Journal of Vascular Surgery
Volume 25, Issue 1 , Pages 131-140, January 1997

Carotid surgery: The past is prologue:☆☆☆

The John Homans Lecture

Presented at the Fiftieth Annual Meeting of The Society for Vascular Surgery, Chicago, Ill., June 11-12, 1996.

  • Jesse E. Thompson, MD
    • ,
  • From the Department of Surgery, Baylor University Medical Center, Dallas, Texas.

Dallas Tex

Received 11 July 1996; accepted 17 July 1996.

Article Outline

 

I feel very honored indeed to be chosen as the Homans Lecturer this year, especially at the time of the 50th anniversary of the Society for Vascular Surgery, yet I have a sense of deep humility when I look back over the list of previous Homans lecturers. It is also a real privilege to present a lecture named for one of the great vascular surgeons of the 20th century, Dr. John Homans. I am deeply grateful to the officers and council for selecting me.

John Homans, the man for whom this lecture is named, was a Boston surgeon and a charter member of The Society for Vascular Surgery. He was born in Boston in 1877, the fourth John Homans to practice medicine in Boston. He attended Harvard College and the Harvard Medical School and trained at the Massachusetts General Hospital. He later spent a year at the Johns Hopkins Hospital under Harvey Cushing.

When the Peter Bent Brigham Hospital opened in 1913, Harvey Cushing, now Surgeon-in-Chief, chose John Homans at age 36 to be a member of his original surgical staff, where he remained for the rest of his career. Basically a general surgeon, he developed a special interest in vascular diseases, especially in venous disease. He described bland thrombosis in the legs as a cause of pulmonary embolism, as differentiated from thrombophlebitis. He was the first to advocate femoral and iliac vein ligation to prevent pulmonary embolism.

At the suggestion of Harvey Cushing, he wrote a Textbook of Surgery which became a classic. During 15 years it was adopted as a standard textbook in 65 medical schools and went through six editions, the last in 1945. In 1939 he published another classic textbook, Circulatory Diseases of the Extremities.

John Homans was a real character, a raconteur of rare ability with a ready and salty wit. He was one of my teachers when I was a medical student at the Peter Bent Brigham Hospital. He was sparkling, unpredictable, and colorful. He was a keen observer, had a logical mind, and his conclusions were based on clear thinking coupled with the facts of the matter. He died in Boston in 1954 at age 77 of a myocardial infarction. He was a true pioneer in vascular surgery.1, 2

Because this is the 50th anniversary of The Society for Vascular Surgery, I thought it would be appropriate and of interest to recount some of the problems we faced in the early days of carotid surgery some 40 years ago. Some of these problems are still unsolved, while many have been resolved.

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History of carotid surgery 

A brief excursion into the history of carotid surgery before 1951 is relevant. As Thomas Carlyle said, “History is the essence of innumerable biographies.”

The word “carotid” is derived from the Greek term “Karótide” or “Karos,” meaning to stupefy or plunge into deep sleep. The ancient Greeks were aware of the significance of the carotid arteries. The 31st metope from the south side of the Parthenon in Athens shows a centaur applying left carotid compression to the neck of a Lapith warrior.3 Ambroise Paré in the 16th century was familiar with the carotid phenomenon and called the carotid arteries the soporales or sleepy arteries.4

The first operations on the carotid arteries were quite naturally ligation procedures for hemorrhage or trauma. Hebenstreit of Germany in 1793 reported a case of carotid ligation for hemorrhage, and the patient is said to have lived.5 John Abernethy in London in 1798 ligated the carotid artery for trauma, but the patient died of cerebral causes.6

The first authentic successful ligation of the carotid artery on record was performed by David Fleming, a young British naval surgeon on October 17, 1803, on a servant who tried to commit suicide by cutting his throat. The patient survived.7, 8

The first successful ligation of the carotid artery in the United States was performed by Dr. Amos Twitchell of Keene, N.H., on October 18, 1807, on a cavalry soldier who had been accidentally shot at a regimental review. The patient made an uneventful recovery. Amos Twitchell, who died in 1850, became the leading surgeon in his area of New England.9 Sir Astley Cooper of London was the first to ligate successfully the carotid artery for cervical aneurysm, on June 22, 1808, and the patient lived until 1821.10, 11

Progress was slow during the ensuing 100 years. It was believed by most physicians, including William Osler, that strokes were caused by intracranial vascular disease.12 This concept is a reflection of how things work in the world of science. We think that discoveries are made, their importance is quickly recognized, and appropriate changes are adopted promptly. Not so. Such was the case with extracranial carotid disease. Autopsies had revealed massive brain infarcts, but it was not recognized that these lesions could be due to extracranial carotid disease because the carotid arteries were not examined during routine autopsies for fear of disfigurement. This failure need not have occurred because a number of physicians had described occlusive lesions in the extracranial vasculature and had related these to the clinical phenomena observed.3 In a landmark paper, J. Ramsay Hunt of New York City in 1914 had called attention to the importance of extracranial lesions in cerebrovascular disease.13

In 1927 Egas Móniz had introduced cerebral arteriography and thus laid the groundwork of a practical method for the diagnosis of occlusive lesions.14

In two papers, in 1951 and 1954, C. Miller Fisher, working in Montreal but later in Boston, made significant contributions; he noted that with severe stenosis of the carotid bifurcation the distal vessels could be entirely free of disease, and suggested that surgical correction should be possible.15, 16

The first successful reconstruction of the carotid artery for frank stroke was performed by Carrea, Molins, and Murphy in Buenos Aires on October 20, 1951, after reading Fisher's article, and was reported in 1955. This was an end-to-end anastomosis between the proximal left external carotid artery and the distal internal carotid artery after partial resection of the stenosed area, together with cervical sympathectomy. The patient lived for 23 years and died of a myocardial infarction in 1974.17

On January 28, 1953, Strully, Hurwitt, and Blankenberg in New York City first attempted thromboendarterectomy of a totally occluded cervical internal carotid artery but were unable to obtain retrograde flow.18

The first successful carotid endarterectomy was performed by Michael E. DeBakey on August 7, 1953, and was reported several years later. The patient was a 53-year-old school bus driver who had had recurring transient ischemic attacks (TIAs) and a mild stroke; he lived for 19 years without further strokes, dying of myocardial infarction in 1972.19

The operation that gave the greatest impetus to the development of carotid surgery was that of Eastcott, Pickering, and Rob, performed on May 19, 1954, at St. Mary's Hospital in London and reported in November of 1954.20 A 66-year-old woman, having suffered 33 TIAs, underwent resection of the carotid bifurcation, followed by end-to-end anastomosis between the common carotid and the distal internal carotid arteries. Hypothermia to 28° C was used for cerebral protection. The patient was relieved of her symptoms and lived 20 years, dying in 1974 at age 86. The second operation at St. Mary's was an endarterectomy, done in June 1954.

My first carotid endarterectomy was performed on April 16, 1957, 39 years ago.21 With increasing experience the various procedures just described were abandoned with the exception of endarterectomy, which has become the standard operation. Table I lists in chronologic order some of the early procedures that were performed for the treatment of extracranial cerebrovascular disease.

Table I. The first carotid reconstructions for cerebrovascular insufficiency, listed in chronologic order
AuthorDate of operationDegree of stenosisProcedureRestoration of flow
Carrea, Molins, & Murphy17October 20, 1951PartialEnd-to-end anastomosis external carotid to internal carotidYes
Strully, Hurwitt, & Blankenberg18January 28, 1953TotalThromboendarterectomy followed by ligation and resectionNo
DeBakey19August 7, 1953TotalThromboendarterectomyYes
Eastcott, Pickering, & Rob20May 19, 1954PartialEnd-to-end anastomosis common carotid to internal carotidYes
June, 1954PartialThromboendarterectomyYes
Denman, Ehni, & Duty22July 14, 1954TotalResection with homograftYes
Lin, Javid, & Doyle23December, 1955PartialResection with saphenous vein graftYes
Murphey & Miller24February 6, 1956TotalThromboendarterectomyYes
February 24, 1956PartialThromboendarterectomyYes
Cooley, Al-Naaman, & Carton25March 8, 1956PartialEndarterectomyYes
Lyons & Galbraith26August 9, 1956PartialSubclavian-carotid nylon bypass graftYes

In the early 1950s most of us were general or thoracic surgeons who were interested in the burgeoning field of vascular surgery. As such we had had little or no experience with cerebrovascular insufficiency. My attention was called to carotid disease and strokes by the neurosurgeons in our hospital, who had been influenced by Dr. Francis Murphey of Memphis and Dr. William Fields in Houston. Thus began a joint endeavor with the neurosurgeons. Eventually the chief of neurosurgery asked us to take over the carotid project, which we did, but with the continued advice and help of the neurosurgeons and neurologists, who saw all the patients in consultation.

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Classification of patients 

It soon became obvious that all strokes were not alike. We learned that there were transient episodes, strokes with all degrees of severity, and patients with carotid lesions that were asymptomatic. It was obviously necessary to classify patients into specific groups. Thus various classifications were developed in different centers, by DeBakey and his colleagues,27 by DeWeese et al.,28 and by others. The one we came to use had four categories: frank stroke, TIAs, chronic ischemia, and asymptomatic bruit or stenosis. There are many subsets in the frank stroke category. Although simple, this classification has served us well over the years.21

There have been many classifications proposed since the 1950s, including the NINCDS,29 the Marseilles classification of Courbier,30 the CHAT,31 and that of the Joint council of the SVS/ISCVS.32

It is important to classify patients with cerebrovascular insufficiency into specific clinical categories. Only in this way can proper selection of patients for surgery be made and results of different methods of therapy within the same category be compared. The outcome early and late is also related to the initial classification.33

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Arteriography 

When we became involved with carotid surgery, all the carotid arteriographic scans in our hospital were performed by the neurosurgeons and later by some of the neurologists, who were very skillful and had low complication rates. At first these were done through a cutdown in the mid-neck. As experience grew, percutaneous punctures low in the neck were done. It was soon learned that unilateral arteriograms were inadequate, so bilateral pictures were obtained. We also found that stenoses as well as total occlusions could cause symptoms. It also became clear that intracranial views were necessary. As x-ray equipment improved, serial films were possible using the Schönander unit. General anesthesia was used in all cases. At that time getting pictures of the vertebral and arch vessels was a problem. Retrograde techniques using needles and short catheters through the common carotid, subclavian, axillary, and brachial arteries were developed. One technique that was tried for a short while was a direct suprasternal notch puncture of the aortic arch with a long #17 gauge needle. This gave good pictures, but also resulted in bleeding into the upper mediastinum, so the technique was abandoned. With the advent of the retrograde femoral Seldinger technique, carotid punctures were abandoned and selective arteriographic scans using local anesthesia took over. Recent developments have included digital subtraction angiography, magnetic resonance arteriography, and color-flow duplex ultrasound.

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Indications for operation 

In the early days it was not clear which patients should undergo surgery. The ones most frequently seen were those who had frank strokes of any degree of severity, including those with coma and hemiplegia. Arteriograms appropriate to the clinical picture were obtained, and total carotid occlusion was a frequent finding. Such severe cases were promptly operated on. Data began to accumulate, however, regarding the outcome of operation on such patients. Thus Wylie et al. in 1964 reported an operative mortality rate of 60% in a small series.34 DeWeese et al. in 1968 reported an operative mortality rate of 34% when such patients underwent surgery within 24 hours.28 In 1966 we reported our results in 45 operated patients with acute profound strokes. Nine patients died, an operative mortality rate of 20%; all nine underwent surgery within 26 hours of onset of the stroke.21 Blaisdell et al. in 1969, reporting for the Joint Study, had an operative mortality rate of 42%, while those who did not undergo surgery had a 20% mortality rate. Patients who underwent surgery more than 14 days after onset had a lower mortality rate of only 17%.35

The recommendation from these studies was that it was inadvisable to perform emergency operation on patients with acute profound strokes or rapidly progressing strokes because of the hazard of producing intracerebral hemorrhage and edema in ischemic brain tissue, with subsequent death, after surgical revascularization. If operation was to be considered, a delay of at least 2 weeks or more was necessary for stabilization.

In 1986 Meyer et al. at the Mayo Clinic reported performing emergency endarterectomy on 34 patients with acute carotid occlusion who had profound deficits. Despite restoring flow in 94% of these patients, the operative mortality rate was 21% and only 38% were improved.36 So the problem of the acute profound stroke remains unsolved.

There is controversy whether to perform emergent, urgent, or elective surgery on patients with fluctuating or unstable strokes, slowly progressing strokes, and crescendo TIAs. With careful clinical judgment and experience, outcome with emergent or urgent operations can be excellent, as reported by a number of surgeons.37, 38, 39

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Total carotid occlusion 

It soon became obvious that the subject of acute profound strokes could not be divorced from the subject of total carotid occlusion because a large proportion of the former are caused by the latter. In the early days we operated regularly on patients with totally occluded arteries. We soon learned, however, that only 40% of these arteries could be opened by carotid endarterectomy. In 112 patients we found that those who underwent surgery within 6 hours of onset of occlusion had 100% restoration of flow. Much to our amazement, patients who underwent surgery after a month still had a 20% patency rate. Chronic occlusion in the absence of symptoms is not an indication for surgery. Chronic occlusion in the presence of symptoms may occasionally justify surgery. If the occlusion is associated with a profound stroke, operation is not indicated. Clinical considerations of the stroke itself are the most important criteria determining operability.40

After an early learning period, it soon became clear that the principal role of carotid endarterectomy was prevention of strokes in patients with TIAs, mild deficits, and asymptomatic but significant carotid stenoses, rather than treatment of severe strokes.41

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Results of operation 

Much progress has been made in carotid surgery over the past 40 years. How do we assess the outcome? In the words of Norman Hertzer, “Results mean everything.”42

The goals of carotid surgery are to relieve symptoms, prevent strokes, and by so doing improve the quality of life, and hopefully to lengthen survival. The evaluation parameters include operative mortality rates, operation-related deficits, long-term strokes, long-term stroke deaths, and long-term survival.43

Of primary concern is the operative mortality rate after endarterectomy. At the outset these elderly patients constituted a high-risk group. Operative mortality data for the first 6 years of our group's experience beginning April 16, 1957, showed that in 272 operations the procedure mortality rate for frank strokes was 8.7%. For TIAs it was 1.7%, and for chronic ischemic and asymptomatic patients it was zero, for an overall mortality rate of 4.8%. After this analysis, we abandoned emergency operation on acute profound strokes, used general anesthesia in most cases, and adopted the routine use of a temporary inlying shunt. The operative mortality rate thus progressively declined. For the next 27 years with 1696 operations, the operative mortality rate for frank strokes was 3.3%, for TIAs 1.2%, and for asymptomatic patients 0.3%, for an overall mortality rate of 1.47%.43 Thus the 33-year experience with 1968 operations gives an overall figure of 1.9%. In a recent 4-year experience, the operative mortality rate for frank strokes has dropped to 1.78%.

In a 1988 survey of 15,960 carotid endarterectomies performed for all indications, Hertzer44 found the overall average operative mortality rate to be 1.4% and the perioperative stroke rate to be 2.2%. In a number of individual series the operative mortality rate has been less than 1% and the perioperative stroke rate less than 2%.45 Thus in the hands of well-trained, experienced vascular surgeons, with proper selection and timing, carotid endarterectomy can be performed safely with low mortality and morbidity rates.

In the early experience about 70% of the operative deaths were from cerebral causes. Once we stopped operating on patients with profound strokes and improved our techniques, deaths from cerebral causes declined markedly, so in recent years operative death has been largely a result of cardiac causes, with an occasional fatality caused by stroke.

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Cerebral protection 

Another problem we faced at the beginning was how to operate on these patients safely without making their deficits worse or producing new deficits, if they were asymptomatic or had TIAs. At first we tested the patient by compressing the carotid in the neck to see if any symptoms developed. If the patient could stand 20 minutes of carotid compression, he could usually tolerate carotid clamping long enough for performance of endarterectomy. Another maneuver was to operate with the patient under local anesthesia and to test the patient by temporary clamping of the carotid for 5 to 10 minutes, as is still done. If the patient could not tolerate carotid clamping, then we had a problem. Early methods of cerebral protection during carotid clamping included general anesthesia, induced hypertension, hypercapnia, hypocapnia, and hypothermia. General anesthesia is indeed helpful by increasing the tolerance of the brain to ischemia and reducing cerebral metabolic demands for oxygen. Except for general anesthesia, the other methods were abandoned.

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Carotid shunting 

The use of a temporary bypass shunt thus came to be the most reliable method for cerebral support. The external shunt was the first technique to be used. As far as I can determine, the case described by Cooley in 195625 was the first reported use of an external shunt during carotid endarterectomy. The shunt consisted of a polyvinyl tube with a 14-gauge needle at its lower end and a 16-gauge needle at its upper or internal carotid end. I first used an external shunt similar to Cooley's using 13-gauge needles on January 6, 1958, and continued to use the external shunt until October 1960, when I first used an intraluminal inlying shunt at the suggestion of Stanley Crawford. I have continued to use the inlying shunt first selectively and then routinely since that time. We described our use of this type of shunt before this Society in 1961.46 The shunt solved the problem of cerebral protection during carotid endarterectomy.

Over the years extensive discussion has centered on the necessity for routine use of the shunt. Some surgeons have employed it routinely, such as Javid and ourselves, some use it selectively on the basis of an assessment of cerebral collateral circulation, and a few state they rarely or never use it. Methods presently available to determine the adequacy of collateral blood flow during carotid clamping are: (1) determination of cerebral blood flow by the xenon method; (2) temporary carotid occlusion under local anesthesia; (3) determination of stump pressure in the occluded distal internal carotid artery; (4) electroencephalographic monitoring; (5) transcranial Doppler monitoring; and (6) somatosensory evoked potential monitoring. I am fully aware that shunting is not necessary in every case; nevertheless, our group prefers routine shunting. With routine use complications are practically nil, which is not necessarily true of the occasional shunter.

There are certain situations, however, in which a shunt is mandatory: in patients with prior strokes, in those with contralateral occlusions, when changes occur during intraoperative monitoring, in those with low stump pressures, and perhaps in patients with positive results of computed tomographic scans.47

In a personal series of 707 operations on patients with TIAs and asymptomatic stenoses using general anesthesia and routine shunting, the operative mortality rate was 0.42%, the incidence of severe deficits was 0.56%, and that of mild deficits 1%, for a total operation-related stroke morbidity rate of 1.56%. A number of other series in the literature using various monitoring methods have shown equally satisfactory results.45

However, all was not well everywhere. In 1977 Easton and Sherman48 reported an alarmingly high rate of complications after carotid endarterectomy performed in two large community hospitals in Springfield, Ill. The operative mortality rate was 6.6% and the perioperative stroke rate was 14.5%, for a combined rate of 21.1%. The implication was that such results might be representative of those in many community hospitals in this country. In 1995 Mattos et al.49 reported an updated study from the same two hospitals 17 years after the original report. They found an operative mortality rate of 1.6%, and a perioperative stroke rate of 5.3%, for a combined rate of 6.3%. This is a dramatic improvement, but as Mattos et al. state, “still not optimal and probably will remain high as long as individual surgeons with high complication rates continue to perform carotid endarterectomies.”49

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Long-term strokes 

The next question was, did carotid endarterectomy really decrease the long-term incidence of stroke compared with the best medical therapy? It is generally accepted that 35% to 40% of untreated patients with TIAs go on to suffer frank strokes if observed up to 5 years or more, at an annual rate of 6% to 10% per year.43 Early reports of nonrandomized clinical series of TIA patients subjected to carotid endarterectomy showed that long-term stroke rates were indeed decreased after operation. In 1965 DeBakey et al.27 reported a long-term stroke rate of 5% during follow-up of 1 to 11 years. In 1970 our group41 reported a rate of 5.4% at 1 to 13 years, or an average of 1.6% per year. DeWeese et al. reported in 197350 a rate of 2.1% per year. A study much later in 1989 by Callow and Mackey51 gave a long-term stroke rate of 2.1% per year and stroke-free rates at 5 and 12 years of 89% and 81%, respectively. Other investigators reported similar results.52

Objections were raised, however, because the studies were not prospective and randomized. As a consequence, several prospective randomized trials were instituted. The outcomes of these trials have substantiated the results of the previously reported clinical series and have shown that carotid endarterectomy does indeed reduce the long-term incidence of strokes in patients with TIAs and mild deficits who have severe degrees of carotid stenosis, i.e., 70% to 99% diameter reduction.

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Randomized trials 

Thus in the NASCET trial the long-term stroke rate for surgical patients was 9% compared with 26% for medical patients.53 In the European trial it was 2.8% for surgical patients, excluding a perioperative morbidity and mortality rate of 7.5%, and was 16.8% for medical patients.54 In the Veterans Administration Symptomatic Trial, in which a 50% stenosis cutoff was used, the stroke rate was 7.7% for the surgical group compared with 19.4% for the medical patients. At 70%, it was 7.9% compared with 25.9%.55 Investigation is continuing in patients with lesser degrees of stenosis, i.e., 30% to 69%.

Another goal of therapy in patients with TIAs is relief of disabling symptoms. In our own series during a 13-year follow-up, 77% were normal and 17% were improved.41 Endarterectomy thus relieves symptoms as well as preventing strokes, improving quality of life.

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Asymptomatic stenoses 

A subject of great interest is the management of patients who have an asymptomatic carotid bruit or stenosis. In the beginning, auscultation of a bruit was the only indication that a patient had a carotid stenosis. There were no other noninvasive tests available at that time. At first, nothing was done if the patient had no symptoms. But then we began to do arteriographic scans and to operate on selected patients with severe stenoses. During an in-depth review in 1966,21 we were struck by the finding that among 16 patients with asymptomatic bruits who did not undergo surgery, five of the 16, or 31%, sustained frank strokes without antecedent episodes of transient ischemia. Thus began our serious interest in asymptomatic bruits.

Consequently two series of patients, an operated and a non-operated, were started and observed prospectively and contemporaneously over the years, though not randomized. The results were published in 1978.56 In 132 patients who underwent endarterectomy, the operative mortality rate was zero and strokes related to operation were 1.2%. These patients were observed up to 15 years, an average of 55 months. TIAs occurred in 4.5% and strokes, both fatal and nonfatal, in 4.6%, while 90.9% remained asymptomatic, giving an incidence of stroke of 1% per year. By contrast, in 138 comparable control patients who did not undergo surgery and were observed up to 16 years, an average of 55 months, 26.8% had TIAs, 17.4% had strokes, and only 55.8% remained asymptomatic, for an incidence of stroke of 3.8% per year. The difference between the two groups was statistically significant in favor of the operated cases.

A number of series in the literature showed results similar to ours.57 In spite of the clinical data, there was still considerable controversy regarding endarterectomy for asymptomatic stenoses because no prospective randomized trials had been carried out. Consequently, several trials were begun. Two major trials have been completed, both ending in favor of endarterectomy. The first was the Veterans Administration Asymptomatic Trial,58 with a division at 50% diameter reduction. The stroke plus TIA rate in the surgical group was 8%, but was 20.6% in the medical group. For stroke only, the rate was 9.4% in the medical compared with 4.7% in the surgical group, thus favoring endarterectomy. The second trial, the ACAS study,59 had a cutoff of 60% diameter stenosis. The stroke rate among the medical patients was 11% compared with 5.1% for surgical patients, a statistically significant difference in favor of surgery.

Although there is still some controversy over various aspects of both trials, it appears that selected asymptomatic patients with significant carotid stenoses benefit from carotid endarterectomy with a reduced incidence of long-term stroke.

Over the years the incidence of carotid endarterectomy rose steadily until 1985, being over 107,000 procedures annually in the United States. Since serious concerns had been raised over the appropriateness and effectiveness of the operation, the incidence plummetted to around 70,000 operations per year. In 1991, results of NASCET and ECST were reported, and the incidence is again on the rise, over 90,000, hopefully for the right indications and with acceptable immediate and long-term results.60

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Long-term survival 

It is difficult to document significant prolongation of survival of patients who have had carotid endarterectomy, although one would expect long-term survival to be somewhat improved in these patients by lowering the long-term incidence of stroke. In our experience with symptomatic and asymptomatic patients observed up to 16 years, we have not been able to show any improvement in survival of the patients who underwent surgery.33, 41 The survival rate of the operated groups is far below that of the normal population of the same age and is a reflection of the incidence of generalized atherosclerotic disease, especially coronary artery disease, in patients with carotid atherosclerosis. Data from the Veterans Administration Asymptomatic Study also showed no difference in long-term survival between operated and nonoperated cases.58

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Risk factors 

At this point, I would like to emphasize the importance of the initial clinical presentation of the patient as related to his prognosis, that is to say the differences between frank stroke, TIA, and asymptomatic stenosis patients. It appears that these patients actually represent three separate stages based on the parameters of operative death, perioperative stroke, long-term stroke, long-term death from stroke, and long-term death. The frank stroke patient has the worst outlook in every category, and the asymptomatic patient has the best outlook. It is thus important to establish an accurate preoperative clinical classification in order to estimate each patient's risk and prognosis.33

There are certain general risk factors that influence the outcome of operation: heredity, age, sex, race, obesity, hypertension, smoking, diabetes, hyperlipidemia, and hypercoagulable states, some of which can be modified by proper medical management and some of which cannot. The major factors influencing the immediate outcome of endarterectomy are: (1) avoidance of operation on patients with acute, profound, and progressing strokes; (2) the presenting neurologic classification; (3) the technical competence of the operating team; and (4) coronary artery disease. The initial classification is an established fact and cannot be changed. The skill and experience of the operating team are factors in operative mortality and stroke morbidity rates. Studies from Connecticut and Kentucky point out that there is an inverse relationship between the number of cases a surgeon does and the immediate outcome; i.e., the fewer the cases, the higher the mortality and stroke rates, and vice-versa.42 This is a factor that can be improved.

The major factors influencing the long-term outcome of endarterectomy are (1) the stage of the atherosclerotic disease; (2) the rate of progression; and (3) associated disorders, especially coronary artery disease.

Atherosclerosis progresses at different rates in different individuals. In general, three rates of progression are observed: rapid, in 10% of patients; moderate, in 60%; and slow, in 20% to 30% of patients. The rate of progression in the individual patient cannot be determined at the initial presentation, but only by careful follow-up at appropriate intervals.33

This brings us to a consideration of coronary artery disease, the major factor limiting both the immediate and especially the long-term outcome of carotid endarterectomy. For the past 30 years, all reported long-term studies following carotid endarterectomy have shown that coronary artery disease is the leading cause of both immediate and long-term deaths. Improved preoperative cardiac assessment and newer therapeutic regimens have improved the perioperative mortality rates to very low levels, 1% to 2%. In our series, 52% of the long-term deaths had cardiac causes.41

The only way that long-term survival can be substantially improved in these patients is by modification of the risk factor of coronary artery disease. Specifically, what is the influence of coronary artery bypass grafting (CABG) on the survival rate of patients who undergo carotid endarterectomy? Data on this matter are scarce, contradictory, and difficult to interpret because of the multiplicity of factors and the numerous subsets of coronary artery disease and carotid disease.

In the series of carotid patients reported by Bernstein et al.61 23 had CABG either before or after the carotid operation. During follow-up of 1 to 10 years, with a mean of 43 months, the survival rate of the patients with CABG was 95%. Of 240 other carotid endarterectomy patients without CABG the survival was only 77%.

Hertzer et al.62 have reported long-term survival data from the Cleveland Clinic on TIA patients having carotid endarterectomy with and without CABG. Thus in patients without CABG, the survival rate was 61% at 5 years and 32% at 10 years, whereas in those with bypass it was 84% at 5 years and 55% at 10 years. In our series of carotid endarterectomy patients, none of whom had CABG, the 5-year survival rate was 71% and the 10-year survival rate 38%.

Mackey et al.63 reported a 5-year survival rate of 73% with simultaneous combined carotid endarterectomy and CABG and 76% in a comparable cohort with carotid endarterectomy alone.

Ricotta et al.64 in a series of 147 patients who all underwent endarterectomy, reported an 83% 3-year survival rate in those without clinical evidence of coronary disease, 93% survival in those having CABG or angioplasty, and curiously enough 100% survival in those with stable coronary disease without CABG. Data from all these sources give us hope that immediate and especially long-term mortality rates from coronary artery disease in carotid patients may be modified by appropriate application of myocardial revascularization by whatever means: CABG, angioplasty, stenting, thrombolysis, antiplatelet or anticoagulant drugs, or other agents.

In 40 years, carotid endarterectomy has become an established and worthwhile procedure for the prevention of strokes. In the early days emphasis was on indications and techniques. Since then the focus has been on natural history, outcomes, and modification of risk factors. But what of the future? What problems remain?

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The future 

How can we best prevent atherosclerotic disease? How can we arrest, modify, or reverse atherosclerotic plaques? How are we going to refine the indications for endarterectomy?

While 20% to 30% of patients with tight stenoses have strokes, why don't the remaining 70% to 80% of individuals with the same lesions have strokes? What factors account for the difference when the stenosis is the same? A number of factors are involved: plaque morphology; integrity of the circle of Willis; the presence of silent cerebral infarcts; status of the cerebral collateral circulation; status of the opposite carotid, external carotid, and vertebral arteries; and combinations of other risk factors as already mentioned, such as smoking, etc. The plaque morphologic features are of great significance. Of special importance is the fibrous plaque cap. Important points here relate to thickness of the fibrous cap, composition of the plaque, why the cap ruptures, and the consequences of cap rupture as related to plaque composition. Likewise, what causes intraplaque hemorrhage?65

How can we prevent recurrent stenosis caused by myointimal hyperplasia? What has cell biology taught us? Mechanically, patching is helpful, but I suspect the ultimate answer will be drugs.

How can we improve the outcome in acute profound strokes? Will thrombolysis be the answer? Perhaps, but at this point, not yet. In the recent NINDS trial66 with intravenous tissue plasminogen activator (tPA), begun within 3 hours of onset, there was no difference between the treatment and placebo groups at 25 hours, although some benefit was observed at 3 months, but the mortality rate was the same. However, at 36 hours the incidence of intracranial hemorrhage with tPA was 6.4% compared with 0.6% in the placebo group, a tenfold difference. Nevertheless, with recent reports of dramatic success with lytic agents, intense further investigation is appropriate.

How can we better differentiate between reversible cerebral ischemia and irreversible frank infarction? What will be the most practical screening test for carotid stenosis?

Will non-invasive methods such as duplex scans replace conventional invasive arteriography? I think this is inevitable, but there are problems here dealing with the arch vessels and intracranial lesions, as well as validation of duplex criteria to conform to the results of the randomized trials based on a standard method of angiographic measurement of carotid stenosis, whether by NASCET, ECST, or some other method. Magnetic resonance angiography will probably be helpful.

How can we eliminate white clot thrombosis in the endarterectomized carotid? This is a hematology problem.

Are there better monitoring methods to detect cerebral ischemia during carotid endarterectomy? Are there other ways to provide cerebral protection during carotid clamping?

What will be the best protocol to manage patients with combined carotid and coronary artery disease in order to prolong survival? This is a major challenge.

Will hospital audits be widely used to improve outcome of carotid surgery?

What further advances will be made in vascular laboratory technology? Will genetic engineering have a role?

A timely and important matter is the role of carotid angioplasty with or without stents. Mortality rates up to 2% and stroke rates as high as 11% as presently reported67 are not acceptable when compared with carotid endarterectomy.

Perhaps we should go by one of the aphorisms of Sir William Osler who said, “The philosophies of one age have become the absurdities of the next, and the foolishness of yesterday has become the wisdom of tomorrow.”68 Time will tell. There is plenty of work to be done. The past is only prologue. When one looks at the progress we have made in the last 50 years and the pace at which technology is advancing today, I have no doubt that most of the problems I have listed will be solved in the next 50 years.

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Journal of Vascular Surgery
Volume 25, Issue 1 , Pages 131-140, January 1997

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