infarction
R.MCA infarction
L.Brainstem infarction

34. Capable or not ??

35. 4-Etiology of Central Nervous System Damage:
Focal ischemia :
emboli .
Global Ischemia :
1. Watershed areas
2. Cerebral perfusion pressure
Autoregulation may be lost in
 Hypothermia (<20˚C)
 Diabetic patient
 Cerebral venous hypertension
3. circulatory arrest .

36. 6-Preoperative evaluation
 Routine screening for Preoperative cognitive
 Cerebral MRI or CT

37. 5-Sources of emboli
A-patient-related sources
(1-Aortic atheroma.
(2-Intraventricular thrombi .
(3-Valvular calcifications .
B- procedure-related sources .
(1-open chamber procedures .
(2-Aoartic cannulation and clamping
(3-Duration of CPB
C-Equipment-related sources .
1- filters
2- oxygenators
3-Use of nitrous oxide .

38. Sources of emboli

39. A-patient-related sources:
1-Aortic atheroma.
2-Intraventricular thrombi .
3-Valvular calcifications .

40. B- procedure-related sources :
1-open chamber procedures .
2-Aoartic cannulation and clamping
3-Duration of CPB

41. 7-Intraoperative cerebral monitoring:
A. Brain temperature
B. Electroencephalogram (EEG)
C. Transcranial Doppler (TCD)
D. Jugular oximetry
E. Noninvasive optical spectroscopy
F. Cerebral perfusion pressure (CPP)

42. 8-Prevention of central nervous system injury
 Embolic load
 Temperature
 Cerebral perfusion
 Euglycemia

43. Embolic load
 TEE screening of descending aorta
 Minimize the time of aortic clamping
 Precirculation of CPB for 30 min with 5-µm filter
 Micropore (20-40µm)filter into cardiotomy return
line
 Use 40-µm filter on arterial inflow line
 De-airing techniques

44. De-airing techniques
 Needle aspiration of LV & LA
 Use of TEE to detect residual intracavitary air
 Titling the patient’s head down
 Bilateral carotid compression

45. temperature
 In a one of largest trials appears that it was not the
hypothermia that was protective but rather the
cerebral hyperthermia that was harmful .
 Avoid rapid rewarming
 To minimize gas bubble formation due to decrease
solubility the temperature gradient between the
arterial inflow blood and the patient must be less
than 10˚C .
 During rewarming arterial blood inflow must not
exceed 37°C.
 Post-operative period may be of equal importance.

46. Cerebral perfusion
 In patient at low risk for CNS injury there were no
significant effects of low MAP
(50-70)
 IN patient at high risk for CNS injury the higher MAP
had lower risk(80-100)
 Avoid hypotension during rewarming

47. Euglycemia
 Hyperglycemia worsen neurologic outcome during
ischemia
 Blood glucose level should be maintained within the
normal range during cardiac surgery
 Avoid glucose priming

48. Pharmacologic cerebral protection
Various agents have the ability to produce EEG
suppression and result in decrease in cerebral
metabolic rate to 50%
 Thiopental 5-8mg/kg
 Propofol 2-3 mg/kg
 Isoflurane (1.5- 2 MAC)

49. Summary
 Prediction of high risk patient
 Perioperative evaluation
 Preventing emboli and maintaining higher perfusion
pressure
 Prevention of hyperthermia
 Monitoring using T C D
 Pharmacological neuroprotection

52. Timing of carotid and coronary surgery
We have 4 important questions:
1. Carotid disease very important ++++
coronary disease supportable
2. carotid disease ++++
coronary disease
3. coronary disease very important ++++
carotid disease supportable
4. coronary disease ++++
carotid disease ++++

53. Efficacy of carotid ENDARTERECTOMY
as treatment for carotid stenosis
 Until the 1990s there was considerable DEBATES as to
whether or not carotid endarterectomy:
Improved survival and yielded lower
incidence of neurologic events in pts with documented
carotid stenosis.

54. C.E.A For Symptomatic carotid
stenosis
 1986 HERTZER: 211 pts
126 pts----- non operative
85 pts------- C.E.A {Follow up: 36 month}
 1991 North American Randomized Study: 659
pts:
328 pts-------C.E.A
331 pts--------M.T
 1991: The veterans affairs cooperative study.
 The European carotid surgery trail randomized to
medical treatment or surgical treatment 2518 pts

55. There for:
 All studies: (Retrospective or randomized) have clearly
established the superiority of carotid endarterectomy
OVER medical treatment for pts with symptomatic
sever carotid artery disease.

56. Efficacy of carotid stenting Versus
conventional surgical endarterectomy:
 Incidence coronary artery disease in carotid
endarterectomy pts:
 Cleveland clinic reported 1985 on : 506 pts:
₋ 7% had normal coronary artery.
₋ 28% mild to moderate.
₋ 30% advanced compensated disease.
₋ 28% sever correctable.
₋ 7% sever inoperable.

59. CAROTID STENTING
 INDICATIONS :
 ( Patients who are at an increased risk with carotid surgery )
 I – High risk factors :
 sever heart disease
 heart failure
 sever lung disease
 age > 75 years
 II – Anatomic features , that make surgery difficult or risky :
 -controlateral carotid radiation therapy to neck ,
 -prior ipsilateral carotid artery surgery ,
 -intra thoracic or intra cranial carotid disease
 -contralateral laryngeal palsy ,
 -previous CEA and recurrent stenosis ,
 -high cervical internal carotid artery leasion ,

60. CAROTID STENTING
 May be considered an alternative to carotid surgery in
average surgical risk patients ,
 In favor carotid stenting :
 -non – atherosclerotic cause of stenosis :
 - fibrodysplasia
 - radiation
 - early post surgical stenosis
 - flap .

62. Risk of myocardial ischemic events:
Short-term risks:
The incidence of myocardial infarction following carotid
endarterectomy 1.5-5%
Long-term risks:
Actuarial survival and reduction in the late mortality
rate were significantly better for the patients with
coronary artery disease who had myocardial
revascularization.

63. Questions
Is not the indication
BUT
timing of the operative procedure.
-Staged procedure
- reversed staged procedure

64. Neuropotection during carotid
and cardiac surgery
OVERVIEW : cerebral complication
 - STROCK
 - Neuropsychological disorders
 - Substantial deterioration of intellectual function
 ARE SERIOUS AND COSTLY HEALTH CARE
PROBLEM
 PHYSICAL / INTELLECTUAL DISABILITY

65. Neuropotection during carotid
and cardiac surgery
Questions
 - Does the number of brain emboli correlate with
occurrence
 -When do brain emboli occur during the course of
both cardiac and carotid surgery
 -Which is the nature gaseous or solid and which is the
composition platelats, fibrine, fat, and cholosteral
 -Is it possible to reduce the neurological complication
by routine TRANSCRANIAL DOPPLER
 (brain macroemboli more than 200 Mm in diametre)

66. Hypoperfusion(14%)
 HypoperfusionBorderzone infarctions(BZ).
 BZ lesions occur after:
1. Cardiac arrest
2. Cardiac surgery
3. Or severe hypotension

67. Intraoperative cerebral monitoring
A. Brain temperature
B. Electroencephalogram (EEG)
C. Transcranial Doppler (TCD)
D. Jugular oximetry
E. Noninvasive optical spectroscopy
F. Cerebral perfusion pressure (CPP)

68. Terminology of Borderzone infarctions

69. Vascular Territories

70. Diagnosis
 The majority of strokes after CABG are identified in the first
2 days
 Delayed stroke, defined as neurological deficit that
develops after initially awakening from surgery without
deficit , representings 65% of postoperative strokes
 CTsingle vessel territory infarcts in 72% , and multiple in
20%
 MRI(DWI)is more sensitive, but may not available
multiple embolic infarcts in watershed areas.
 perfusion( BP,CPB) watershed territory infarcts.

71. Effect of reduced CBF
infarction
Penumbra

72. Diagnosis
CT:L.MCA infarction DWI:R.thalamic lacune

73. Assessment of collateral flow

74. Postoperative Coma after
cardiac surgery
Intracerebral Hemorrhage
Neurosurgery evaluation
Blood pressure control
Correct coagulopathy, if present
CT brain
EEG
MRI brain Repeat CT brain
Serial neurological
examination
Persistent coma
Drug- induced altered Consciousness
Minimize sedation
Correct metabolic derangements
Hypoxic ischemic
encephalopathy
Ischemic stroke
(multifocal):
Operative factors:
CPB time
DHCA time
Hypotension
Nonconvulsive status epilepticus
Antiepileptic medications
Evaluate for underlying cause

76. Synchronous carotid artery stenting
and open heart surgery
 Carotid artery stenting followed immediately by
cardiac surgery .
 CREST trial compared stenting to surgery on the
collective incidence of stroke heart attack death .
 Found : there was no significant difference out to four
years follow up .

79. Cost
 Significant more in-hospital morbidity.
 Longer Length of stay(25 days).
 Mortality 21%

80. In such a dark room a surgeon dreams
of such carotid

86. Aortic surgery with DHCA
Patient characteristics
 History of CVA
 Diabetes
 Previous aortic surgery
Operative Variables
 Urgent operation
 CPB duration
 DHCA duration
 Increase use of fresh
frozen plasma
Lancet 1998;351(9106):857-861

87. Neuroprotection during carotid
and cardiac surgery
 SUMMARY
 The necessity to further develop innovate technical
methods to better assess the embolic risk of a patient
prior to a cardiovascular operations

90. 6-Preoperative evaluation
Elderly patients: at increased risk
 Atherosclerosis
 Cerebrovascular disease
 Underlying cognitive dysfunction

91. Overview
Coronary artery bypass
graft(CABG):
[Cardiopulmonary
bypass(CPB)]emboli
 Stroke
 Coma
 Encephalopathy
 Neurocognitive decline
 Peripheral nerve injuries
[off-pumpbeter outcomes]
Valve replacement & Aortic
arch surgery:
[Deep Hypothermic
circulatory arrest(DHCA)]
Higher rate of mortality &
morbidity(emboli)
Risk factors:
Duration of surgery
Advanced age
DM
HTN

92. CNS injury after cardiac surgery
CNS injury ranges in severity from subtle
changes in personality, behavior and
cognitive function to fatal brain injury

93. Classification of CNS injury
 TYPE I : injury is defined as death due to stroke or hypoxic
encephalopathy ,nonfatal stroke , TIA, stupor or coma
 Type II :a new deterioration in intellectual function,
confusion , agitation, disorientation, memory deficit , or
seizure without evidence of focal injury .

94. Sources of emboli
A-patient-related sources:
 1-Aortic atheroma.
 2-Intraventricular thrombi .
 3-Valvular calcifications .
B- procedure-related sources :
 1-open chamber procedures .
 2-Aortic cannulation and clamping
 3-Duration of CPB
C-Equipment-related sources :
 1- filters
 2- oxygenators
 3-Use of nitrous oxide .

95. Preoperative evaluation
Elderly patients: at increased risk
Atherosclerosis
Cerebro vascular disease
Underlying cognitive dysfunction
Cerebral MRI or CT

96. Neurocognitive functions
- Attention
- Cognitive speed
- Memory
- Executive Function
- Fine motor function
 These disturbances more pronounced in :
Deep hyperthermia & circulatory arrest

97. Prevention of CNS injury
Embolic load
Temperature
Cerebral perfusion
Euglycemia

99. Stroke
 The stroke rate after CABG has remained stable in the
last 3 decated at about 2%
 The incidence of stroke with aortic valve surgery and
combined CABG/valve surgery associated with a
higher risk of stroke and mortality (bucerius et al,2003)
 Mortality rate after CABG:3%
 in perioperative stroke after CABG : 32%

101. Cardiac Surgery with CPB
 Patient characteristics
 Older age
 History of CVA
 Peripheral vascular D.
 Diabetes
 Hypertension
 Previous cardiac surgery
 Preoperative infection
 Female gender
 Carotid artery disease
 Reduced EF
 Chronic renal insufficiency
 Proximal aortic atherosclerosis
 Operative Variables
 Urgent operation
 CPB duration>2 hours
 Intraoperative hemofiltration
 High-transfusion requirement
 Intermittent clamping of aorta
 Atrial fibrillation
 Low cardiac output syndrome
Lancet 1998;351(9106):857-861

102. AF & CABG
 AF after CABG is common : up to 32%
 AF is common in stroke after CABG :37%
 Without AF, stroke occurred after # 3 days
 With AF  stroke occurred after # 6 days
 AF+ low cardiac output risk of stroke
 AF+ anticoagulating patients risk of stroke

103. AF

105. Treatment
 Early recanalization of the occluded artery
 IV-tPA is contraindicated
 Intra-arterial thrombosis for acute stroke within 6
hours of onset has been demonstrated to be a
potential treatment option that may lead to
recanalization and neurologic recovery (Fukuda st al,2003)

106. Coma
 Postoperative coma after cardiac surgery indicate
bihemispheric cortical injury or a brainstem lesion.
 Failure to awaken after surgery
 Causes:
 intracerebral haemorrhage
 hypoxic- ischemic encephalopathy
 multifocal ischemic stroke
 Severe metabolic encephalopathy
 Management according to the evaluation

108. Encephalopathy
 Delirium after cardiac surgery 7-14% , and increase to 32% in older
adults(other causes : DEMENTIA)
 Post Op. delirium
 increase rate of respiratory insufficiency
 Longer ICU stay
 Increase mortality
 421 CABG12% showed encephalopathy at post Op. (day 4),but 80%
had a normal mental state at discharge.
 In our retrospective study : of 1615 CABG only 14 patients showed
Delirium at post Op., most of them returned normal at discharge.
(Khalifa,Othman,2008)
(Breuer et al,1983)

109. RFs of encephalopathy after CS
 Patient characteristics
 Older age
 History of CVA
 Peripheral vascular D.
 Diabetes
 Hypertension
 Reduced EF<30%
 AF
 Operative Variables
 Urgent operation
 Operative time>3 hours
 CPB duration>2 hours
 Intraoperative
hemofiltration
 High-transfusion
requirement
 Intra-aortic ballon pump
 Use of pressor agents
Bucerius et al,2004

110. Cognitive Decline(CD)
 CD after CABG is due to cerebral micro-emboli
during cardiopulmonary bypass
 The rate of CD after surgery is # 25% at 3Ms 32% after
12Ms,increasing to 42% at 5 years
 Recent studies7.7%at 3 months , and 12.3% at 12
months (keiz et al,2005)
 The effect of avoiding CPB(off-pump CABG) has not
been proven to reduce CD (Van Dijk et al,2007)

111. Aortic Surgery
 Surgery of aorta or aortic arch  complete circulatory arest +
profound hypothermia
 Proximal & descending aorta(aneurysm , dissection) :
elephant trunk procedure:2 stages
 Profound hypothermia is neuroprotective , however can
produce abnormal bleeding , especially over one hour.
 During rewarming further impaired coagulation
 Compared with CPB,DHCA is associated with increased
neurological morbidity

112. Neurological complications
 Compared with CABG, ascending aortic surgery higher
mortality(10%) & stroke(7%)
 for stroke The 2 main risk factors :
1. Emergency surgery(17% vs 3.4%)
2. The duration of DHCA(stroke after 40 Ms, mortality >60
minutes)
 Stroke after aortic surgery
1. Increase ICU stay
2. Increase intubation duration & mortality
 65% of stroke are embolic,13% hemorrhagic

113. IC HEMORRHAGE

114. RFs for stroke after Aortic surgery
Patient characteristics
 History of CVA
 Diabetes
 Previous aortic surgery
Operative Variables
 Urgent operation
 DHCA duration
 CPB duration
 Increase use of fresh
frozen plasma
Goldstein et al,2001

115. RFs for cognitive decline after AS
 CD after AS up to 28%
 DHCA>one hour  impairment from 2Ws up to 6 months.
 A rare neurological complication is a clinical syndrome
resumbling progressive supranuclear palsy(PSP)vertical
gaze palsy, gait unsteadiness, dysarthria, dysphagia, and
tremor MRI  infarction in brainstem (Mokri et al,2004)
 In children after surgery for congenital heart lesion
complete PSP + acute chorea syndrome. MRI: normal?!
(Robinson et al,1988)

116. PSP

117. RFs for cognitive decline after AS
Patient characteristics
 Advanced age
 Diabetes
 Hypertension
Operative Variables
 DHCA duration>25Ms
Goldstein et al,2001

118. Conclusion
Prediction of high risk patient
Perioperative evaluation
Preventing emboli and maintaining
higher perfusion pressure
Prevention of hyperthermia
Monitoring using TCD
Pharmacological neuroprotection

126. Risk factors
- Age
- Diabetes
- Peripheral Vascular disease
- Renal failure
- Aneurysmal disease
- Left main coronary disease
- Emergency
- Heart failure
- Duration of bypass
- Intra-Aortic balloon pump

127. Carotid endarterectomy for
asymptomatic carotid stenosis:
 HERTZER group:
290 pts had carotid stenosis 50%
 VETERANS affairs cooperative study:
444 pts
 Results of the Asymptomatic carotid Atherosclerosis
study:
1662 pts
All studies: Documented:
A significant advantage of carotid endarterectomy OVER
continued medical management for patients with sever
asymptomatic carotid artery stenosis.

128. CNS injury ranges in severity from subtle changes
in personality, behavior and cognitive function to
fatal brain injury

130. “I am not afraid of death, I just don't
want to be there when it happens.”