Professor Kazem Fathie, M.D., F.A.C.S., F.I.C.S., Ph.D.

TRANSIENT ISCHEMIC ATTACK ENDARTERECTOMY DEFINITION

Irreversible disability is traditionally associated with cerebral vascular disease (CVA) and certain deaths are associated with the CVA. Despite enormous progress already made in the diagnosis and treatment of this catastrophic disease, unfortunately, many still do not know the prevention of this very serious problem. It is under-estimated that there are 2 million fatalities from vascular disease every year. Certain information for the general public and the medical profession must be disseminated to change this.

If we believe that certain chains of events produce the CVA, we could easily approach the recognition that the disease can be diagnosed before the catastrophic event. There are factors, such as, hypertension, hypercholesterolemia, atherselerosis, cardiac abnormalities, diabetes mellitus, which make the recognition easier.

The earliest sign of the CVA is what is known as the transient ischemic attack (TIA). The history and careful examination, plus evaluation of the factors named above could bring one to suspect this problem in any given patient. The other findings may be a history of diplopia, atherosclerosis of the retinal arteries, speech difficulties, motor or sensory changes, abnormalities of cerebellar function. etc. Funher, radiological examination, such as, angiography, brain scanning, study of the cerebrospinal fluid, may also assist in making the diagnosis.

MAKING THE DIAGNOSIS

By far the best method (also according to Doctor Cluk Milucan) in making the diagnosis of cerebral arterial disease is angiography. There are five items which would bring one to suspect involvement of the carotid arteries:
1. Blindness in one eye during the TIA attack.
2. Emboli in the retinal vessels.
3. Bruit over the carotid artery.
4. Significant lowering of the retinal arterial pressure on the affected side. 5. Any sign of retinal artery ischemia.

Recently, the Joint Committee for Stroke Prevention submitted the following criteria for diagnostic angiography to be done:

1. Uncertainty as to the diagnosis of stroke.
2. If the patient improves and then becomes worse.
3. If retinal ischemia is found (temporary or permanent).
4. If there is a carotid bruit, angiography should be done.

This angiography should be complete cerebral, carotid and arch studies, selective or bilateral in location.

TRANSIENT ISCHEMIC ATTACK

Transient ischemic attacks are usually described as related to the carotid or vertebral-basilar arterial systems.

1. Carotid Artery System. The classic history for transient ischemic attack in the carotid system is one of swift onset of contralateral weakness or numbness of the arm or leg. Dysphagia occurs if the dominant hemisphere is involved. Impaired vision of the eye on the side of the diminished carotid flow takes place. This clinical phenomenon usually indicates a decrease in regional cerebral perfusion, and occasionally may be confused with other neurological disease (such as, seizure). Transient ischemic attack produces a neurological deficit, the onset of which is usually sudden with gradual progression of the symptomatology.

2. Vertebral-Basilar Arterial System. Damage to this system is also characterized by a very swift onset of symptoms with neurological phenomenon such as ataxia, monoparesis, hemiparesis, quadriplegia, numbness (frequently shifting from one side to the other), vertigo, defects in either visual field, diplopia, dysarthria, aphasia and occasionally, clouding of consciousness. Vertigo is perhaps the most common symptom of TIA in this distribution (the diagnosis should not be made on this one symptom alone, however).

CEREBRAL INFARCT

Arterial thrombosis and atheroscerosis with occlusion of the cerebral arteries (as a result of this atherosclerosis) is the single most common cause of stroke in more than 50 percent of patients. The stroke may take place in the carotid or the vertebral systems. They are classified as follows:

1. Carotid Arterial System. Cerebral infaretion occurs in the carotid arterial system abruptly over a matter of many minutes to a very few hours. In some cases, neurological impairment may occur during sleep, and therefore may be maximum when first discovered. In other cases, it might require several hours (to a day) to develop. Thirty to 50 percent of the cases have had previous transient ischemic attacks. Violent headaches as a result are rare. The spinal fluid is clear, but atherosclerosis and carotid bruit are usually found. There may also be hypertension, local vascular disease, retinal emboli, and other evidence of retinal arterial ischemia.

2. Vertebral-Basilar Arterial System. Neurological symptoms develop early in a few hours or days, in a step-wise or stuttering fashion. Thus the erroneous impression that the occlusion is complete may be given. Ocular manifestations include a number of defects in the visual fields, nystagmus, or impaired extra-ocular movement. Rarely the patient may develop intranuclear ophthalmoplegia. All or any limb combination may have weakness and impaired function. There may be sensory changes and impairment of consciousness.

3. Infarction Secondary to Embolic Arterial Occlusion. One of the first considerations is to determine the origin of the embolus. It may be from:

A. Ulceration of an atherosclerotic plaque at the carotid bifurcation (such as in vaivulu heart disease or myocardial infarction), or
B. Cardiac dysrythmia (due to vaivular heart disease or myocardial infarction).
C. Small number due to bacterial endocarditis.

4. Intracerebral Hemorrhage. This accounts for 20-25 percent of all Hemorrhaging into the brain substance may come from any artery, vein or capillary. About 70 percent of cerebral hemorrhage occurs in the internal capsule, 20 percent in the brain stem or cerebellum and 10 percent elsewhere in the cerebral hemishperes. The significant points in the diagnosis of hemorrhage into the cerebral hemispheres are:

A. No previous history of TIA.
B. Severe headaches (very common).
C. Rapid evolution of neurological symptoms.
D. Impairment of consciousness, sometimes progress to coma.
E. Elevated blood pressure.
F. Bloody cerebrospinal fluid.

Cerebral hemorrhage results in death in 80-90 percent of cases. Pontine hemorrhage are usually extensive, producing a sudden loss of consciousness with respiratory arrythmia, bilateral meiosis, lack of reflexes. There may be eye movement or head turning, and bilateral involvement of the corticospinal tract (and cranial nerve nuclei). Hyperreflexia may occur in some cases. Cerebellar hemorrhages usually occur very abruptly. Typically there is occipital headache, vomiting, vertigo and ataxia. When loss of consciousness occurs (within a few hours) the patient presents with Cheyne-Stokes respirations, marked constriction of the pupils, deviation of the eyes away from the lesion, and contralateral hemiplegia. In one case in five, the onset is catastrophic with a sudden loss of consciousness, absent focal signs and death within two days.

SUBARACHNOID HEMORRHAGE

This term describes the disorder in which ruptured, sacular or berry aneuryms bleed into the subarachnoid space. It is to be distinguished from intracerebral hemorrhage (that which bleeds into the brain substance itself). Characteristics of this disease are the sudden onset of extraordinaffly excruciating headache and (occasionally) there is some loss of consciousness. Locallizing neurological signs are often absent except for a partial ocular motor palsy with outward deviation of the eye and pupillary dilatation. lntracranial hemorrhage from vascular malformations can also occur (as well as hypertensive encephalopathy) making the diagnosis difficult.

MEDICAL TREATMENT

Medical treatment of this disease should include a step by step monitoring of the patient’s acute state, including watching his blood pressure, cardiac condition, bladder management, feeding, positioning, etc. Anti-coagulation therapy is indicated only in those cases where fresh thrombosis has occurred without evidence of actual cerebral hemorrhage. Some neurologists feel that it is important to anti-coagulate their stroke patients, particularly if the patient has had a transient ischemic attack. Some differ with this idea, for fear of further complicating the patient’s picture. The primary objective for anti-coagulation therapy is to prevent the formation of emboli (from the thrombus). These aims of anti-coagulation are:
1. To stop focal transient ischemic attacks,
2. To prevent cerebral irifaretion,
3. To stop progression of the disease,
4. To prevent formation of emboll from the heart, and
5. To decrease the number of complications.

The possible reason why anticoagulation has limited effectiveness is that the arterial thrombus begins as a white plaque composed mainly of platelets and fibrin. A deficiency of fibrinolysis and increased platelet adhesiveness may be present in occlusive ceyebrovascular disease. Thus, platelet inhibitors may play a useful role in the management of patients with cerebral thrombo-embolism. This is especially true of patients with cardiac valvular prostheses. Certain typical procedures should be followed in anticoagulation therapy:
1. Determine the clotting and prothrombin time before beginning anticoagulation therapy,
2. Adminisister concentrated Heparin Sodium in repository form (200-400 mgm), subdermally as soon as possible and then daily at 9:00 AM and 9:00 PM,
3. Determine the clotting time less than one hour before each dose and adjust the dosage so as to maintain the Lee-White clotting time between 20 and 30 minutes,
4. Give Coumadin compounds such as Cournadin Sodium or other Coumadin derivatives orally, each evening between 6:00 and 8:00 PM. The dosage depends on the previous prothrombin time.
5. Reduce praftombin time to 20 or 30 percent of the control value. 6. Continue the use of Heparin and keep on with it until the prothrombin time has reached this level.
7. Have Vitamin K1 Oxide for emergency use at hand and a medical ID card stating that the patient is taking anticoagulation medication.
8. Caution the patient to avoid the excessive use of alcohol and aspirin.
9. Advise the patient to be alert for melena or hemauria, and to seek medical advice for dental work.
10. Continue the use of Heparin and Coumadin until the patient has been without a TIA attack for at least several months to one year.

VASODILATOR THERAPY

Vasodilation therapy has been advised for TIA for many years. There are a large number of medications and preparations, such as, Papaverine (and derivatives), carbon dioxide, low molecular weight Detran, Glyserol, Cyclospasmol, Pavabid and others.

SURGICA.L MANAGEMENT

In summary, the surgical management of TIA would be advisable if the lesion is accessible to surgical approach. To eliminate the immediate neurological disorder, nothing would be better than the removal of the occlusive material, perfuse the brain, oxygenate the cortex and optimally monitor the patient’s blood pressure. It is unfortunate that many continue medical therapy past the time that surgical intervention should have begun. Certain factors make the possibility of cerebral infarct quite likely when they occur with the transient ischemic attack. They are hypertension, cardiac abnormalities, increased serum cholesterol, high blood sugar, obesity, cigarette smoking, decreased physical activates, etc. The three factors that have been determined to be most important in the development of stroke are hypertension, cardiac disease and TIA.

Surgical approach for carotid endarterectomy has been known by many surgeons, but good cerebral blood flow during the procedure is essential to maintain the condition of the patient. Doctor Parker Tower reported 219 operations, of whom 171 patients had arterio- sclerotic stenosis of the internal carotid artery with good result following enderarterectomy. In the patient with lateralizing transient ischemic attack less consistent good result may be expected in those patients with significant stenosis and less specific symptoms.

A small number of patients, have significant stenosis without a bruit, but this asymptomatic stenosis has an unpredictable prognosis and may be operated upon with rather low mortality and morbidity. The use of local anaesthesia and shunting when necessary proved to be a safe technique for the author. Timing of the operation is important and should not be delayed once the diagnosis is proven by cerebral angiography. Some authors believe that if the patient has had the symptoms for longer than two days, the findings are irreversible. During surgery it is essential to prevent cerebral metabolism, give adequate brain protection (with medications and hypothermia), perfuse the brain and measure shunting pressure continuously. Hypercarbia, hypocarbia, and steroid therapy have been also suggested.

INDICATIONS FOR OPERATION

It has been said that the ideal patient for carotid endarterectomy is one who has no neurological deficit on physical exaznination and who has a stenotic lesion at the ortice of the internal carotid artery. He will present with a history of transient ischemic attack, either hemi-hemispheric, vertebral or basilar, or nonspecific, or a carotid bruit will be present even though the patient is asymptomatic. The operative mortality and morbidity in this group of patients is close to 1% and 0.5% respectively.

CONTRAINDICATIONS TO OPEPATION

The patient with acute stroke is a poor surgical candidate for any cerebral vasculuization procedure, including endarterectomy. This patient has acutely injured and necrotic neural tissue and if the carotid stenosis or occlusion is relieved at the time, the arterial pressure is actually increased in the injured area. Complete occlusion of the carotid vessels are the worse cases to be tackled immediately, while partial occlusion of the carotid arteries are regarded to be best for surgery. Although these indications and contraindications for endartetectomy are not rigid, each case has to be dealt with on its own merit at the time.

THIS SERIES OF TIA MANAGED BY ENDARTERECROMY A REPORT OF 110 CASES

Atherosclerosis and atheroma may cause partial or total occlusion of the carotid artery, with extension of cholesterol deposits into the branches of the common carotid and internal carotid arteries. Such occlusion can result in CVA or TIA, sometimes with devastating neurological symptoms, including paralysis, speech difficulties and blindness. Occlusion of the cerebral vessels will result in tampering with the following systems:

1. Conveyance of oxygen to the tissue and carrying away the carbon dioxide
2. Conveyance of glucose and metabolites
3. Removal of waste products
4. Regulation of tissue fluid with regard to water and acid base levels
5. Regulation of temperature
6. Production and absorbtion of cerebro- spinal fluids
7. Take part in the work of the blood-brain barrier.

Furthermore, one should realize that the damage which is found is not limited to the area, but means that changes have taken place in the brain and the entire nervous system, such as, destruction, vascular lesions, edema, infarction, and hemorrhages.

Observation for the combined stenosis of the carotid vessel along with occlusion of the vertebral-basilar artery should always be kept in mind. Four-vessel angiography is mandatory prior to enderectomy surgery in order to recognize multiple or solitary occlusions of the common carotid arteries. You may also find post-stenotic lesions of the bifurcation, patency of the anterior cerebral vessel, absence of the vertebral artery, occlusion of the vertebral artery and partial occlusion of the internal carotid vessels. Pre-stenotic lesions beyond the bifurcation should be recognized and evaluated by x-ray studies. Sometimes a slightly punched-out lesion at the bifurcation with post-stenotic dilatation is seen. Also, sometimes there is occlusion of the internal carotid vessel due to increased intracranial pressure which also must be recognized.

Internal carotid patency along with cross-filling of the anterior, middle cerebral and the posterior communicating vessels needs to be evaluated. Sometimes a catheter defect can be found in the artery and must be differentiated from actual disease. Complete occlusion of the middle cerebral artery, posterior communicating and anterior cerebral vessels should also be recognized through angiography. Sometimes the defect can be found by crossfilling from the other side. Occasionally soft atheromata can be recognized through angiography at the level of bifurcation, but rarely can emboli be seen in the cerebral vessels unless it has caused complete occlusion. Areas of true infarct may be responsible later for encephalomalacia. Thus, embolization may be difficult to recognize unless it has caused a space occupying lesion along with the cerebral hemorrhage.

A study of 102 patients with carotid artery occlusion revealed that 8 had bilateral occlusion, making a total of 110 endarterectomies. The 61-70 age group had the largest incidence of the disease (49.1%). Forty-two percent of the patients were men and 59% women. Many of the patients had a family history of heart disease and stroke.

Of the cases studied the most prominent neurological symptom was weakness, speech difficulties (37.9%), and numbness of the upper and lower extremity (48.5%). It should be mentioned that the next most common complaints were dizziness and headaches. Almost 70 percent of the patients had no visual difficulties, while the rest had diplopia, blurring, blindness, hemianapsia, etc. High blood pressure was seen in 47.6 percent and heart attack, diabetes, and atherosclerosis followed.

Retinal atherosclerosis was found in 60.2 percent, carotid artery bruit in 41.7 percent. Of the patients who complained of visual disturbance, this could be found on neurological examination in only 90.2 pecent of cases. Laboratory data revealed that 13.8 percent had elevated cholesterol and 37.9 percent had high BUN determinations. Diabetes was commonly found (63.8 %). Prior to surgery the prothrombin time was normal in 48.2 percent of these patients. Angiography was positive in 86 percent of patients, EEG was abnormal in 46.4 percent and brain scan was positive in only 10 percent of the patients.

Circulation was established in 91.8 percent during surgery. The time of arterial ligation and complete occlusion of the vessel to the restablishment of circulation to the brain was 7-8 minutes in 73 patients (66.4%). The symptoms were improved in almost 107 patients (97.3%).

There were only four mortalities. One patient died 21 days post- operatively from hemorrhage and severe anemia. Another died of complete thrombosis of the circle of Wiffis, and a third from cardiac arrythmia and fibrillation on the third day post-op. The length of hospitalization averaged 5-10 days for most of the patients. There are 96.4 pecent alive, and those who died did so 2-36 days after surgery (see appendix for all tables).

SUMMARY

Any unilateral blindness, emboli of the retinal vessels, bruit over the carotid artery, or any sign of ischemic retinopathy may indicate occlusion of the carotid vessels, and require angiography to detect such occlusion. Recognition of transient ischernic attack, especially in conjunction with hypertension, hypercholestolemia, cerebral infarct, diabetes mellitus, and the presence of cardiac abnormalities requires consideration of management by endarterectomy in order to prevent the catastrophic results of this disease.

This study is now being updated to include 60 more patients. Pre- liminary results indicate that the relative percentage remains the same as in the larger group.

To eliminate the immediate neurological disorder, nothing would be better than to remove the occlusion, perfuse the brain, oxygenate the cortex and monitor the blood pressure optimally. It is unfortunate to continue medical therapy and ignore the fact that surgical therapy is effective (if angiographic studies are positive) in obviating catastrophic events of this disease.

APPENDIX SUMMARY OF TIUS SERIES IN TABLES

1. TOTAL ENDARTECTOMIES.
Total Patients 102
Bilateral Cases 8
Total Enduterectomies 110

 

2. AGE RANGE FOR THIS SERIES:
AGE PATIENTS %
40 1 1.0
40-50 5 4.0
51-60 30 29.4
61-70 50 49.1
71-80 16 15.6

 

3. GENDER DISTRIBUTION:
SEX PATIENTS %
FEMALE 42 41.2
MALE 60 58.8


4. INITIAL COMPLAINT (NEUROLOGICAL):
SYMPTOM NUMBER %
Limb weakness 50 48.5
Speech difficulty 39 37.9
Numbness of the upper limb 35 34.0
Dizziness 30 29.1
Nausea (or vomiting) 9 8.7
Headaches 24 23.3
Balance difficulty 19 18.4
Lightheadedness 15 14.5
Syncopal attack 20 19.4
Facial numbness 12 11.6
Limb paresthesias 18 17.4
Poor memory 8 7.7
Paralysis of:
upper
limb
9 8.7
face 12 11.6
lower
limb
6 5.8
History AS or Increased cholesterol 8 7.7
Found unconscious 6 5.8
Convulsions 4 3.9
Dysphagia 5 4.8
Palsy of:
3rd
nerve
1 1.0
6th
nerve
1 1.0

 

5. VISUAL DISTURBANCES:
(39 HAD VISUAL DISTURBANCES – 38.2%)
Type Temporary Unilateral Bilateral Nonspecific
Blurring (16) 41% (8) 50% (8) 50%  
Diplopia (16) 31% (4) 33% (6) 50%  
Blindness (6) 15% (5) 83% (1) 17%  
Hemianopsia (1) 3% (1) 100%    
Light Flashes (1)3% (1) 100%    
Designs (1) 3% (1) 100%    
Dim vision (1) 3% (1) 100%    
Tunnel vision (1) 3% (1) 100%    

 

6. FAMILY HISTORY:
  Number %
Heart disease 22 21.3
Strokes 13 12.6
Diabetes 6 5.8
Arteriosclerosis 3 2.9
High Cholestrol 0 0.0

 

7. PHYSICAL EXAMINATION FINDINGS: (NEUROLOGICAL)
Finding Number %
Retinal AS or ischemia 62 60.2
Carotid artery insufficiency 43 41.7
Hyperactive DTR’s 28 27.2
Limb weakness 27 26.2
Facial paralysis 10 9.7
Positive Rhomberg 8 7.7
Dysarthria 13 12.6
Carotid bifurcation AS 31 30.0
Numbness of:
Upper limb 8 7.8
lower limb 6 5.8
Dizziness 4 3.9
Facial palsy 9 8.7
Gait problems 5 4.8
Facial numbness 4 3.9
Limb paresthesias 3 2.9

 

 

8. BLOOD PRESSUPE DISTRIBUTION
Diastolic Number % Systolic Number %
51-60 (5) 4.9 90-100 (4) 3.9
61-70 (18) 17.7 101-130 (26) 25.5
71-80 (26) 25.5 131-150 (33) 32.4
81-90 (23) 22.6 151-200 (37) 36.2
91-100 (14) 13.7 >200 (2) 2.0
101-110 (9) 8.8      
111-120 (4) 3.9      
121-130 (3) 2.9      

 

9.VISUAL
DISTURBANCES
(PHYSICAL
EXAMINATION)
Type Temporary Unilateral Nonspecific
Blurring (7) 70.0% (6) 85.7% (1) 14.3%
Diplopia (1) 10.0% (1) 100%  
Blindness (1) 10.0% (1) 100%  
Hemianopsia (1) 10.0% (1) 100%  

 

10. LABORATORY TESTS:
Test Normal High Low
Cholestrol (50) 86.2% (8) 13.8% (0)
BUN (35) 60.4% (22) 37.9% (1) 1.7%
LDH (54) 93.1% (4) 6.9 (0)
SGOT (51) 87.9% (7) 12.1% (0)
Glucose (21) 36.2% (37) 63.8% (0)

 

11. PROTHROMBIN TUAE PRIOR TO SURGERY:
Normal (53) 48.2%
Abnormal (15) 13.6%
Not done (36) 32.7%
On film (6) 5.5%

 

12. LEE AND WHITE TIME BEFORE SURGERY:
Normal (40) 35.4%
Abnormal (30) 27.3%
Not Done (34) 30.9%

 

13. ANGIOGRAPHY FINDINGS:
  Partial Occlusion Total Occlusion  
Right Carotid (65) 85.5% (11) 14.5% 14.5%
Left Carotid (63) 88.7% (8) 11.3%  
(Cerebral Vessels absent = 3)

 

14. EEG RESULTS:
Normal (34) 30.9%
Abnormal (51) 46.4%
Not done (16) 14.5%
Not available (9) 8.2%

 

15. BRAIN SCANS
Organic
   Normal (72) 65.5%
   Abnormal (11) 10.0%
   Not done (27) 24.5%
Dynamic
   Normal (21) 63.6%
   Abnormal (5) 15.7%
   Not done (7) 21.2%

 

17. SURGERY PERFORMED:
Left endarterectomy (54) 49.1%
Right endarterectomy (56) 50.9%
Unilateral (both) (102) 92.7%
Bilateral (both) (8) 7.3%

 

18. CIRCULATION ESTABLISHED:
(Internal Carotid Artery)

Established at surgery (101) 91.8%
Not established (9) 8.2%

 

19. IMPROVAL AFTER SURGERY:
Did not improve (3) 2.7%
improved (107) 97.3%

 

20. TIME SPAN BILATERAL SURGERY:
2 weeks (2) 25.0%
24 weeks (2) 25.0%
3 Months (1) 12.5%
6 Months (1) 12.5%
lyr 8mos (1) 12.5%
2yr 9mos (1) 12.5%

 

21. COMPLICATIONS FOLLOWING SURGERY:
9 cases = 8.2%
Complication When Developed Result
Tissue hemorrhage with anemia 21st day deceased
myocudial infarction 1st day lived
GI bleeding (old ulcer) 3rd day lived
Unknown thrombosis day of surgery deceased
Occlusion left middle cerebral vsl 5th day lived
Hematoma of incision day of surgery lived
Arrythmia of Heart 3rd day lived
Thrombosis basal artery 1st day lived
Stroke 5th day lived

 

22. MORTALITY RATES:
Alive (106) 96.4%
Deceased (4) 3.6%

 

23. CAUSE OF DEATH:
Case number 1: Cerebral vascular insufficiency.
Case number 2: Cardiac arrest. secondary to myocardial infarct
Case number 3: Left common carotid occlusion from AS.
Case number 4: Arrythrnia causing embolus and CVA.

 

24. TIME OF DEATH:
Case number 1: 9 days
Case number 2: 2 days
Case number 3: 36 days
Case number 4: 12 days

 

25. TIME PATIENT SENT HOME.
Days after surgery Number
5- 10 days 66
11-15 days 19
16-20 days 7
21-25 days 2
26-30 days 0
Over 30 days 10

BIBLIOGRAPHY

1. MOSKOWITZ, KAPLITT, SOBEL, SAWYER and MELLINS: “Angiographic Manifesmtions of Gas Enderarterectomy”. The New York State journal of Medicine, October 15, 1971. pp. 2395-2400.

2. PAPACOUPOLOS, C.D. Cerebral Vascular Insufficiency”, text book

3. BAKER, W.H.: “The Selection of Patients for En&rterectomy’ journal of Iowa Medical Society, December 1971, pp. 725-728

4. IMPARATO, BRACCO, and KIM: “Comparisons of Three Tech- nics for Femoral-Popliteal Arterial Reconstruction”. Annals of Surgery, March 1973, pp. 375-380.

5. KILLEN and FOSTER: “Considerations in the Technic of Arterial Reconstruction Following Carotid Sinus Endancrect- orny”. The American Surgeon, April 1973, pp. 207-211.

6. KAPLITT and ROBINSON: “Appraisal and Reappraisal of Card- iac Therapy”. American Heart Journal, January 1971, Vol. 1, pp. 136-140.

7. STANSEL, OGDEN and SHAPIRO: “Retroperitoneal Iliac Endarterectomy”. Connecticut Medicine, 1973, pp. 102-107.

S. CONNOLY and STEMMER: “Endarterectomy of the External Carotid Artery”. Arch. Surg., Vol. 106, June 1973, pp.799-802.

9. ROSENTAL, GASPAR and MOVIUS: “Intraoperative Arterio- giraphy in Carotid Thromboendaxtertectomy”. Arch. Surg. Vol. 106, April 1973, pp. 906-808.

10. SULLIVAN, BLAKELY and BANOWSKY: ” Transaortic End- arterectomv”. Arch. Surg. Vol. 106, June 1973, pp. 873-876.

11. KIELY, LUMLEY and TAYLOR: “Extended Endarterrectomv of the Profunda Femoris Artery”. Arch. Surg. Vol. 106, April 1973, pp. 605-609.

12. HEIFETZ, SCHRAMEK, YAHEL and BIRKHAHN: “Clinical Forums”. Anaesthesia, 1973, Vol. 28, pp. 82-87.

13. GROVES, LOOP and SILVER: “Endarterectomv as a Supple- ment to Coronary-Saphenous Vein Bypass Surgery”. The journal of Thoracic and Cardiovascular Surgery, pp 514-522.

14. DEWEESE, ROB, SATRAN, MARSH, JOYNT, SUNNERS, and NICHOLS: “Results of Carotid Endarterectomv for Transient lschemic Attacks- FiveYe2.rs Later”. Ann. Surg., 1973, 258-264.

15. THOMPSON and PATMAN: “Carotid Endarterectomv Cerebrovascular Insufficiency. NebraskaM.J., 1972. 24-27.

16. CLAUSS, SANOUDOS, RAY and MOALLEM: “Carotid Endart- crectomy for Cerebrovascular lschemia”, Surg. Gyn. & Obstet. June 1973, Vol, 136, pp. 993-1000.

17. ENGELL, BOYSEN, LADEGAARDPEDERSON and HENRIK- SEN: “Cerebral Blood Flow Before and After Carotid Endarter- ectomy”. pp 14-19.

18. HICKEY, EHRENFIELD, HAMILTON and LARSON: Surg. February 1972, Vol. 175, No. 2, pp. 268-273.

19. URSCHEL, RAZZVK, WOOD and PAULSON: ” Distal C02 Coronary Artery End2rtercctomy”, The Annals of Thoracic Surgery, Vol. 14, No. 1, July 1972, pp. 10-15.

20. BRADHAM, BRADHAM and CHARLESTON: “Excraluminal Carotid Endarterectomv”. Arch. Surg., Voi. 105, 1972,123-124.

21. SMITH, RAYMOND, SIMMONS and HINSHAW: “A Safe Ap- proach to Carotid Endarterectomy”. California Medicine, the Western journal of Medicine, December 1971 pp. 15-18.

22. DAVIES, THORVURN and POWELL: “Endartertectomv of the Internal Carotid Artery”. California Medicine, The Western journal ofmedicine, April 1972, pp. 15-18.

23. WALTZ, SUNDT and MICHENFELDER: “Cerebral Blood Flow During Carotid Endarterectomy”. Circulation, Vol. XLV, May 1972, pp. 1091-1096.

24. FATHIE, KAZEM: “Fathic Shunt – Its Application in Carotid Artery Occlusion and the Procedure of Endarterectomv”. journal of Iowa Medical Society, March 1972, pp. 125-129. n