SHORT TERM AND LONG TERM OUTCOMES AFTER CAROTID

ENDARTERECTOMY- SINGLE CENTRE EXPERIENCE

THESIS

Submitted for the partial fulfillment for the requirement of the degree of

MCh in Vascular Surgery

By

Dr. P.Shivanesan

MCh Vascular Surgery Resident

2014 – 2016

DIVISION OF VASCULAR SURGERY, DEPARTMENT OF CVTS

SREE CHITRA TIRUNAL INSTITUTE FOR MEDICAL

SCIENCES AND TECHNOLOGY

THIRUVANANTHAPURAM – 695011, India

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Travancore, an erstwhile province of pre-independent India, was ruled by

Maharaja Sree Chitra Tirunal Balarama Varma until the country became

independent in 1947. The Government of India took over the province after

independence and was incorporated into the state of Kerala.

Known for their munificence, the royal family of Travancore considered

themselves ‘dasas’ (servants) of Lord Padmanabha, the reigning deity of

Travancore. Interestingly, they wore turban instead of a crown as a mark of respect

to the Lord. Their philanthropy finds expression in their countless contributions to

the country, then and now.

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The Sree Chitra Tirunal Institute for Medical Sciences & Technology

(SCTIMST), Thiruvananthapuram is an Institute of National Importance

established by an Act of the Indian Parliament. It is an autonomous Institute under

the administrative control of the Department of Science and Technology,

Government of India.

The Institute signifies the convergence of medical sciences and technology

and its mission is to enable the indigenous growth of biomedical technology,

besides demonstrating high standards of patient care in medical specialties and

evolving postgraduate training programmes in advanced medical specialties,

biomedical engineering and technology, as well as in public health.

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ACKNOWLEDGEMENT

I have great pleasure to place on record my debt of gratitude to

Prof M Unnikrishnan, Professor and Head of the Division of Vascular Surgery, Dept of CVTS,

SCTIMST, my revered teacher and mentor, who provided me updated information, suggested

improvisations and guided me to imbibe vascular surgical skills during the course.

I wish to thank Prof. Sylaja.P.N, Professor, Dept of Neurology for her contribution and

guidance in the conduct of this study .I am also grateful to Prof. TR Kapilamoorthy, Professor

and Head, Dept of Imaging Sciences and Interventional Radiology, for his guidance in the

conduct of this study. I am very much grateful to Prof. Jayakumar K, Professor and Head,

Department of CVTS, SCTIMST for his whole hearted support during my course.

I would like to express my sincere gratitude to Dr Balasubramoniam KR previous

Consultant, in Division of Vascular Surgery for his support and guidance. I am grateful to

Mr.Jayakumar, for his assistance in the statistical analysis.

I also appreciate the help and the company of my colleagues Dr Sidharth Viswanathan,

Dr Ajay Savlania., Dr Prakash G, and Dr Vijay Richard. Last but not the least I would like to

thank the nursing staff & the patients for their cooperation.

Dr.P.Shivanesan ………………

Thiruvananthapuram Date

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DECLARATION

I, P.Shivanesan, hereby declare that the project in this book was undertaken by me under the

supervision of Prof M. Unnikrishnan MCh, Professor and Head of Division of Vascular Surgery,

Dept of CVTS, Sree Chitra Tirunal Institute for Medical Sciences and Technology,

Thiruvananthapuram.

Date: Dr. P.Shivanesan

Forwarded Resident, Vascular Surgery

The candidate, P.Shivanesan, had carried out the minimum required work in this project

Prof. Unnikrishnan M Prof. Jayakumar K

Head, Division of Vascular Surgery Head of the Department

Dept of CVTS Dept of CVTS

SCTIMST, Thiruvananthapuram SCTIMST, Thiruvananthapuram

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CERTIFICATE

Certified to be the bonafide record of Dr.P.Shivanesan the work done at

Vascular Surgery division, Department of CVTS, as part of MCh Programme in

Vascular Surgery at Sree Chitra Tirunal Institute for Medical Sciences and

Technology, Thiruvananthapuram, for a period of three years from January 1st,

2014 to December 31st, 2016.

Prof Unnikrishnan M

Head, Division of Vascular Surgery,

Dept of CVTS

SCTIMST, Thiruvananthapuram

Dr.Sylaja.P.N

Professor, Department of Neurology.

SCTIMST,

Thiruvananthapuram

Prof Kapilamoorthy TR

Head, Department of Imaging Sciences and

Interventional Radiology

SCTIMST, Thiruvananthapuram

Prof Jayakumar K

Head, Department of CVTS

SCTIMST,

Thiruvananthapuram

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INDEX

Sl. No Particulars Page No.

General Contents 1-5

i Introduction 7

ii Aims of the study 9

iii Review of Literature 10

iv Materials and Methods 26

v Results 33

vi Clinical images 48

vii Discussion 52

viii Conclusions 58

ix References 59

TAC, IEC approval and Plagiarism check certificates

Proforma

Abbreviations

Appendix 1,2

Master Chart

-

72,74,76

77

79

80,81

82

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INTRODUCTION

Stroke remains leading cause of death and disability worldwide. Around

80% of the stroke is ischemic, with extra cranial carotid artery disease being

responsible for nearly 40% of these cases1. Since several natural history studies

demonstrated that carotid stenosis is a leading risk factor for disabling stroke and

death, carotid endarterectomy (CEA) became the major treatment of choice to

prevent stroke in these patients sooner than later2, 3

. The randomized control trials

clearly established the safety and efficacy of CEA over best medical management

both in symptomatic and asymptomatic carotid artery disease4, 5

.

The significant benefit of CEA in preventing stroke due to symptomatic

carotid artery disease was confirmed in various randomized control trials including

North American Symptomatic Carotid Endarterectomy Trial (NASCET), European

Carotid Surgery Trial (ECST) and Veteran Administration (VA) Symptomatic

Stenosis Trial4, 5, 6

. These studies have shown that there is a clear benefit of CEA

for stroke risk reduction in symptomatic patients with stenosis of 70% to 99%, and

a lesser, but still significant, benefit of CEA in symptomatic stenosis of 50% to

69%. Management of asymptomatic carotid disease is increasingly controversial

because the long-term risk for stroke is not as high in asymptomatic as in

symptomatic patients. But compared to symptomatic patients, the benefit of CEA

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in asymptomatic patients with 60% or greater stenosis, even though statistically

significant, is less impressive7, 8

. Carotid artery stenting (CAS) is evolving into an

effective procedure in preventing stroke. But current evidences support the

superiority of endarterectomy over CAS both in randomized and non randomized

control trails including the Carotid Revascularization Endarterectomy versus Stent

Trial (CREAST) 9.

The safety and efficacy of CEA have been reciprocated in many individual

institutional reports. For example in a report from Johns Hopkins Hospital, the

perioperative stroke and death rate was 2.5% and 0.8% respectively10

. In India,

many institutions now perform CEA regularly. But unlike the western countries,

there are only two institutional reports pertaining to the outcomes of CEA from our

country, including our own results published in 2008 which included 39 patients

who underwent CEA11, 12

.

Since there is no national registries to study the outcomes of CEA in

different institutions in our country, the individual institutional results remains the

bench mark for comparing results of CEA with one’s own experience. Our institute

has a well organized stroke team comprising Neurologist, Vascular Surgeon,

Interventional Radiologist and Neurosurgeon. This study aims at assessing the

outcomes of the procedure done since 1997 in our institute.

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AIM OF THE STUDY

1. To assess short term and long term outcomes after carotid endarterectomy

2. To evaluate factors determining the outcome of the procedure

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REVIEW OF LITERATURE

Stroke is among the leading causes of mortality and disabilities in the world

with > 80% being ischemic stroke1. A major preventable cause of ischemic stroke

is atherosclerotic extracranial carotid artery disease. Even though association

between the extracranial carotid artery disease and ischemic stroke was known

since 19th century, the most important breakthrough was contributed by

publications of C.Miller Fischer, who studied on pathophysiological correlation

between the occlusion of carotid artery disease and the ischemic stroke13

. He first

predicted the surgical treatment for the carotid atherosclerosis can prevent the risk

of ischemic stroke. Successful first carotid endarterectomy (CEA) was done in

1953 by Debakey14

. In 1954, Eastcott et al described the first successful surgery of

carotid occlusive disease in which the bifurcation of the carotid artery was resected

and then internal common carotid artery was anastamosed with the internal carotid

artery15

.

The second half of 20th century saw a rapid increase in number CEA done

both for symptomatic and asymptomatic carotid artery stenosis. Though there was

an initial speculation about the potential benefit of CEA due high complication

rated published in initial studies16

, the randomized trials conducted in 1990s

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established the definitive safety and efficacy of CEA in management of

symptomatic and asymptomatic carotid artery disease, also its superiority over the

medical management of these patients.

The North American Symptomatic Carotid Endarterectomy trial (NASCET)

and European Carotid Surgery Trial (ECST) are the major randomized control

trials comparing CEA with medical management for symptomatic carotid artery

disease4,5,17

. In NASCET the end point was reported in 2 different intervals- 2

years for high grade (70%-99%) stenosis and 5 years for moderate (50%-69%)

stenosis. In high grade carotid artery stenosis an absolute risk reduction of 17% for

any ipsilateral stroke was observed at the end of 2 years and in moderate stenosis

group the absolute risk reduction was 6.5% for any ipsilateral stroke at the end of 5

years. Similarly in ECST for symptomatic patients with 80%-99% carotid stenosis,

the 3yrs ipsilateral stroke rate was 6.8% in surgical arm but it was 20.6% in

medical arm and an absolute risk reduction of 13.8% was observed.

The major randomized trials which provided the benchmark for outcomes

associated with CEA in asymptomatic patients are Asymptomatic Carotid

Atherosclerosis Study (ACAS) and Asymptomatic Carotid Surgery Trial

(ACST)7,8

. In ACAS study 1662 asymptomatic patients with >60% carotid stenosis

was randomized to medical management or CEA. At 5yrs follow up the total event

rate was 5.1% in surgical arm versus 11% in the medical arm. The European trial

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ACST randomly assigned 3120 patients with >60% stenosis either to optimal

medical management or CEA. The 5yr stroke and death rate was 6.4% in CEA and

11.8% in medical arm. Both these trials showed an absolute and relative reduction

of approximately 5% and 50% respectively for surgery over best medical

management.

Various factors have been described which affect the perioperative outcome

following CEA. This includes, Age, gender, contralateral carotid occlusion,

surgery for restenosis, congestive heart failure, chronic obstructive lung disease,

chronic renal insufficiency, recent coronary artery bypass graft, ulcerated plaque,

diabetes mellitus, hypertension, peripheral vascular disease

In NASCET and ACAS trial, patients with >80yrs were either excluded

from the study cohort whereas in ECST and ACST trial they formed a very small

number within the study cohort and hence was considered as a high risk for CEA.

But when a subgroup meta-analysis done using both NASCET and ECST data

showed a comparable surgical result and better benefit for elderly patients who

underwent CEA. Literature is often conflicting about the actual risk of CEA in

patients > 80yrs.With available evidence, octogenarians are not to be considered as

high risk for perioperative outcome following CEA18

.

The influence of gender on perioperative outcome is controversial but most

studies indicate a lesser benefit for women than that for men19-21

. Various reasons

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are attributed to this finding. A systematic analysis of various studies addressing

this issue was done by den Hartog AG et al22

. They concluded that higher embolic

potential and different plaque morphology in females was the main gender specific

factors influencing the outcome. Other reasons that were put forward were smaller

diameter of the ICA, hormonal influence and more restenosis in women when

compared to men.

Significant other system diseases such as coronary artery disease, COPD and

CKD also have a negative impact on the outcome after CEA. Ouriel et al from

Cleaveland clinic analyzed the outcome of CEA in high risk group patients which

included: presence of significant coronary artery disease (requiring CABG or

coronary angioplasty within previous 6 months), severe COPD and serum

creatinine >3mg/dl. The rate of composite end point (stroke and MI) and also rate

of individual end points (stroke/death/MI) were significantly higher in this high

risk patients23

. And the same reason was quoted for including these high risk

patients for CAS. But this fact is not universally accepted because, various single

centre studies have demonstrated safety even in patients considered high risk due

to various co-morbid conditions. Gasparis et al reviewed 788 consecutive patients

with isolated CEA and defined a high-risk cohort using similar criteria. Over all

stroke and death rate was not statistically significant between the high risk patients

and low risk patients. The authors questioned the existence of high risk CEA and

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concluded that it should be restricted to only anatomical factors such as

reoperations or irradiated neck24

Contralateral carotid occlusion is considered to be major anatomical factor

associated with increased risk of perioperative stroke. Presence of bilateral disease

is also a marker of widespread significant atherosclerotic disease including

coronary artery disease hence it is associated with increased perioperative

morbidity and mortality. Post-hoc analysis of NASCET database showed a

significantly high combined event rate in patients with contralateral carotid

occlusion25

. In similar way post hoc analysis from ACAS trail also failed to show

any benefit in asymptomatic patients with contralateral carotid occlusion and also

cautioned that it may be harmful26

. But the available evidence is contradictory and

multiple studies have shown excellent outcome in this subset of patients. Rockman

et al retrospectively analyzed the 338 patients with contralateral carotid occlusion

who underwent CEA in their institute. Among both asymptomatic and

symptomatic group of patients, there was no statistical difference in the

perioperative neurological symptoms when compared with those patients who did

not have contralateral carotid occlusion27

. Even the long term outcome was

reported to be similar to patients without contralateral carotid artery occlusion.

AbuRahma et al, as a sub group analysis of their randomized trial, noted that both

the perioperative and the long term combined event rate following CEA was

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comparable in patients with and without CEA28

. Thus based on most of the

available high quality evidence in the literature, the presence of contralateral

carotid endarterectomy does not seem to increase the perioperative or long term

outcome following CEA. And many centers do not consider contralateral carotid

occlusion as an anatomical risk factor for surgery to favor CAS.

Carotid reoperation is a technically challenging surgery when compared to

primary CEA. It is associated with increased perioperative stroke rate and also

complications such as cranial nerve injury and bleeding is high in these patients.

Hertzer et al from Cleveland clinic reported their experience of 153 reoperations in

2228 consecutive CEAs. They noted a high combined stoke and mortality rate in

redo surgeries when compared to primary CEA ( 5.1%vs 1.9%, P=0.024)29

.In their

series, Aburahma et al noted 15.3% transient cranial nerve injuries in redo CEA

compared to 4.9% in primary CEA. But no statistical difference between two

groups in permanent cranial nerve injuries30

. But the recent studies have

documented that even redo CEA can be safely done31

. Cho et al in their

retrospective analysis of 64 consecutive redo CEA showed a low perioperative

stroke rate (<3%) and no operative mortality. The outcome was sustained in the

long term follow up also and they concluded that redo CEA can be performed

safely with excellent short term and long term durability32

. Centers were CAS is

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routinely done, would opt for an endovascular management of these patients since

the main issue of increased cranial nerve palsy in redo CEA can be avoided.

Similar to redo CEA, the setting of prior cervical irradiation is also

technically demanding surgery with often dissection if difficult in the irradiated

operative field and also delayed wound healing can be anticipated. Only few series

are available in literature addressing this issue. Perioperative stroke and death rates

are distributed over a wide range in these studies (0.0% to 4.0% and from 0.0% to

3.3%, respectively33-36

.Hence local risk factors such as redo CEA and prior cervical

radiation are associated with slightly increased in stroke and death rate also cranial

nerve injury rates. Hence CAS was suggested CEA in these situations. But meta-

analysis suggest that both CEA and CAS is effective in either redo CEA or in

irradiated filed albeit minor increase in temporary cranial nerve injuries. Also CAS

is associated with increased recurrent stenosis which has to be taken into account

when taking decision37-38

.

Even though surgical technique of carotid endarterectomy has been

standardized and routinely done in many centers worldwide, there are few aspects

of surgery in which there is still controversy prevails. This include, type of

anesthesia (either local or general), method of endarterectomy (Conventional vs

eversion technique) use of shunt during surgery (Selective shunting vs routine

shunting vs no shunting) and arteriotomy closure( primary or patch closure and

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also type of patch). Various randomized trials and non randomized trials have been

published literature to address each of this issue, but still a many question remains

unanswered.

Reported advantages of doing CEA under local anesthesia (LA) or regional

anesthesia (RA) include predicting the need for selective shunting during surgery,

lower rate of perioperative myocardial infarction, decreased neurological events

and decreased hospital stay39-41

. Disadvantages of RA include increased discomfort

for the patient, anxiety for the operating surgeon, risk of seizures and also there are

chances that it may compromise the technique in teaching setup. Meta-analysis

from Cochrane database also did not show any significant advantage of CEA done

under LA/RA42

. General anesthesia versus local anesthesia (GALA) trial, a

multicenter randomized control trial of 3500 patients, randomized to CEA under

either GA or LA reported that there was no statistically significant difference in the

rates of perioperative stroke, death, or MI between the two anesthetic methods43

.

So the surgeon with proper discussion with the patient can choose any of either of

this two anesthetic technique depending on the clinical situation and own

preference.

Some surgeons prefer eversion endarterectomy over conventional CEA

technique, since no need to use patch and anastomosis can be completed quickly.

Eversion carotid endarterectomy versus standard carotid endarterectomy

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(EVEREST) trial is a large multicentre randomized control trial, which included

1353 patients randomized to eversion or conventional CEA. At 4 yr follow up no

significant differences in the clinical outcomes between the two CEA methods was

observed44

. Eversion technique offers distinct advantages in certain anatomical

situations like elongated or kinked ICA, other than this choosing a technique

depends on surgeon’s experience in performing a particular technique of

endarterectomy.

One of the long standing debate in CEA concerns with use of shunts during

surgery- routine use of shunts verses selective use of shunts verses routine non use

of shunts. Routine use of shunt allows surgery to be performed in a uninterrupted

manner, which decreases surgeon’s anxiety and also reduces the complexity of

cerebral monitoring equipment. It is easy to do and especially facilitates

performing CEA in a teaching environment. Theoretically it also decreases the

ischemia-reperfusion injury. Excellent results have been reported in several

series45-47

. But there are several arguments against use of routine shunting such as

increased risk of embolic phenomenon while inserting the shunt which can lead to

stroke, chances of damage to ICA and also it is unnecessary in 85% of the

patients48, 49

. To avoid these drawbacks some have advised routine non shunting

during CEA and have proven excellent results50,51

. Samson et al with their

experience with routine non shunting in 654 patients, provided an excellent

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outcome even in the setting of contralateral carotid artery occlusion52

.But in all

these studies there is a small incidence of stroke sometimes attributed to

intraoperative cerebral ischemia due to carotid clamping53

. So third option is

selective shunting, wherein shunts are used in those patients who experience or at

risk of cerebral ischemia during surgery. Several techniques are described for

monitoring to detect cerebral ischemia during surgery so that selective shunting

can be accomplished. These techniques including stump pressure,

electroencephalogram (EEG) transcranial Doppler (TCD), somatosensory evoked

potential (SSEP) cerebral oximetry monitoring cervical block anesthesia (CBA).

Cerebral monitoring using stump pressure (SP) was the earliest used method

to predict the risk of intraoperative ischemia. It is usually measured by inserting a

needle into distal common carotid artery after clamping ECA and proximal CCA.

Exact cutoff point varies between studies (anywhere between 25-70mm of Hg) and

never has been determined. Jacobs et al reported that with using SP <45mm of Hg

as a cut off for shunting, observed that only 21% of the patients required shunting

and their perioperative mortality and combined event rate were 0.5 and 1.5%,

respectively54

. With the introduction of newer modalities like TCD and EEG,

various studies were performed to validate SP. Harada et al performed a

prospective study with keeping EEG as a gold standard found that SP had a very

low positive predictive value. In this study 11% of the patients would not have

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received shunt and 64% would have received unnecessarily shunt if the ischemia is

determined only by SP criteria of <50mm of Hg. Similarly using TCD Finocchi et

al observed that SP did not correlate well with the ischemia55, 56

.

Intraoperative EEG is the most frequently used method of cerebral

monitoring and has been reported in more than 100 studies. Standard criteria for

intraoperative ischemia are at least a 50% decrease in fast background activity, an

increase in delta wave activity, or complete loss of EEG signals. Schneider et al

with their experience with routine EEG and selective shunting in 564 CEAs

reported that with routine use of EEG intraoperative stroke can be apparently

eliminated. In their series the perioperative stroke and combined event rate was

0.9% and 1% respectively57

. But drawbacks of EEG includes the fact that it can

vary by anesthetic agent used, arterial oxygen tension, and systemic blood

pressure, its inability to detect subcortical ischaemia and can detect only cortical

ischemia, has a high false-positive rate and in those with recent stroke, its

sensitivity is reduced. Some studies used SSEP to detect intraoperative ischemia

because unlike EEG, SSEP can detect ischemia of the deeper brain tissue. But it

was found to be no more sensitive or specific than EEG. A meta-analysis by

Wober et al found that SSEP is not a reliable method of monitoring cerebral

ischemia and it is associated with extremely poor positive predictive value58

.

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In TCD a middle cerebral artery (MCA) velocity is measured by placing a

Doppler probe across the petrous temporal bone. When there is marked decrease in

the MCA flow velocity, it is an indication to shunt. Main advantage of TCD is that

it can detect microemboli intraoperatively, possibly alerting the surgeon to avoid

further manipulation which can cause a stroke59

. Halsey et al reported their results

of 1495 CEA mostly done under GA that were monitored using TCD. They

observed that in patients with persistent ischemia detected by TCD, shunting

protected against stroke and thus concluded that perioperative stroke can be

reduced by selectively shunting only those patients with persisting severe ischemia

detected by TCD60

. The main drawback with TCD is that it is unusable in 15-20%

of the patient. It is very much operator-dependent and requires a great deal of skill

while the probe is bulky tends to encroach on the surgical site and often needs

constant adjustment that may be difficult perioperatively. As with stump pressures,

values for MCA velocity that correlate with critical cerebral blood flow have not

been determined and different investigators have proposed different thresholds at

which shunting should occur. Despite the potential benefits and utility of TCD,

there is no level one evidence to support its use as an independent modality to

determine cerebral hypoperfusion.

In selective cerebral shunting under cervical block anesthesia (CBA),

surgery is done in an awake patient under block and patients’ neurological status

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during carotid clamping can be continuously monitored and so that the need for

shunting can determined. The assessment of motor function on the side of the body

contralateral to surgery can be done by asking the patient to move their arm,

squeeze fingers or if their arm is under drapes they can be provided with a squeaky

toy or a fluid bag connected to a pressure transducer to squeeze when commanded.

In addition to testing motor function this also shows that the patient understands

and can obey commands. Studies have shown that intraoperative monitoring of

patients under CBA is more sensitive and specific than other modalities. Hans et al

evaluated 314 consecutive CEAs under CBA with EEG and SP measurement; a

shunt was used in 10% when a neurological deficit occurred. But using SP < 40mm

of Hg and EEG ischemic changes criteria shunt was required in 57% and 59% of

patients respectively61

. This indicates that both SP and EEG were less sensitive

than intraoperative neurological examinations under CBA. Similar results were

also seen by McCarthy et al, who concluded that both TCD and SP are not as

effective as neurological examinations under CBA62

. The main limitations of CBA

are the patient’s anxiety, claustrophobia and cervical spine rigidity. Inspite of its

reliability there is no robust evidence demonstrating a difference in stroke or

mortality rate between general and regional anaesthesia for CEA.

Other modalities that have been described for perioperative cerebral

monitoring includes cerebral oximetry, near infrared spectroscopy, jugular venous

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bulb oxygen saturation and Xenon-133 washout assay. Most of these are under

investigational phase and often has cumbersome equipments to use in day today

practice63

.

After extracting the plaque, the simplest and most effective method of

closing the arteriotomy is by simple closure without patching. But now there is

level 1 evidence available which showed the superiority of patch closure when

compared with primary repair. The British Joint Vascular Research Group RCT

compared 104 patients undergoing primary closure with 109 patients treated by

patch closure with either autologous vein or Dacron. Six strokes occurred in the

primary closure group and two in the patch group, and six perioperative

thromboses were noted in the primary closure group versus none in the patched

group64

. Meta-analysis by Bond et al found that all short term and long term end

points were significantly better with patch closure than with primary closure65

.

But even though literature supports patching, there is very little evidence to

support the type of patch material to be used. Various patch material that has been

used includes Great saphenous vein (GSV), jugular vein, Dacron, PTFE and

Bovine pericardial patch. Saphenous vein patching has been used extensively with

good results, although problems specific to saphenous vein patching include

wound complications at the harvest site, potential compromise of a valuable

conduit for later bypass procedures, and the devastating complication of patch

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rupture66

. But many studies shows similar outcome with saphenous vein patch

when compared with other patch materials. Goldman et al compared saphenous

vein and internal jugular vein with knitted Dacron in 275 CEAs and found no

significant differences in perioperative morbidity, mortality, or early restenosis

among any of these groups67

.

Percutaneous treatment of carotid stenosis has been extensively investigated

and outcomes compared with those of CEA by a large number of RCTs, registries,

and clinical studies. None of the trails have conclusively proved non superiority of

CAS with that of CEA. CREST is the most recent and largest RCT designed to

compare the efficacy of CAS and CEA in standard-risk patients9. At the end of

four years, there was no significant difference in the estimated 4-year rate of the

primary endpoint (composite of stroke, death or MI) between the CAS and the

CEA groups. The risk of periprocedural stroke/death was significantly higher in

CAS than in CEA (4.4% vs. 2.3%; P = .005), and that of MI was significantly

higher in CEA (1.1% vs. 2.3%; P = .003). Periprocedural risk of stroke/death was

higher after CAS for symptomatic patients (6.0% vs. 3.2%; P = .02). CREST

confirmed higher periprocedural stroke hazards from CAS in symptomatic patients

but raised concerns about the cardiac risks after CEA. The recent Cochrane meta-

analysis which included 16 trials concluded that CAS was associated with an

increased risk of periprocedural stroke or death compared with CEA.

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Many centers routinely do CEA in our country but is paucity of literature

available from India pertaining to outcome of CEA. One of those is a report from

our institute which included 39 patients in the early part of our experience11

. The

other report was from Mishra et al, who documented the perioperative outcome of

CEA in their series of 49 patients. The perioperative mortality was 1.89% and

stroke was 1.89% in their series. Only three patients required shunting and all

arteriotomy was primarily closed12

.

Our institute, being tertiary care centre with a well organized stroke team,

routinely manages patients with extracranial carotid artery disease with

multidisciplinary team approach. This study aims at assessing the outcomes of the

procedure done since 1997 in our institute.

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METHODS AND METHODOLOGY

Retrospective analysis of patients operated in our institute between January

1997 to November 2015 was done. Patient’s demographic details, operative

procedure accounts and post operative follow up were noted from the hospital

records.

Indication for surgery (Inclusion criteria):

1. Symptomatic patients with >70% stenosis

2. Symptomatic patients with ulcerated plaque >60% stenosis

3. Asymptomatic patients with progressive increase in stenosis over and above

80%, despite medical management

4. Asymptomatic patients with >60% stenosis with contralateral carotid

occlusion

Exclusion criteria:

1. Symptomatic patients <60% stenosis and asymptomatic patients <80%

stenosis

2. Patient who underwent Carotid artery stenting(CAS) during the study time

period

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3. Patients who underwent concomitant Coronary revascularization along with

CEA

All patients were evaluated with CT/MRI brain as per Stroke protocol

followed in our institute. Neck vessel Doppler was also done to measure the

velocities across the stenosis. Degree of stenosis was calculated both by

CTA/MRA images (NASCET Criteria) and by duplex velocity criteria. Apart

from routine blood investigations (which included hemogram, coagulation

profile, liver and renal function test), all patients underwent baseline non

invasive cardiac workup including ECG, echocardiogram and chest X-ray.

Further invasive testing for cardiac fitness was decided by the cardiologist

based on patient’s cardiac symptoms and functional class. If found to have

significant cardiac disease, the patient is either advised concomitant coronary

revascularization with CEA or percutaneous coronary intervention (PCI)

followed by staged CEA. All patients were started on dual antiplatelets (Aspirin

and Clopidogrel) with high dose statin therapy (Atorvastatin 40/80mg or

Rosuvastatin 20/40mg). Blood pressure and glycemic profile were monitored

and controlled accordingly. Around 2-4 days prior to procedure, clopidogrel

was withheld but Aspirin was continued during the perioperative period.

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Operative Procedure details:

All the patients underwent the procedure under general anesthesia using

neuro-protective pharmacotherapy. Low molecular weight dextran is started at the

rate of 10-20cc/hr in the beginning of the surgery. The patient was positioned with

neck extended and chin turned to opposite side. Incision was along the anterior

border of sternocleidomastoid muscles (SCLM), from the angle of mandible to 5

cm above clavicular head. The carotid sheath was opened and the common carotid

artery (CCA) was dissected and looped for control. External carotid artery (ECA)

and Superior thyroid artery (STA) were controlled and looped. Without disturbing

the carotid bifurcation the distal internal carotid artery (ICA) beyond the disease

was dissected and looped for control. Heparin (1 mg/kg) was given intravenously.

Neuro productive medications such as Methyl Prednisolone (30mg/kg) and

Thiopentone (1mg/Kg) were administered. ICA, CCA, ECA and STA were

clamped in sequence. The arteriotomy begins 2 cm on the distal CCA and

proceeded over the carotid bulb, gradually extending to visualize the atheromatous

endpoint in ICA. A subintimal plane was created and the plaque was extracted

feathering away from ICA end point with gentle traction while the ICA clamp was

momentarily released (Fig 8,9). The endarterectomised artery was then carefully

irrigated with heparinised saline and any loose intimal tags were peeled off .We

routinely used shunt during the proceure ( Pruitt Inhara shunt, LeMaitre® vascular,

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USA or Brener shunt, Bard Peripheral Vascular Inc, Tempe, AZ, USA) which was

first inserted into the CCA end followed by ICA end and snugged(Fig 10). Stump

pressure was measured by placing a rubber shod on the CCA end, using an arterial

line extension attached to T segment of the shunt. Once the stump pressure was

recorded, continuous perfusion pressure to brain was recorded with the removal of

rubber shod (Fig 11). Systemic arterial pressure was monitored via the radial

arterial line and around 90 mm of mean blood pressure is maintained while

ipsilateral carotid is cross clamped. The arteriotomy was then repaired using a

patch (Supramaleolar great saphenous vein mostly)[Fig 12]. In patients with

peripheral vascular disease or those having poor quality vein, Bovine pericardial

patch was used [Fig 13]. Before completing the suture line, the carotid shunt was

removed and clamps reapplied. Patient was then placed in Trendelenberg position

and adequate de-airing was done after which the sutures were tied. ECA first and

then CCA clamp was released, and initial perfusion restarted to ECA. ICA was

perfused a minute later. Hemostasis secured and heparin reversal with protamine

was done. A suction drain was placed and the wound was repaired in layers. The

patient was then shifted to the ICU and kept on assisted ventilation. Once the

patient becomes awake and neurological assessment is done, he/she was extubated.

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Post operative management:

Post operatively strict blood pressure control was maintained and when

required infusion of vasodilators such as nitroglycerine (NTG) and/or Sodium

nitropruside (SNP) was started to maintain the systolic blood pressure less than

120mm of Hg. Anti edema measures, which include intra venous steroids and

diuretics, were started and continued minimum for 2-3 days after procedure. Low

molecular Dextran was continued for 48 hours. From post op day (POD) 1 oral

feeds started and a single antiplatelet medication was started (usually Aspirin).

Patient was observed in Intensive care unit (ICU) for 24-48 hours and then shifted

to the ward. On POD 5 or 6, sutures were removed and patient was discharged.

Postoperative surveillance:

Patients were followed up by the neurologist and vascular team at 3rd

month,

6th month and 1 year after surgery. Then after, yearly reviews were done in the

stroke clinic. Patients were reassessed for any fresh neurological deficit and

NIHSS score & mRS were measured. Duplex scan was done at 3rd

month, 1st year

and then yearly. All demographic data, vitals, duplex findings and neurological

assessment is recorded in a data sheet. If any restenosis was found or patient

develops ipsilateral symptoms, the case was again discussed in the comprehensive

stroke meet and further treatment was initiated.

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Definitions:

Symptomatic patients:- Patients with carotid stenosis are considered symptomatic if

they present with a history of stroke, amaurosis fugax, or transient ischemic

attacks (TIA) involving the ipsilateral carotid territory that occurred within 180

days of the initial assessment

Asymptomatic patients:- Patients with no neurologic symptoms referable to the

cerebral hemisphere ipsilateral to the carotid stenosis or a history of previous

neurologic events without subsequent event within 180 days.

Stroke:- Defined as a cerebral infarction that manifests as sudden onset of focal

neurological deficits that persists for more than 24 hours

Transient Ischemic Attacks: Defined as a temporary focal neurologic deficit that

persists for <24 hours with a return to baseline or complete resolution of the event.

Minor stroke:- A new neurologic event that persists for more than 24 hours but

completely resolves or returns to baseline within 30 days with NIHSS score of ≤4

Major stroke:- A new neurologic event that persists for >24hours with NIHSS

score >4

Post Procedural myocardial Infarction:- Chest pain or equivalent symptoms

consistent with myocardial ischemia and ECG evidence of ischemia including new

ST segment depression or elevation> 1mm in 2 or more contiguous leads along

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with elevation of cardiac enzymes (CK-MB or Troponin T) to a value 2 or more

times the institute’s laboratory upper limit of normal

Cranial Nerve injury:- Temporary or permanent deficits secondary to injury to

cranial nerves that occured as a result of a carotid intervention, particularly those

that have not resolved by 30 days and 6 months after the initial procedure

Statistical comparison for continuous variables was performed with

Student’s t test and categorical variables using Fisher’s exact test. p<0.05 was

considered statistically significant. Kaplan Meier life-table analyses were

performed to assess stroke-free and overall survival and compared using log-rank

test.

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RESULTS

Demographic details and disease status:

The mean age group of the study cohort was 62.9yrs and majority

were males (83%)[Fig 1]. Predominantly smokers (60.5%) and hypertensives

(85.2%)[Fig 2].Coronary artery disease was present in 61 (27.4%) and peripheral

artery disease was present in 16(7.17%) patients [Fig 4]. Concomitant significant

(>50% stenosis) steno occlusive disease of Vertebro-basilar territory was present in

36(16.1%) patients and of intracranial vessels (ipsilateral/contralateral) was present

in 21(9.41%) patients. Contralateral ICA occlusion was present in 27(12.1) patients

[Fig 3]. The demographic details of the study group are summarized in Table-1.

Among the study group 213 (95.5%) patients had symptomatic carotid

disease and only 10 (4.5%) patients were asymptomatic [Fig 5]. All these

asymptomatic patients were having contralateral occlusion. In the symptomatic

patients, 143 (67.13%) had stroke as their presenting symptom and remaining 70

(32.86%) patients presented with TIA. Majority (90.24%) patients had >70%

stenosis of the ICA. All patients underwent conventional carotid endarterectomy

except in 5 (2.25%) patients in whom eversion endarterectomy was done mainly

because of anatomical indications such as coiled ICA/in ICA with significant kink.

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Plaque was ulcerated in 62.33% patients. Except in 2, shunt was used in all

patients. In one patient the ICA was very narrow in caliber hence shunt couldn’t be

used and in other patient eversion endarterectomy was done, hence shunt was not

used during the procedure. All patients were patched during conventional CEA,

majority (92.37%) being autologous supra malleolar saphenous vein patch. In 13

patients (5.82%) Bovine pericardial patch was used either because of poor quality

of the vein or presence of significant peripheral vascular disease, in whom wound

healing is likely to be impaired (Table-2).

Perioperative Outcome:

In asymptomatic patients, none developed perioperative adverse events.

Among symptomatic group, 2 (0.93%) patients had major stroke in the immediate

post operative period. One major stroke was due to post operative hyper perfusion

syndrome related intra cranial hemorrhage. At 3month follow-up, both these

patients made excellent neurological recovery with no disabling permanent deficit

(mRS<2). Six (2.81%) patients developed transient neurological events (minor

strokes) with total/near-total recovery within a week. Perioperative cardiac event

was seen in 6(2.81) patients, mostly ST elevation MI which was managed

conservatively. Two (0.93%) patients had immediate post operative mortality, one

due to MI and other patient due to aspiration related ARDS. Cranial nerve palsy

was present in 19(8.52%), commonly involving hypoglossal nerve (78.96%),

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majority being transient (89.48%). Apart from hypoglossal nerve,

glossopharyngeal nerve and marginal mandibular branch of facial nerve was

involved in 2 patients each. Table 3 summarizes the peri-operative outcomes

Factors affecting the perioperative outcome:

Patient related factors that determine the perioperative outcome

(neurological outcome and mortality) was assessed. The variables with which the

outcome was assessed was as follows- Age < 65yrs, female sex, presence of

comorbid conditions (HTN, DM, DLP, Smoking, CAD, PAD), presence significant

vertebral/intra cranial disease, contralateral carotid occlusion, presenting

symptomatology (TIA/Stroke) and surgery within 6 weeks from onset of

symptoms (Table 4 & 5). In multiple logistic regression analysis none of the above

mentioned variable significantly affected the perioperative outcome. Even with

contralateral occlusion, the outcome was not significant when compared with those

who did not have CCO.

Long term outcome:

Mean follow up of the patients was 29.7months . At the end of 1 year follow

up 3 (1.34%) patients sustained stroke of which 2 patients had a non fatal stroke

and the other patient succumbed to fatal stroke. Overall there were 5 (2.24%)

mortalities at the end of 1 year of which 4 patients died due to acute cardiac events.

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Restenosis (>50%) was seen in one patient and he was managed conservatively.

Beyond 3 yrs, one patient developed contralateral stroke which improved

completely and there was 2 mortalities mainly due to cardiac cause. Asymptomatic

restenosis (>50%) was seen in 1 patient at the end of 1 year and 6 patients at the

end of three years including 1 occlusion. All these patients were managed

conservatively and were on regular follow up. Long term stroke free survival was

98.2%, 94.6% and 93% at the end of 1, 3 and 5 years respectively.

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Table- 1) Demographic details and risk factors

Number %

Total Number (n) 223

Male 185 83%

Mean Age 62.9yrs

Risk Factors

HTN 190 85.20%

DM 126 56.50%

Smoking 135 60.50%

DLP 56 25.10%

Other system

PAD 16 7.17%

CAD 61 27.35%

Concomitant steno-occlusive disease

Vertebro-basilar 36 16.14%

Intracranial branches 21 9.41%

Contralateral occlusion 27 12.10%

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Table- 2) Disease status and Intraoperative features

Disease status Number %

Symptomatic 213 95.51%

Stroke 143 67.13

TIA 70 32.86

Asymptomatic 10 4.49%

Degree of Stenosis

50-69% 22 9.86%

70-89% 114 51.12%

90-99% 87 39.02%

Intra Operative Features

Ulcerated plaque 139 62.33%

Conventional CEA 218 97.75%

Eversion CEA 5 2.25%

Shunt used 221 99.10%

Vein Patch 206 92.37%

Bovine pericardial patch 13 5.82%

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83.00%

17.00%

Fig 1-Sex Distribution

Male

Female

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

HTNDM

SmokingDLP

57%

85%

61%

25%

Fig 2-Comorbid Illness

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12%

9%

16%

0%

2%

4%

6%

8%

10%

12%

14%

16%

18%

C/l CCO Sig Intracranial disease Sig Vertebral disease

Fig-3 Disease in other cerebral vascular territories

27%

7%

0% 5% 10% 15% 20% 25% 30%

CAD

PAD

Fig-4 Coronory & Peripheral Vascular disease

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:

Asymptomatic

4.5%TIA

33%

Stroke

67%

Symptomatic

95.5%

Fig-5 Clinical Status

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Table 3.Peri-operative outcomes

Outcome Number %

Ipsilateral Neurological Events

Major*

2 0.93%

Minor#

6 2.81%

Cardiac Event 6 2.81%

Mortality 2 0.93%

Others

Cranial Nerve paresis 19 Total 8.52%

12th N-15 78.96%

10th N-2 10.52%

7th N-2 10.52%

Wound complications 1 infection 0.45%

8 hematoma 3.58%

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Table- 4- Univariate analysis of predictors of perioperative adverse

Neurological events (Major/minor)

Variable studied

Peri - OP Neurological

Events Total (N=223) p value

Yes (N=8) No (N=215)

N % N % N %

Age <65 4 50 135 62.8 139 62.3 0.463

Sex- Male 7 87.5 178 82.8 185 83 0.728

Female 1 12.5 37 17.2 38 17

TIA 4 50 62 28.8 66 29.6 0.198

Stroke 4 50 139 64.7 143 64.1 0.396

Vertebral disease 3 37.5 33 15.3 36 16.1 0.095

IC vessels stenosis 1 12.5 20 9.3 21 9.4 0.761

DM 5 62.5 121 56.3 126 56.5 0.727

HTN 5 62.5 185 86 190 85.2 0.066

Smoking 5 62.5 130 60.5 135 60.5 0.908

PAD 0 0 16 7.4 16 7.2 0.423

CAD 0 0 61 28.4 61 27.4 0.077

DLP 1 12.5 55 25.6 56 25.1 0.402

Timing of surgery<2

weeks 4 50 100 46.5 104 46.6 0.846

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Table- 5- Univariate analysis of predictors of immediate

postoperative mortality

Immediate mortality

Total (N=223) p

value Variable Studied Yes (N=2) No (N=221)

N % N % N %

Age <65 2 100 137 62 139 62.3 0.269

Sex- Male 2 100 183 82.8 185 83 0.52

Female 0 0 38 17.2 38 17

TIA 1 50 65 29.4 66 29.6 0.525

Stroke 1 50 142 64.3 143 64.1 0.676

Vertebral disease 0 0 36 16.3 36 16.1 0.533

IC vessels stenosis 0 0 21 9.5 21 9.4 0.647

DM 2 100 124 56.1 126 56.5 0.213

HTN 2 100 188 85.1 190 85.2 0.554

Smoking 2 100 133 60.2 135 60.5 0.251

PAD 0 0 16 7.2 16 7.2 0.693

CAD 1 50 60 27.1 61 27.4 0.47

DLP 1 50 55 24.9 56 25.1 0.415

Timing of surgery<2

weeks 1 50 103 46.6 104 46.6 0.924

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Table 6-Peri-operative outcome comparison between patients with

CCO and no CCO

Outcome

CCO

(n = 27)

No CCO

(n = 196)

p

value

Patients % Patients %

Death 0 0.0 2 1.0 > 0.99

Major stroke* 0 0.0 2 1.0 > 0.99

Minor/Transient events† 1 3.7 5 2.6 > 0.99

Peri-operative MI 0 0.0 2 1.7 > 0.99

MI = Myocardial infarction i.e., elevation in cardiac enzymes or ECG changes

* Major Stroke-A new neurologic event that persists for >24hours with NIHSS score >4

† Minor Stroke-A new neurologic event that persists for more than 24 hours but completely

resolves or returns to baseline within 30 days with NIHSS score of ≤4

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Table- 7-Late outcome

Outcome Number %

1 year outcome

Stroke 3 1.34%

Death 5 2.24%

Re-stenosis rate* 1 0.44%

Beyond 3 years outcome

Stroke 1 0.44%

Death 2 0.89%

Re-stenosis rate* 6 2.69%

* ≥50% by duplex or CT angiography

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Fig 7-Kaplan Meier Survival Curve

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Fig-8- Intraoperative picture showing ulcerated plaque (yellow arrow)

and a free floating thrombus (Black arrow)

Fig-9- Carotid endarterectomy specimen showing smooth feathered end

of the plaque (black arrow) and ulceration within (yellow arrow)

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Fig-10- Pruitt Inhara shunt insitu

Fig-11- A) Shows stump pressure mean of 31mm of Hg B) Shows shunt

pressure mean of 68mm of Hg

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Fig-12- Patch closure of the arteriotomy using saphenous vein patch

Fig-13- Patch closure of the arteriotomy using bovine pericardial patch

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Fig-14- CT Angiogram showing significant stenosis of Carotid bulb and proximal ICA

Fig-15- CT-angiogram, volume rendered 3-dimentional image showing patent

ICA at 12 years follow up

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DISCUSSION

There is robust clinical evidence for safety and efficacy of carotid

endarterectomy in preventing subsequent stroke in patients with symptomatic and

asymptomatic carotid artery disease4-8

. The recommended benchmark for post

CEA combined event rate (stroke and mortality) is 1.5% for asymptomatic patients

and 5% for symptomatic patients69

. In our present study, the asymptomatic patients

formed only a minority of the study population, i.e. 10 patients that too in

association with CCO, but no adverse event were observed in them. Among the

symptomatic patients the perioperative major stroke rate was 0.93% and mortality

of 0.93%, both of which was within the recommended benchmark outcome. The

transient neurological events were seen in 2.81% patients and all these outcomes

were within the recommended bench mark.

Reports from latest randomized controls trials such as ICSS and CREST,

failed to prove non inferiority of CAS when compared to CEA and still CEA

remains the treatment of choice especially in symptomatic patients9, 70

. Various

individual risk factors are considered to influence the outcome of CEA which

includes age >80yrs, female sex, co-morbid illness (DM, HTN, DLP, CAD, PAD),

anatomical factors (previous ipsilateral CEA, high or low bifurcation, previous

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neck irradiation), tandem lesions in intracranial vessels, significant vertebrobasilar

disease, contralateral carotid occlusion, symptomatic status

(asymptomatic/TIA/Stroke) and ipsilateral cerebral symptoms within 2 weeks

before surgery71, 72

. And these risk factors are quoted as an indication to choose

CAS rather than CEA as a modality of treatment. The mean age of our study group

was lesser (63yrs) than the published large institutional series18

. Hence 65 yrs of

age was taken as a cut off for assessing the risk. Moreover percentage of female

patients in the study group was also less (17%) to be considered as a major factor

and none of the patients had previous ipsilateral CEA. In the current study none of

these other factors influenced poor post operative outcome (both perioperative

poor neurological outcome and mortality). May be the event rate is very low in our

study, hence we couldn’t get a significant value when assessing these factors.

Studies have also shown similar results, with only anatomical/local risk factors

have slightly raised adverse events and in all other patients CEA can be performed

successfully with low morbidity and mortality71

.

The influence of CCO on CEA outcome still remains controversial. Both

NASCET and ACAS trial have showed adverse neurological outcome in this

subset of patients even though they included only few patients with CCO25, 26

. On

the other hand many authors have demonstrated peri-operative outcomes in

patients with CCO that are comparable to the non-occluded cohort73-75

. It is

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hypothesized that patients who undergo carotid intervention in the face of CCO

might have heavier disease burden particularly in intracranial and/or extracranial

cerebrovascular system. Also their cerebral collateral vascular reserve,

predominantly of the hemisphere ipsilateral to the occluded carotid artery may be

significantly compromised76

. In our study, none of the patients with CCO

developed any adverse neurological events. This can be attributed to routine use of

shunt and pharmacological cerebro-protection. A plausible rationale for routine

shunting in patients with CCO can be inferred if the concept of total brain

circulation is considered in these patients. The stenosed ICA not only supplies the

ipsilateral hemisphere but is also responsible for sustenance of perfusion to

significant portion of the contralateral hemisphere particularly the peripheral

(watershed) territories. When an ischemic event occurs, such as in carotid cross-

clamping, these watershed zones are at greatest risk of hypoperfusion due to

compromised collateral blood flow. The use of routine shunting with continuous

intra-operative monitoring of shunt perfusion pressure, and hence cerebral

perfusion, seems to be vital adjunct technique especially in this subset of patients.

Routine shunting during CEA is also an area of controversy and literature

still doesn’t shed proper evidence to advocate specific method of shunting and

cerebral monitoring (routine vs. selective vs. no shunting) 48

. In our study we

routinely shunted all the patients (except in 2). In our practice we insert the shunt

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after completely removing the plaque and this avoids any chance of distal

embolisation that can happen during insertion of shunt, which is an adverse event

quoted against usage of routine shunting. Patients tolerate this short period of

cerebral ischemia until shunting even in those having very low stump pressures.

But there are several arguments against use of routine shunting such as increased

risk of chances of damage to ICA (dissection) and also it is unnecessary in 85% of

the patients48, 49

. So many have suggested either routine non shunting or selective

shunting77, 78

. But in all these studies there is a small incidence of stroke often

attributed to carotid clamping induced cerebral ischemia. More over even though

many methods of cerebral monitoring has been described including EEG, TCD,

SSEP, stump pressure etc, most of them are cumbersome to do in operating room

and none of them have been proven to be most sensitive method of monitoring

cerebral ischemia79

. In our experience routine shunting allows the surgeon to

perform the surgery without anxiety especially in a teaching environment like our

institute. The same has been reported in large series from Cleveland clinic

experience by Hertzer at al45

.

All procedures were done under general anaesthesia in our institute even

though many advocate use of local anaesthesia/regional anaesthesia for the same.

The only randomized control trial which compares GA vs LA (GALA Trial) failed

to show any statistical difference in the rates of perioperative stroke, death, or MI

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between the two anesthetic methods43

. GA has advantages avoiding discomfort/

claustrophobia for the patient, helps in avoiding unnecessary fluctuation of blood

pressure during surgery and also reduces anxiety for the surgeon.

There is robust evidence in literature showing superior clinical and

anatomical outcome with patching over primary closure of the arteriotomy after

CEA and near abolition of perioperative ICA thromsbosis65, 80

. Various patch

materials are available including autologous vein patch (saphenous vein/external

jugular vein), PTFE, polyester and bovine pericardium. But optimal patch material

yet to defined. In majority of our study group supra malleolar saphenous vein was

used as a patch material and in those patients with poor vein/significant peripheral

arterial disease Bovine pericardial patch was used. Various complications are

described specific to saphenous vein patching such as wound complications at the

harvest site, aneurysmal expansion of the patch and rupture of the patch in up to

4% of these patients66, 67

. In the present study we never experienced patch rupture

or aneurysmal expansion during the follow up. Since bovine pericardium was used

in only 13 patients, direct comparison of these two types of patch material was not

done. Currently there is no strong evidence to show superiority of one patch

material over other, but Margovsky et al showed in their animal model that platelet

accumulation over the vein patch was much lower than that on prothetic patch

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(Dacron/PTFE)81

. So whenever available, saphenous vein still remains the optimal

patch for arteriotomy closure.

In the published institutional series, the incidence of restenosis had been

reported between 1-37%82- 83

. It varies between definition applied, detection

method and duration of follow up. In a review by Lattimer et al only 0-8% patients

had symptoms related to restenosis and majority remained asymptomatic84

. Present

study showed restenosis rate of 0.4% at 1 year and 2.7% beyond three years, which

is comparable to the reported literature. None of these patients were symptomatic

for the same and remained asymptomatic during follow up, avoiding any

reintervention. This low rate of restenosis in our study is probably due to routine

patch angioplasty done in our patients since there is level 1evidence which shows

patch angioplasty following CEA reduces the incidence of restenosis than primary

closure. Meta-analysis by Bond et al found that both short term and long term

outcomes were significantly better with patch closure than with primary closure65

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CONCLUSION

Our study demonstrates that carotid endarterectomy could be performed

safely with low risk of perioperative stroke or death in the setting of symptomatic

carotid artery disease. Encouraging long-term benefit in stroke prevention could be

accomplished even in patients with risk factors such as contralateral carotid

occlusion or those who undergo surgery as early as with 2 weeks from the

neurological event. Routine shunting during CEA has vital benefits in abating

adverse neurological outcomes during surgery. Patch angioplasty benefits not only

in short term but also in long term outcome after surgery by keeping the internal

carotid artery patent and disease free.

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PATIENT INFORMATION PROFORMA

PROFORMA No:

AGE/SEX

RISK FACTORS:

Hypertension

Diabetus

Coronary Artery disease

Peripheral Arterial disease

Dyslipedemia

Smoker

PRESENTING NEUROLOGICAL SYMPTOMS

Type of Event (stroke/TIA)

Duration since onset

Completely recovered or not

Modified Rankin Score (mRS)

National Institute of Health Stroke score (NIHSS)

PREOPERATIVE IMAGING

Neck Vessel Doppler

CT Angio

Aortic Arch

Ipsilateral Carotid Vessels

Contralateral Carotid Vessels

Vertebral System

Intracranial Disease

MR Angio

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Aortic Arch

Ipsilateral Carotid Vessels

Contralateral Carotid Vessels

Vertebral System

Intracranial Disease

Intraoperative Findings

Bifurcations

Lesion characteristics

Type of patch used

Mean shunt pressure

Stump pressure

Duration of carotid clamp

Immediate Post OP

Stroke(minor/major)

Cardiac Event

Respiratory distress

Bleeding

Reperfusion Syndrome

Uncontrolled Hypertension

Cranial Nerve Palsy

Wound Infection

Follow Up

3 Months/12 months

Any New neurological Event

Neck Vessel Doppler

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LIST OF ABBREVIATIONS

CEA - Carotid endarterectomy

CAS - Carotid Artery Stenting

CCA - Common Carotid Artery

ECA - External Carotid Artery

ICA - Internal Carotid Artery

GA - General Anaesthesia

LA - Local Anaesthesia

COPD - Chronic Obstructive Pulmonary Disease

CAD - Coronary Artery Disease

PAD - Peripheral Artery Disease

CVD - CerebroVascular Disease

DM - Diabetes Mellitus

HTN - Hypertension

CKD - Chronic Kidney Disease

DLP - Dyslipedemia

CT Angio - Computed Tomography Angiography

MR Angio - Magnetic Resonance Angiography

NIHSS Score - National Institute of Health Stroke Scale Score

mRS - modified Rankin Scale

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APPENDIX 1- NIHSS Score

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APPENDIX 2- modified Rankin Scale

S No Name Age Age Sex H No Symptomatic (Y/N) TIA Stroke Side (L/R) % Stenosis C/L ICA Occlusion (Y/N) Vertebral disease (>50%) IC vessels stenosis(>50%)

1 SADASIVAN CK 77 >65 M 389899 Y N Y R 90% N N N

2 RAMAN Y 75 >65 M 384542 Y Y N R 60% N N N

3 BABU ASARI M 59 <65 M 193761 Y N Y R 70% N N N

4 PATHAEI K 47 <65 F 391185 Y N Y R 90% N N N

5 VASUDEV WADHWANI 53 <65 M 391269 Y N Y R 90% N N N

6 SOLOMON 79 >65 M 392297 Y Y N R 80% N Y N

7 VIJAYAN NAIR M 57 <65 M 391601 Y Y N R 90% N N N

8 VIJAYAKUMAR B 67 >65 M 394071 Y Y N R 90% N N N

9 NOORUDHEENKUTTY A 60 <65 M 394159 Y N Y L 95% N Y N

10 SAJI G NAIR 46 <65 M 393259 Y N Y R 80% N Y Y

11 VIJAYAMMA K 81 >65 F 394510 Y N Y L 80% N N N

12 BAHULEYAN 59 <65 M 393760 Y N Y L 90% N N N

13 SARASU GOPALAN 58 <65 F 394649 Y Y N R 80% N Y N

14 SATISH KUMAR DOSHI 64 <65 M 396250 Y Y N L 80% Y N N

15 ALAVIKUTTY M 68 >65 M 396268 Y N Y L 70% N Y N

16 CYRIAC THOMAS 67 >65 M 397010 Y N Y L 60% N N N

17 KUNJU KUNJU 72 >65 M 397394 Y Y N L 80% N N N

18 PARAMESWARAN NAIR 73 >65 M 397013 Y Y N L 80% N N N

19 GOPINATHAN NAIR 74 >65 M 397378 Y Y N R 80% N N Y

20 BHANUMATHY AMMA 75 >65 M 397383 Y N Y R 90% N N N

21 SASIDHARAN UT 63 <65 M 398730 Y N Y R 80% N N N

22 RAJU LOORTHU SAMY L 45 <65 M 399426 Y N Y R 80% N N N

23 SAINABA M 67 >65 F 400207 Y N Y R 90% N N N

24 MALAISAMY L 33 <65 M 400292 Y N Y L 80% N N N

25 SARASWATHY C 47 <65 F 400989 Y Y N R 90% N N N

26 THOUFEEK M 69 >65 M 401080 Y N Y L 80% N N N

27 DAISY JOY 68 >65 F 401402 Y Y N R 90% N N N

28 SURESH K 51 <65 M 401304 Y N Y R 80% N N N

29 BALAKRISHNAN KP 63 <65 M 401739 Y N Y R 80% N N N

30 VIJAYA KUMARAN B 65 <65 M 400259 Y Y N L 80% N N N

31 KURIKESU JOHN 70 >65 M 402103 Y Y N R 95% N Y N

32 RAJENDRAN NAIR M 63 <65 M 401260 Y Y N R 95% N N N

33 RAMAKRISHNAN K 59 <65 M 402370 Y N Y R 90% N N N

34 PADMAKUMAR PR 46 <65 M 403332 Y N Y R 80% N N Y

35 RAMACHANDRAN NAIR N 67 >65 M 403599 Y N Y L 90% N Y N

36 RAMACHANDRAN NAIR TR 59 <65 M 404063 Y N Y L 80% Y N N

37 HILARY A 73 >65 M 244076 Y N Y L 90% N N N

38 RAMACHANDRAN K 56 <65 M 405142 Y N Y R 80% N N N

39 VISHWANATHAN PILLAI KP 76 >65 M 222294 Y N Y L 90% N N Y

40 JALALUDEEN M 68 >65 M 403093 Y N Y R 90% N N N

41 ABBAS M 62 <65 M 406070 Y Y N R 90% Y Y N

42 ABDUL KAREEM 53 <65 M 406633 Y Y N L 90% N Y N

43 SOSAMMA GEORGE 65 <65 F 407098 Y Y N R 90% N N N

44 SAROJINI AMMA 68 >65 F 400747 Y N Y L 95% N N N

45 GEORGE THOMAS 65 <65 M 395261 Y Y N L 80% N N N

46 SURENDRAN M 78 >65 M 371648 Y Y N L 90% N N N

47 VIMALA K 64 <65 F 372899 Y Y N L 90% Y N N

48 ABDUL AZEEZ 61 <65 M 371509 Y N Y L 70% N N Y

49 PHILIP TP 78 >65 M 373627 Y N Y R 70% N N N

50 SUBRAMANIAM MV 61 <65 M 374191 Y Y N L >90% N N N

51 ABDUL RAZAK A 76 >65 M 378213 Y N Y R 70% N N N

52 MOHANAN TN 69 >65 M 379493 Y N Y L 90% N N N

53 IBRAHIM KS 53 <65 M 377845 Y N Y R 75% N Y Y

54 ALAVI M 76 >65 M 379955 Y N Y L 70% Y N N

55 WALTER THOMAS 73 >65 M 348086 Y N Y L 70% N N N

56 JOSEPH KO 72 >65 M 380586 Y Y N L >90% N N N

57 LIAQUATH ALI G 69 <65 M 380687 Y N Y L 70% N N N

58 FRANCIS P 60 <65 M 380838 Y Y N R >90% N N N

59 SARASWATHYKUTTY ANTHARJANAM 65 <65 F 381128 Y N Y L 65% N N N

60 GOPALAKRISHNAN ACHARY 80 >65 M 380835 Y Y N R 90% N N N

61 SATHYABHAMA S 58 <65 F 381176 Y N Y L 90% N N Y

62 VAMADEVAN S 84 >65 M 382024 Y N Y R 80% N N N

63 MARSHAL KA 65 <65 M 381504 Y N Y L 70% N N N

64 FAZEELATHUNISHABAGUM N 62 <65 F 380418 Y N N R 90% Y N N

65 MARY CD 68 <65 F 382197 Y N Y R 65% Y Y Y

66 BALACHANDRAN 56 <65 M 383287 N N N R 70% Y N Y

67 AHAMED KUNJU NAVAS 56 <65 M 383270 Y N Y L 70% N N N

68 JOSEPH KURIAKOSE 69 >65 M 384703 Y Y N R 70% N N N

69 PRABHAKARAN NAIR 66 >65 M 383225 Y Y N L 70% Y N N

70 THANKAPPAN KK 62 <65 M 236735 Y N Y R 70% N N N

71 KURUP GV 65 <65 M 388511 Y N Y R 90% N Y N

72 YOHANNAN N 52 <65 M 387151 Y N Y R 90% N N N

73 GOPINADHAN NV 65 <65 M 388889 Y N Y L 90% N N N

74 RAJESWARAN S 63 <65 M 388601 Y N Y L 80% N N N

75 GOVINDAN P 50 <65 M 355743 N N N L 80% Y N N

76 THOMAS TV 61 <65 M 356123 N N N L 75% Y N N

77 SOMARAJAN P 58 <65 M 206048 Y N Y R 50% N N N

78 CHAKKI KP 57 <65 F 357615 Y N N R >90% N N N

79 SAMUEL JOSEPH 61 <65 M 357922 Y N Y L 80% N N N

80 SREEDHARAN PILLAI K 72 >65 M 357315 Y N Y R 90% N N N

81 MADHAVAN G 68 <65 M 358757 N N N L 90% Y N N

82 ASHOKAN CK 50 <65 M 359341 Y N Y L 60% Y Y N

83 MUTHAIAH M 65 <65 M 359277 N N N R 90% Y N N

84 JACOB RC 72 >65 M 362260 Y N Y R 90% N N N

85 JOSEPH PA 72 >65 M 362609 Y N Y R 80% N N N

86 JAMES KA 56 <65 M 360206 Y N Y R 80% N N N

87 PRITHIVI RAJ S 58 <65 M 363167 Y N Y R 70% N N N

88 SUJI K 42 <65 F 363247 Y N Y L 60% N N N

89 SASIDHARAN C 61 <65 M 365272 Y N Y L 70% Y N N

90 PRABODHA CHANDRAN P 73 >65 M 9809874 Y N Y R 70% N Y N

91 RAJAN V 56 <65 M 242217 Y N Y R 70% N Y Y

92 XAVIOUR KA 58 <65 M 352483 Y N Y R 90% N N Y

93 ABDUL KAREEM H 69 >65 M 368012 Y N Y R 90% N N N

94 CHAMI TN 74 >65 M 370052 Y N Y R 90% N Y N

95 ANTONY KJ 68 >65 M 370391 Y N Y R 75% N N N

96 VALSAMMA TG 52 <65 F 362279 Y N Y L 60% N N N

97 SOWBACKYAVATHI S 58 <65 F 367534 Y Y N L 70% N N Y

98 MUTHULIPU 41 <65 M 364508 Y N Y L 90% N N N

99 VISWAMBHARAN ASARI R 68 >65 M 370488 Y N Y R 70% Y N N

100 GOPALAKRISHNAN NAIR V 79 >65 M 367962 Y Y N R 90% N Y Y

101 APPUKUTTAN PILLAI 69 >65 M 351233 Y N Y L 65% N N N

102 ABDUL JABBAR S 62 <65 M 338243 N N N L 70% Y N N

103 VASAVAN N 66 >65 M 341106 Y N Y R 90% N N N

104 GANGADHARAN K 65 <65 M 339028 Y Y N L 70% N Y Y

105 ISMAIL HAJI M 60 <65 M 337933 Y N Y R 70% N N N

106 BALAKRISHNAN M 77 >65 M 339291 Y Y N R 70% N N N

107 JOHN THEKKEL (FR) 77 >65 M 340250 Y N Y L 90% N N N

108 SANTHAKUMARI V 63 <65 F 340541 Y N Y R 70% N N N

109 BHASKARAN KR 75 <65 M 341033 Y N Y L 70% N N N

110 ANTO TL 61 <65 M 341349 Y Y N R 95% N N N

111 SEKKARIYA P 67 <65 M 342984 Y N Y L 90% N N N

112 INDIRA PEETHAMBARAN 72 >65 F 344243 Y N Y R 90% N Y N

113 SAJI VT 48 <65 M 343211 Y N Y R 70% N N N

114 IYAPPAN L 62 <65 M 343698 Y N Y L >90% N N N

115 GEORGE THOMAS K 68 >65 M 343355 Y Y N L 70% N N N

116 SOMARAJAN D 59 <65 M 345098 Y Y N L 80% N N N

117 BALACHANDRAN S 71 >65 M 346119 Y Y N L 80% N Y N

118 JOHN O 80 >65 M 346191 Y Y N L 80% N N N

119 SARASWATHY AMMA 60 <65 F 346343 N N N L 90% Y Y Y

120 PERIYASAMY M 82 >65 M 347410 Y N Y R 75% N N N

121 YAGNA NARAYANAN R 59 <65 M 344250 Y N Y T 75% N N N

122 CHINTAMANI P 64 <65 F 347987 Y N Y L 75% N Y Y

123 SHARMA RH 69 >65 M 346395 Y N Y L 70% N N Y

124 VASU KK 74 >65 M 348961 Y N Y L 65% N N N

125 GURUVAMMAL K 72 >65 F 349071 Y N Y R 90% N N N

126 CHANDRA MOHAN S 56 <65 M 349759 Y N Y R 90% N N N

127 KUNJUSANKARAN K 87 >65 M 264462 Y N Y R >90% N N N

128 MOHAMMED KHAN A 60 <65 M 349919 Y N Y L 70% N N Y

129 CHELLAMMAL P 65 <65 F 354759 Y N Y R 90% N Y N

130 MATHEW ALEX CHALAKUZHY 56 <65 M 354775 Y N Y R 80% Y Y N

131 SEBASTIAN THOMAS 66 >65 M 338379 Y N N L 90% Y N N

132 SREEKANDAN NAIR G 64 <65 M 353153 Y N Y L 90% N Y N

133 VIJAYAMMA B 60 <65 F 353828 Y Y N L 80% N N N

134 SUGATHAN V 60 <65 M 320228 Y Y N L 90% N N N

135 RAMACHANDRAN PILLAI M 71 >65 M 9206150 Y N N L 70% N Y N

136 JOSEPH DOMINIC 70 >65 F 322633 N N N R 70% Y Y N

137 KUNJAMMA GEORGE 61 <65 F 324304 Y N Y L >80% N Y N

138 SURENDRAN D 50 <65 M 234038 Y N Y R 80% N N N

139 VELAYUDHAN R 55 <65 M 329843 Y N Y L 70% N N N

140 VASANTHA BAI AMMA TP 69 >65 F 329760 Y N Y L 90% N N N

141 RENGAN N 75 >65 M 331756 Y N Y L 90% N N N

142 IBRAHIM KUNJU S 73 >65 M 332018 Y N Y L 70% N N N

143 MOHAMMED SHIYAM 47 <65 M 334264 Y N Y R 65% N N N

144 SREEKUMAR PS 60 <65 M 336522 Y N Y R >90% N N N

145 JAGATHAPPAN NAIR 63 <65 M 335341 Y N Y L 90% N N N

146 VIJAYA LEKSHMY KR 75 >65 F 319648 Y N Y R 90% N N N

147 PREMAVATHY K 60 <65 M 325796 Y Y N R 90% N N N

148 JOSEPH CD 72 >65 M 327737 Y N Y L 90% N N N

149 CHANDRAGADAN 75 >65 M 325356 Y Y N L >90% N Y Y

150 NARAYANAN PILLAI 75 >65 M 318741 Y Y N L 50% Y N N

151 KESAVAN NAIR 78 >65 M 333718 Y N Y L 70% N N N

152 BHARGAVI AMMA 76 >65 F 334305 Y N Y L >90% N N N

153 SIVADASAN PILLAI 65 <65 M 309121 N N N R 70% Y N N

154 SEKAR S 48 <65 M 309638 Y N Y L >90% N N Y

155 BAHADOOR KHAN S 59 <65 M 310262 Y N Y R 60% N N N

156 ELIYA LONAPPAN 69 >65 F 311319 Y N Y R 75% N N N

157 PONNAIAH K 54 <65 M 314661 Y N Y L >90% N N Y

158 GANGADHARAN PILLAI 65 <65 M 255252 Y Y N L 50% Y N N

159 SAID MUHAMMED V 72 >65 M 316391 Y N Y R 75% N N N

160 LEELAMONY G 61 <65 F 318958 Y N Y R 60% N Y N

161 JOSEPH PJ 55 <65 M 320007 Y Y N L 70% N N N

162 BABU D 58 <65 M 9601439 Y N Y L 75% N Y N

163 NABEESA BEEVI M 65 <65 F 249983 Y Y N L >80% N N N

164 CHANDRASHEKHARAN CK 82 >65 M 321523 Y N Y L >90% N N N

165 VARGHESE C 64 <65 M 206090 Y N Y R 70% N N N

166 RAVEENDRAN G 70 >65 M 291701 Y N Y L 90% N N N

167 NAZIMUDEEN A 53 <65 M 293259 Y N Y R 80% N N N

168 HALEEMA BEEVI M 51 <65 F 292274 Y N Y L 70% N N N

169 SALIM PM 58 <65 M 293226 Y N Y R 70% N N N

170 NARAYANAN M 66 >65 M 297187 Y N Y L 90% N N N

171 KUTTY RAJ N 49 <65 M 298114 N N N L 80% Y N N

172 JOHN LUKOSE 52 <65 M 298118 Y N Y L 80% N N N

173 VINCENT P 54 <65 M 299222 Y N Y L >80% N N N

174 THOMAS PG 74 >65 M 301633 Y N Y R 70% N N N

175 RAJAN P (ADV) 57 <65 M 301836 Y N Y L 90% N N N

176 SIVAN PILLAI K 60 <65 M 300891 Y Y N L >80% N N N

177 PALRAJ C 58 <65 M 276778 Y Y N L 90% N N N

178 JOGINDER SINGH 60 <65 M 281446 Y N Y R >90% N N N

179 MAIDEEN PICHA A 75 >65 M 284043 Y N Y R 70% N N N

180 MANI V 52 <65 M 285580 Y N Y L 70% N Y N

181 GOPINATHAN TS 67 >65 M 285725 Y Y N R 70% N N N

182 VELAPPAN NAIR V 57 <65 M 286225 Y N Y R 90% N N N

183 SHAJI FAZILUDDIN 47 <65 F 288049 Y N Y R >90% N N N

184 MUTHUKUTTY E 65 <65 M 286950 Y Y N L 90% N N N

185 THANKAPPAN K 60 <65 M 289564 Y Y N L 90% N N N

186 VADIVEL M 56 <65 M 9907265 Y N Y R 60% N N N

187 AMINA CA 52 <65 F 8709192 Y N Y R 90% N N N

188 MOIDEEN KUTTY C.K 52 <65 M 191154 Y Y N L 70% N N N

189 CHETTIYAR K SHYLASWARAN 39 <65 M 191071 Y N Y R 80% N Y N

190 ROHINI C 59 <65 F 9006209 Y Y N R 70% N N N

191 JACOB.K.VARGESE 56 <65 M 9805775 Y Y N L 70% N N N

192 ANUSUYA R 47 <65 F 204022 Y N Y L 90% N N N

193 SUBRAMANYAM P 65 <65 M 204498 Y Y N R 80% N N N

194 SAHADEVAN.K 62 62 M 216847 Y Y N R 95% N N N

195 NARAYANAN NAIR K 73 >65 M 219007 Y N Y L 80% N N N

196 DANIEL K.G 71 >65 M 9305282 Y Y N L 70% Y N N

197 NARAYANAN K.K 60 60 M 222409 Y N Y L 70% N N N

198 ABDUL KHADER L.S.M 68 68 M 223070 Y Y N R 90% N N N

199 MADHAVAN K.S 74 >65 M 228841 Y N Y R 80% N N N

200 MOHANAN.K 50 <65 M 235580 Y Y N R 75% N Y N

201 THAMPURAN.R 69 >65 M 237469 Y N Y R 70% N N N

202 SHELLY.T.D 30 <65 M 238087 Y Y N L 70% N N N

203 ELIAS D 70 >65 M 239047 Y Y N R 60% N N N

204 KRISHNAN S 48 <65 M 248794 Y N Y L 80% Y N N

205 SURENDRAN K 49 <65 M 259050 Y Y N R 70% N N N

206 HARIDASAN C.K 34 <65 M 259916 Y Y N R 80% N N N

207 IBRAHIM K.B 57 <65 M 260462 Y N Y L 60% N N N

208 KRISHNAN K.T.K 58 <65 M 267982 Y Y N L 99% N Y N

209 MOHAMMED ABOOBACKER K.T 58 <65 M 268411 Y N Y L 70% N Y N

210 MADHUSOODANAN NAIR S 61 <65 M 271365 Y N Y L 80% N N N

211 BHASKARAN NAMBIAR 57 <65 M 227252 Y Y N L 60% N N N

212 NATARAJAN K 57 <65 M 270479 Y Y N R 70% N N N

213 HARIDAS S 60 <65 M 262359 Y N Y R 80% N N N

214 PAPPACHAN C.A 59 <65 M 251466 Y N Y R 90% N N N

215 SOMARAJAN D 69 >65 M 225585 Y N Y R 80% N N N

216 SULOCHANA D 58 <65 F 274204 Y N Y L 75% N N N

217 RAGHAVAN K.V 54 <65 M 202438 Y N Y R 60% N N N

218 ABDUL KABEER.K 38 <65 M 188313 Y N Y L 65% N N N

219 VASAVAN K 67 >65 M 180262 Y Y N L 75% N N N

220 GEORGE M.K 69 >65 M 206312 Y N Y R 80% N N N

221 BHASKARA KURUP P 74 >65 M 195244 Y Y N R 90% N N N

222 GOVINDHAN T 62 <65 M 200344 Y N Y L 90% N N N

223 PONNAMMAL K 67 >65 M 9404161 Y Y N L 65% N N N

E-4

DM HTN Smoking PAD CAD DLP Timing of surgery <6 weeks (Y/N)Tehnique Ulerated plaque Patch Peri-op minor stroke Peri-op major stroke Peri-op cardiac events Wound morbidity

Y Y Y N N y N C Y V N N Y N

N Y N N N n Y C Y V N N N N

Y Y N N Y n Y C N V N N N N

Y Y N N N y Y C Y V N N Y N

N Y Y N N n N C Y B N N N N

N N Y N N n Y C Y V Y (c/l) N N N

N Y Y N N n Y C N V N N N N

Y Y Y N N n N C Y V N N N N

N Y Y N N n N C Y V N N N N

N Y Y N Y n N C N V N N N N

Y Y N Y Y n N C Y B N N Y N

Y Y Y N Y n N C y V N N N N

N Y N Y N n N C N B N N N N

Y N N N N n N C N V Y N N N

Y Y N N N n Y C Y V N N N N

N Y Y N Y n N C N V N N N N

N Y Y N Y n N C Y V N N N N

Y Y N N Y y N C Y V N N N N

Y N N N N y Y C Y V N N N N

Y Y N Y N y Y C Y B N N N N

N Y Y N N n N C N B N N Y N

N Y Y N N n N C N V N N N N

Y Y N N N n N C Y B N N N N

N Y N N N n N C N V N N N N

N Y N N N y N C N V N N N N

N Y Y N N n N C Y V N N N N

N Y N N Y n N C Y B N N N N

N Y Y N N n Y C Y V N N N N

Y Y Y N N n N C N V N N N N

Y N Y N N n Y C Y V N N N N

N Y Y N N n N C N V N N N N

Y Y N N Y y N C Y V N N N N

Y Y Y N N n N C Y V N N N N

Y Y Y N N n N C Y V N N N N

Y Y N N Y n N C Y B N N N N

N Y Y Y N y Y C N B N N N N

Y Y Y N Y n N C Y B N N N N

Y Y Y N Y n Y C Y B N N N N

Y Y Y N Y n N C Y V N N N N

Y N Y N N n Y C Y B N N N N

Y Y Y N Y n N C N V N N N N

Y Y N N N n N C Y V N N N N

Y Y N N N y N C Y V N N N N

N Y N N N y N C Y V N N N N

N Y N N N n Y C N V N N N N

Y Y N N N y Y C N V N N N N

Y Y N Y Y n N C N V N N N N

Y Y Y N N y Y C N V N N N N

Y Y Y N Y y N C Y V N N N N

Y Y Y N N y N C Y V N N N N

N Y Y N N y N C N V N N N N

Y N Y N Y n N C N V N N N N

Y Y Y N N n Y C Y V N N N N

N Y Y N Y n N C Y V N N N N

N N Y N N n N C Y V N N N N

N Y Y Y N n N C N V N N N Hematoma

N Y Y N Y n N C N V N N N N

Y Y N N N n Y C N V N N N N

N Y N N N n N C N V N N N N

Y Y N Y N y N C N B N N N Infection

N N N N N n N C N V N N N N

N Y Y N Y y N C Y V N N N N

Y Y Y N Y y N C Y V N N N N

Y Y N N N n Y C N V N N N N

Y Y N N N n N C N V N N N N

Y N Y N N n Y C Y V N N N N

N N N N Y n Y C N V N N N N

N Y Y N N n N C Y V N N N N

N Y Y N N n Y C Y V N N N N

Y Y Y N Y n Y C Y V N N N N

Y Y Y N Y n Y E N NA N N N N

N Y N N N n Y C Y V N N N N

N Y Y N Y n N C N V N N N Hematoma

N N Y N N n Y C N V N N N N

N Y Y N N y Y C N V N N N N

Y Y Y N Y n Y C N V N N N N

Y N Y Y N y N C Y V N N N N

Y Y N N Y n N C N V N N N N

Y Y Y N N n N C Y V N N N N

N Y Y N Y n Y C N V N N N N

N Y Y N N n N C N V N N N N

Y Y N N N n N C N V N N N N

Y Y N N N n Y C Y V N N N N

Y Y N N N y N C Y V N N N N

Y Y Y N Y y N C N V N N Y N

N N Y N N n Y C N V N N N N

Y Y Y N N n Y C N V N N N N

N Y N N N n N C Y V N N N N

Y Y Y Y Y n Y C Y V N N N N

Y Y Y N N n N C N V N N N N

Y Y Y Y N n Y C N V N N N N

Y Y Y N Y y Y C N V N N N N

N Y N N N n Y C Y V N N N N

Y Y N N N n N E Y V N N N N

Y Y N N N n N C Y V N N N N

Y Y N N N n Y C Y V Y N N N

N Y N N N n Y C Y V N N N N

Y Y Y N N y Y C N V N N N N

Y Y Y N N n N C N V N N N N

Y Y N N N y N C N V N N N N

Y Y N N N n N C Y V N Y N N

N Y Y N Y n N C N V N N N N

Y Y N N N y Y C N V N N N N

Y Y Y N N n N C N V N N N N

N Y Y Y N n Y C N V N N N N

N N N N Y y N C Y V N N N N

Y N N N N n Y C N V N N N N

Y Y N N N n N C Y V N N N N

Y Y N N N n Y C Y V N N N N

Y Y Y N N n Y C N V N N N N

Y Y N N N n N C Y V N N N N

Y Y N N N n N C Y V N N N N

Y N N N N n N C Y V N N N N

Y Y Y N N y N C N V N N N N

Y Y N N N n Y C Y V N N N N

N Y Y N Y n N C N V N N N N

Y Y Y N Y n N C Y V N N N N

Y Y N N N n Y C N V N N N Hematoma

Y Y N N N n N C Y V N N N N

N Y N N N n N C Y V N N N N

Y N N N N n Y C Y V N N N N

N N N N N n N C Y V N N N N

Y Y Y N N y Y C N V N N N N

Y Y N N N n N C N V N N N N

Y Y N N N n N C Y V N N N N

N Y Y N N n N C N V N N N N

N Y N N Y n N C Y V N N N N

Y N Y N N n N C Y V N N N N

N Y N N Y n N C N V N N N N

Y N Y N N n N C N V N N N N

N Y Y N N n Y C N V N N N N

Y Y Y N N n N C Y V Y N N N

Y Y N N N n N C N V N N N N

Y Y Y N Y n Y C Y V N N N Hematoma

Y Y Y N Y n Y C Y V N N Y N

N Y Y N N n Y C N V N N N N

Y Y N N N y N C N V N N N N

Y Y Y N Y y N C Y V N N N N

Y Y Y Y Y n N C Y V N N N N

Y Y N N N n Y C Y V N N N N

N Y N N N n N C Y V N N N N

Y Y Y N N n N C Y V N N N N

N N Y N N n Y C N V N N N N

Y Y Y N N y N C Y V N N N N

Y Y N N Y n N C N V N N N N

N Y N N N y Y C Y V N N N N

Y Y N N Y y Y C Y V N N N N

Y Y Y N Y n Y C Y V N N N N

N Y Y N N y N E N NA Y N N N

N Y Y N N n N C Y V N N N N

Y Y Y N N n N E N NA N N N N

Y Y N N N n N C Y V N N N N

Y Y Y N N y Y C Y V N N N N

N N Y N N n Y C Y V N N N N

Y Y N N N n Y C Y V N N N N

N Y N N N n Y C Y V N N N N

Y Y N N Y n N C Y V N N N N

N N Y N N n Y C Y V N N N N

N Y Y N N n Y C Y V N N N N

Y Y N Y N y N C Y V N N N N

Y Y N N N n N C N V N N N N

Y Y Y N Y n Y C N V N N N N

Y Y N N Y n N E Y NA N N N N

Y Y Y N Y n Y C Y V N N N N

N Y Y N Y n Y C N V N N N N

N Y Y N N y Y C N V N N N N

Y Y Y N N n Y C Y V N N N N

N Y N N N n Y C N V N N N N

N Y Y N N n Y C Y V N N N N

Y Y Y N Y y N C N V N N N N

Y Y Y N N y Y C N V N N N N

N Y N N N n Y C Y V N N N N

Y Y Y N N n N C N V N N N Hematoma

Y Y N N Y n N C N V N N N N

N Y Y N N n N C N V N N N N

N N Y Y Y y Y C Y V N N N N

Y N Y N N n Y C N V N N N N

Y Y N N N n N C N V N N N N

Y Y Y N N n N C N V N N N N

N N Y N N n Y C Y V N N N N

Y Y Y N N y Y C N V N N N N

N Y Y N N n N C N V N N N N

Y Y N N N n N C Y V N N N N

N N Y N N y Y C Y V N N N N

Y N Y N N n Y C Y V N Y (H) N Hematoma

Y Y Y N Y y Y C Y V N N N N

N Y Y N N y Y C Y V N N N N

Y Y Y N N n Y C Y V N N N N

N N Y N Y n Y C Y V N N N N

N Y N N N n N C Y V N N N N

N Y N N N n Y C Y V N N N N

Y Y Y N N n Y C Y V N N N N

Y Y Y N Y y N C Y V N N N N

N N Y N N n N C Y V N N N N

N Y Y N N n Y C Y V N N N N

N Y Y N Y y N C Y V N N N N

Y Y Y Y N n Y C Y V N N N N

N Y Y Y N n Y C Y V N N N N

Y Y Y N N y Y C Y V N N N N

N Y Y N N n Y C Y V N N N N

Y Y N N Y n Y C Y V N N N N

N Y N N N y N C Y V N N N Y

Y Y Y N N n Y C Y V N N N N

N N Y N N y Y C Y V N N N N

N N N N N n N C Y V N N N N

N Y N N N n N C Y V N N N Y

Y Y Y N N y Y C Y V N N N N

N Y Y N N n N C Y V N N N N

N Y Y N N y Y C Y V N N N N

N Y Y N N n Y C Y V N N N N

N Y Y N N y Y C Y V N N N N

Y Y Y N N n Y C Y V N N N N

N Y Y N N y Y C Y V N N N N

N Y Y N Y n N C Y V N N N N

N Y Y N N n Y C Y V Y N N N

N Y Y N N n Y C Y V N N N N

N Y Y N Y y N C Y V N N N N

N N Y N N n N C Y V N N N N

Y Y N N N n Y C Y V N N N N

Y Y N N Y n N C Y V N N N N

N Y Y N N y Y C Y V N N N N

N Y N N N n Y C Y V N N N N

N Y Y N Y n Y C Y V N N N N

E-4 Bovine=13

Nerve praxia/palsy Mortality Follow-up Re-stenosis Follow Up

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

CN XII N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N Y Doing well Nil NA

N N Doing well Nil 6

N N Doing well Nil 6

N N Doing well Nil 6

N N Doing well Nil 6

N N Doing well Nil 6

N N Doing well Nil 6

N N Doing well Nil 6

N N Doing well 75% 24

N N Doing well Nil 15

N N Doing well Nil 24

N N Doing well Nil 24

N Y (renal and respiratory failure) NA NA -

N N Doing well Nil 24

N N Doing well Nil 24

N N Doing well Nil 10

N N Doing well Nil 24

N N Doing well Nil 24

CN XII N Doing well Nil 10

N N Doing well Nil 24

CN XII N Doing well Nil 24

N N Doing well Nil 9

N N Doing well Nil 24

N N Doing well Nil 24

CN XII N Doiing well Nil 24

N N Doing well < 50% 24

N N Doing well Nil 24

N N Doing well Nil 12

N N Doing well 50% 24

N N Doing well Nil 24

N N Doing well < 50% 24

N N Doing well Nil 24

N N Doing well Nil 12

N N Doing well Nil 4

N N Doing well Nil 24

CN XII N Doing well Nil 22

N N Doing well Nil 4

N N Expired - 1 yr, MI Nil 12

CN XII N Doing well <50% 36

CN X N Doing well Nil 36

N N Doing well Nil 36

N N Doing well Nil 25

N N Doing well Nil 36

CN XII N Doing well Nil 36

N N Doing well Nil 36

N N Doing well Nil 35

N N Doing well Nil 36

N N Doing well Nil 22

N N Doing well Nil 36

N N Doing well <50% 36

N N Doing well Nil 36

N N Stroke - 8 months and expired Nil 8

N N Doing well Nil 36

N N Doing well < 50% 36

N N Doing well <50% 36

N N Doing well <50% 24

N N Expired - 1 yr - MI Nil 12

N N Doing well <50% 36

N N Doing well Nil 36

N N Doing well Nil 36

N N Doing well Nil 36

N N Doing well <50% 36

N N Doing well <50% 36

N N Doing well Nil 36

N N Doing well Nil 48

CN XII N Doing well Nil 48

N N Doing well 60% 39

N N Doing well Nil 38

CN X N Doing well <50% 48

N N Doing well <50% 48

N N Doing well Nil 48

N N Doing well Nil 37

N N Doing well Nil 37

N N Doing well Nil 36

CN VII N Doing well Nil 35

N N Expired 6 months later - MI Nil 6

N N Doing well <50% 35

N N Doing well Nil 35

CN XII N Doing well <50% 48

CN XII N Doing well Nil 34

N N Doing well Nil 33

N N Doing well 60% 33

N N Doing well Nil 33

N N Doing well <50% 48

N N Doing well 80% 48

N N Doing well 60% 48

N N Doing well Nil 32

N N Doing well <50% 31

N N Doing well Nil 31

N N Doing well Nil 48

N N Doing well Nil 30

N N Doing well Nil 28

N N Doing well Nil 48

CN VII N Doing well Nil 48

N N Doing well Nil 48

N N Doing well <50% 48

N N Doing well Nil 51

N N Doing well Nil 51

N N Doing well Nil 50

N N Doing well Nil 49

N N Doing well Nil 48

N N 1 yr follow-up Nil 12

N N Doing well <50% 45

N N Doing well Nil 48

CN XII N Doing well Nil 62

N N Doing well <50% 42

N N Doing well Nil 62

N N Doing well Nil 40

N N Doing well Nil 49

N N Doing well Nil 48

N N Died MI - 4 months Nil 4

N N Doing well Nil 49

CN XII N Doing well Nil 60

N N Doing well Nil 42

N N Doing well Nil 42

N N Doing well <50% 61

N N Doing well 70% 60

N N Doing well 50% 59

CN XII N Minor stroke in 3 months - follow-up of 1 yr Nil 3

N N Doing well Nil 56

N N Doing well Nil 56

N N Doing well Nil 54

CN X N Doing well Nil 53

N N Doing well Nil 53

N N Episode of ACA-MCA territory stroke 1 yr later Nil 52

N N Doing well Nil 52

N N Doing well Nil 52

N N Doing well Nil 74

N N Follow-up of 3 yrs Occluded 36

N N Doing well Nil 73

N N Doing well Nil 72

N N Doing well Nil 71

N N Doing well Nil 69

N N Doing well Nil 69

N N Doing well Nil 69

N N Follow-up of 3 yrs Nil 36

N N Doing well Nil 66

N N Doing well Nil 66

N N Doing well Nil 64

N N Follow-up of 12 months Nil 12

N N Doing well Nil 83

N N Doing well Nil 80

N N Doing well Nil 79

N N Doing well Nil 79

N N Doing well <50% 79

N N Doing well Nil 77

N N Doing well Nil 76

N N Follow-up of 12 months Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 144

N N Doing well Nil 6

N N Doing well Nil 12

CN XII N Died due to MI in 3 yrs Nil 36

N N Doing well Nil 24

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 6

N N Doing well Nil 72

N N Stroke on c/l side at four yrs Nil 48

N N Doing well Nil 12

N N Doing well Nil 6

N N Doing well Nil 12

CN XII N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 6

N N Doing well Nil 8

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 10

N N Died due to MI in 3 yrs Nil 36

N N Doing well Nil 60

N N Doing well Nil 72

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 3

N N Doing well Nil 3

N N Doing well Nil 6

N N Doing well Nil 12

N N Doing well Nil 24

N N Doing well Nil 24

N N Doing well Nil 10

N N Doing well Nil 12

N N Doing well Nil 12

N N Doing well Nil 12

10th-3

7th-2