The Evolution of Surgery for the Treatment and Prevention of Stroke

• carotid endarterectomy
• history
• stroke prevention
• surgery

Thomas Willis, the man for whom this lecture is named, was an Englishman and a leading neuroanatomist of the 17th century. Born in 1621, he attended Oxford University, graduating from Christ Church College in 1639. While still at Oxford, he became Sedleian Professor of Natural History in 1660. He did much experimental work with his associate Richard Lower. He performed injection experiments on cadavers and noted that if he injected the carotid artery on one side, the dye solution would come forth from the carotid on the opposite side.

In 1664 Willis published his monumental work Cerebri Anatome, the most complete and accurate account of the nervous system that had hitherto appeared. In it he contributed the term “neurology” to medicine, a word derived from the Greek, meaning “sinew,” “tendon,” or “bowstring.” The word was translated and introduced into the English language in 1681 in Samuel Pordage's translation of Willis' work.

Cerebri Anatome contains a classification of the cerebral nerves, the first description of the eleventh nerve, and a description of the hexagonal network of arteries at the base of the brain that we know as the circle of Willis. Although others had described the circle before Willis, he was the first to grasp its physiological and pathological significance. He records the clinical histories of two patients in whom he suggests that the anatomic configuration of the arteries at the base of the brain could prevent apoplexy. The book was illustrated by Christopher Wren, an associate of Willis at Oxford, later to become England's leading architect and designer of St Paul's Cathedral, numerous other English churches, and many historic secular buildings.

Willis moved to London in 1666 and acquired the largest fashionable practice of his day. He continued his careful clinical observations and made a number of other important contributions. He was the first to recognize that lesions in the region of the internal capsule will produce hemiplegia. He was the first to notice the characteristic sweetish taste of diabetic urine. He described myasthenia gravis. He gave the first account of epidemic typhoid fever and typhus. He was the first to describe and name puerperal fever. He described the phenomenon of Willis' paracusis: a deaf person who can hear only in the presence of noise.

Thomas Willis died in London on November 11, 1675, of pneumonia at age 54. He is buried in the north transept of Westminster Abbey. He was indeed a remarkable man.^{1 2 3 4}

Changing concepts of the etiology, diagnosis, and treatment of ischemic stroke syndromes in the past 45 years have been responsible for widespread renewal of interest in this disease. Increasing awareness of the extracranial location and segmental nature of atherosclerotic occlusive disease in a large proportion of patients with cerebrovascular insufficiency was followed by the development and use of appropriate vascular surgical techniques for removing or bypassing offending plaques, thus increasing cerebral blood flow or eliminating sources of cerebral emboli. Since extracranial carotid lesions are those most frequently encountered, surgery of the carotid artery has become a subject of heightened interest and importance.^{5 6}

It is the purpose of this article to review the historical aspects of surgery for stroke, emphasizing surgery of the carotid artery but discussing briefly surgery of the vertebral artery and the great vessels of the aortic arch. As Thomas Carlyle said, “History is the essence of innumerable biographies.”

The first recorded reference to the nervous system is found in ancient Egyptian records. The Edwin Smith Surgical Papyrus, composed about 3500 BC, or more than 5000 years ago, contains the first use of the word “brain,” along with a description of its coverings and the fluid beneath them.²

The word “carotid” is derived from the Greek term karotide or karos, meaning to stupefy or plunge into a deep sleep. According to Rufus of Ephesus (circa AD 100) the term was applied to the arteries of the neck because compression of these vessels produced stupor or sleep.² The ancient Greeks were aware of the significance of the carotid artery: the 31st metope from the south side of the Parthenon in Athens depicts a centaur applying left carotid compression to the neck of a Lapith warrior.

With the advent of Hippocrates (460 to 370 BC), ancient descriptive neurology was born. It was known that paralysis and convulsions followed injuries to the brain, with paralysis on the opposite side to the wound. Hippocrates described paralysis of the right arm with loss of speech in what is probably the first written description of aphasia. In one of his aphorisms Hippocrates stated, “Unaccustomed attacks of numbness and anesthesia are signs of impending apoplexy,” a description of a TIA. Apoplexy, a Greek word meaning “struck with violence,” first appeared in the Hippocratic writings.²

Galen (AD 131 to 201) was aware that hemiplegia resulted from a lesion in the opposite side of the brain but did not know about softening or hemorrhage as a cause of apoplexy, which he attributed to an accumulation of phlegm in the arteries of the brain.² With Galen as the authority, European medicine remained at a dead level for nearly 14 centuries until the time of Vesalius, who in 1543, with the publication of his magnificent De Fabrica Humani Corporis, threw overboard Galenical traditions.¹

Ambroise Paré⁷ in the 16th century was familiar with the carotid phenomenon and stated, “The two branches they call carotides or soporales, the sleepy arteries, because they being obstructed or any way stopt we presently fall asleep.”

The 17th century saw the work of Thomas Willis and Richard Lower, mentioned above in connection with the circle of arteries at the base of the brain.

Johann Jakob Wepfer, a Swiss physician, in 1658 was the first to describe carotid thrombosis, extracranially and intracranially, in a patient with a completely occluded and calcified right internal carotid artery. In his Apoplexia, he traced the carotid and vertebral arteries from their origins to the arterial circle at the base of the brain and noted that apoplexy could result from cerebral hemorrhage. In Apoplexia, examples of completed stroke, progressing stroke, TIA, and reversible ischemic neurological deficit were described.^{2 3 8}

Jean Luis Petit⁹ in the 18th century discovered that the brain may survive deprived of the contribution of one carotid artery. His patient had an aneurysm of the bifurcation of the right common carotid artery that was cured spontaneously. Seven years later, autopsy showed the lumen of the vessel to be completely occluded by organized thrombus.

The first operations on the carotid artery were quite naturally ligation procedures for trauma or hemorrhage. Hebenstreit of Germany, in his translation of Benjamin Bell's Surgery in 1793, mentions a case in which the carotid artery was injured during operative removal of a scirrhous tumor. The surgeon ligated the vessel to arrest hemorrhage, and the patient lived for many years. This is thought to be the first case on record of ligature of the carotid.^{10 11 12}

John Abernethy of London, a pupil of John Hunter, in 1804 reported a case of carotid ligation performed some years previously, probably in 1798. The patient, a man, was gored in the neck by the horn of a cow, and hemorrhage was profuse. Compression controlled the bleeding temporarily only to have it recur when pressure was released. Abernethy was compelled to ligate the common carotid artery. He states, “In attempting to secure the carotid artery I passed behind it. . . . a blunt hook with an eye in the point, and having previously introduced a ligature into it I drew back the instrument and thus enclosed the artery.” Hemorrhage was controlled, and the patient appeared well. However, the man died 30 hours later of cerebral causes, and Abernethy abandoned the procedure.^{10 12 13 14}

With the beginning of the 19th century, the history of carotid surgery becomes more accurate as dates of operations are given with exactness. The first successful ligation of a carotid artery was performed by David Fleming on October 17, 1803. Fleming was a young naval surgeon aboard His Majesty's Ship Tonnant, the greatest two-decker in the British navy, carrying 80 guns and cruising off the Spanish coast during the Napoleonic era. Mark Jackson, a servant, attempted to commit suicide by cutting his throat on October 9, 1803. The knife had grazed the outer and muscular coats of the carotid artery but left the artery intact. Eight days later on October 17, the carotid ruptured. Fleming cut down on the artery proximal to the rupture and ligated it. He had not done this before, nor had he heard of Abernethy's case. The patient survived and made an uninterrupted recovery. The case was reported in 1817 by Dr Richard Warren Coley, an assistant surgeon on HMS Tonnant. This was the first authentic successful case of ligation of the carotid artery on record.^{15 16}

The first case of ligature of the carotid artery in the United States was that of Mason F. Cogswell of Hartford, Conn, performed November 4, 1803; the report was published in October of 1824. The patient, a 38-year-old woman, had an extensive tumor of the left side of her neck that completely enveloped the carotid artery. During the course of its removal, the carotid artery had to be ligated and divided. The patient did well at first, but on the 20th day she died as a result of hemorrhage from the wound. Cogswell stated, “The circumstances attending this case were such as entirely to establish the practicability and safety of dividing the carotid artery on the living subject.”^{10 12 17}

The first successful ligation of the carotid artery in the United States was performed by Dr Amos Twitchell of Keene, NH, on October 18, 1807. John Taggart, a cavalry soldier, age 20, in a mock fight at a regimental review, was accidentally wounded in the neck by a pistol shot on October 8, 1807. The wound was treated by simple dressings, although Dr Twitchell commented, “There was a good deal of arterial excitement.” Taggart improved rapidly, however, until the 10th day when the internal carotid artery ruptured, and “the blood jetted forcibly in a large stream to the distance of three or four feet.” Twitchell stopped the hemorrhage by compression, then made an incision lower in the neck and ligated the common carotid artery with the patient's mother acting as his assistant. To his surprise, backflow bleeding continued from the distal vessel. He then packed the wound with dry sponges and the bleeding stopped. Fourteen days later, after all the packing was removed, the wound granulated in, and the patient made an uneventful recovery. This case occurred 8 months before Astley Cooper's successful operation. At the time, Twitchell was ignorant of any other previous ligations of the carotid artery. The case was not reported until 1842, in the short-lived New England Quarterly Journal of Medicine and Surgery. Amos Twitchell, who died in 1850, became the leading surgeon in his area of New England.^{10 18}

Sir Astley Cooper in London was the first to attempt ligation of a carotid artery for cervical aneurysm on November 1, 1805. This patient died of sepsis on the 21st day with a left hemiparesis. Cooper repeated the operation on June 22, 1808, at Guy's Hospital. The patient was 55 years of age and had a pulsating tumor the size of an egg at the angle of the jaw. Two ligatures were applied to the artery, which was divided. The patient made a perfect recovery with no untoward symptoms and lived until 1821. This was the first successful case of ligature of the carotid artery for aneurysm.^{19 20}

The first successful ligation of the carotid for aneurysm in the United States was performed by Dr Wright Post of New York City on January 9, 1813. After a stormy postoperative course, the patient eventually survived.¹²

Benjamin Travers, on May 23, 1809, first successfully ligated the left carotid for carotid-cavernous fistula, with disappearance of signs and symptoms. In 1885 Victor Horsley first successfully ligated the carotid in the neck for an intracranial aneurysm. The patient was well 5 years later. By 1868 Pilz was able to collect 600 recorded cases of carotid ligation for cervical aneurysm or hemorrhage with a mortality rate of 43%.¹⁴

The American surgeon John Wyeth in 1878 published an extensive report detailing 898 collected cases of common carotid ligation. He found the mortality to be 41% in contrast to that after ligature of the external carotid, which was only 4.5%.²¹

Until fairly recently, the prevailing notion held by most physicians was that strokes were caused by intracranial vascular disease. William Osler, in his textbook entitled The Principles and Practice of Medicine in the seventh edition of 1909 (the last edition that he himself wrote), attributed apoplectic stroke largely to cerebral hemorrhage. No mention is made of extracranial occlusive disease, and in the section dealing with cerebral softening, where embolism and thrombosis are mentioned, emphasis is on blockage of intracranial vessels.²² This is somewhat curious in view of the fact that several authors had already described occlusive lesions in the extracranial segments of the main arteries supplying the brain and noted the association of these lesions with symptoms of cerebral ischemia.

William Heberden (1710-1801), a prominent London practitioner, described symptoms of transient cerebral insufficiency recurring in hours, days, or even months before the final episode of hemiplegia.^{3 23}

Gull,²⁴ in 1855, wrote of a case of occlusion of the innominate and left carotid.

W.S. Savory,²⁵ in 1856, published a landmark article on cerebral ischemia. In it he described the case of a 22-year-old woman who had no pulsation in any of the vessels of the head, neck, or upper extremities. She had symptoms involving the left eye and right side of her body, both motor and sensory, as well as dizziness and convulsions. At postmortem examination, she had obliteration of the left carotid and both subclavian arteries. Savory commented on the relationship between the vascular occlusions and the clinical phenomena observed.

In 1856 Virchow described carotid thrombosis associated with ipsilateral blindness but found the lumens of the ophthalmic and central retinal arteries to be patent.⁸

Broadbent,²⁶ in 1875, reported the case of a 50-year-old patient with absent pulses in both radial arteries. At autopsy, the origins of the innominate, left carotid, and subclavian arteries were tightly constricted, whereas the vessels distal to the narrowing appeared full and healthy.

Penzoldt,²⁷ in 1888, reported a case of thrombosis of the right common carotid artery. The patient developed a sudden permanent blindness in the right eye and later sustained a left hemiplegia. At autopsy, the right common carotid was thrombosed and the right cerebral hemisphere had a large area of softening.

In 1905 Chiari²⁸ described ulcerating plaques at the carotid bifurcation and on the basis of detailed pathological examinations found that emboli could break away from carotid-sinus area plaques and cause strokes. He was among the first to propose that occlusive disease of the extracranial blood vessels could be responsible for neurological symptoms.³

A landmark article was that of J. Ramsay Hunt²⁹ of New York City in 1914, who called attention once again to the importance of extracranial occlusions in cerebrovascular disease. He recognized that both partial and complete occlusions of the innominate and carotid arteries could be responsible for cerebral syndromes of vascular origin and even used the term “cerebral intermittent claudication.” He suggested that extracranial obstructions had been largely overlooked and emphasized the importance of examining the cervical carotid system in patients with strokes. He also emphasized “the occurrence of unilateral vascular changes, pallor or atrophy of the disk with contralateral hemiplegia, in obstruction of the carotid artery.”

The next significant contribution was the report of Egas Móniz³⁰ of Portugal, who in 1927 first described the technique of cerebral arteriography for the study of cerebral tumors, using sodium iodide as the contrast medium, and thus laid the groundwork of a practical method for the diagnosis of occlusive lesions. The first report of carotid thrombosis demonstrated by arteriography was that of Sjöqvist³¹ in 1936. The following year, 1937, Móniz, Lima, and de Lacerda³² reported four patients with occlusion of the cervical portion of the internal carotid artery in whom the diagnosis had been established by arteriography. Egas Móniz won a Nobel Prize in 1949, not for cerebral arteriography but for his work on prefrontal lobotomy.

Chao and associates³³ of Peking, China, in 1938 reported two cases similar to those of Móniz. They used thorium dioxide as the contrast medium and found the internal carotid artery occluded in both cases. Portions of the internal carotid artery were resected, and slight improvements in the patients' symptoms were reported. By 1951 Johnson and Walker³⁴ were able to collect 107 instances of carotid thrombosis, all diagnosed by arteriography, and suggested that carotid occlusion was probably more frequent than generally realized.

In two important articles published in 1951 and 1954, C. Miller Fisher,^{35 36} working in Montreal and later in Boston, reemphasized the relationship between and frequency of disease of the carotid artery in the neck and cerebrovascular insufficiency. He defined the basic nature of the lesion as atherosclerosis, noted again partial and complete occlusions, and described several syndromes associated with such occlusive disease. He observed that with severe stenosis of the carotid bifurcation, the distal vessels could be entirely free of disease. He realized the importance of these observations and stated, “It is even conceivable that some day vascular surgery will find a way to bypass the occluded portion of the artery during the period of ominous fleeting symptoms. Anastomosis of the external carotid artery or one of its branches with the internal carotid artery above the area of narrowing should be feasible.”

Between 1916 and 1921, several surgeons reported successful repair of the cervical carotid artery for trauma, aneurysm, or tumor removal. Later in 1952, John Conley of New York reported anastomosing the distal ends of the internal carotid artery and external carotid artery to restore flow to the brain after tumor resection, a procedure previously reported by LeFevre³⁷ in France in 1918. In 1953, Conley³⁸ reported 11 cases in which the superficial femoral or saphenous vein had been used as an interposition graft to reconstruct a resected cervical carotid artery after tumor surgery.

Surgical methods of treating carotid artery occlusive disease prior to 1951 were (1) stellate ganglion block, (2) cervical sympathectomy, (3) removal of thrombi with reestablishment of blood flow, (4) ligation and excision of the carotid bifurcation, and (5) intracranial ligation of the carotid artery with silver clips. The reasons given for using these methods were (1) the release of vasospasm in the vessels supplying the brain by interrupting periarterial sympathetics and (2) the prevention of forward embolism from clots in the cervical vessels. The methods listed had little or no success in the treatment of strokes due to extracranial vascular disease.^{39 40}

A Portuguese surgeon, J. Cid Dos Santos,⁴¹ in 1946 introduced thromboendarterectomy for restoring flow in peripheral vessels, a major breakthrough.

In 1951 E.J. Wylie introduced into the United States the procedure of thromboendarterectomy for the removal of atherosclerotic plaques from the aortoiliac segments, but it had not been used on the carotid artery.⁴²

Fisher's prophecy of surgical reconstruction of the carotid artery in the neck as therapy for occlusive disease was soon fulfilled. The first successful reconstruction of the carotid artery was performed by Carrea, Molins, and Murphy⁴³ in Buenos Aires in 1951, after they read Fisher's article, and was reported in 1955. A 41-year-old male patient had recurring symptoms of right hemiparesis, aphasia, and left amaurosis over a 6-month period before being referred to the neurosurgical service of Dr Raul Carrea by Dr Guillermo Murphy. A left percutaneous arteriogram demonstrated an atherosclerotic plaque with severe stenosis in the internal carotid artery. On October 20, 1951, Dr Molins, a vascular surgeon, and Dr Carrea performed an end-to-end anastomosis between the left external carotid and the distal internal carotid arteries after partial resection of the stenosed area, together with cervical sympathectomy. The patient made an uneventful recovery and died 23 years later from myocardial infarction. His neurological status was normal except for loss of vision in the left eye.

On January 28, 1953, Strully, Hurwitt, and Blankenberg⁴⁴ in New York operated on a patient with a frank stroke and a totally occluded internal carotid artery. They performed a thrombectomy but were unable to obtain retrograde flow; consequently, a section of the internal carotid was resected. They suggested that thromboendarterectomy should be feasible in such cases when the distal vasculature was patent.

The first successful carotid endarterectomy was performed by Dr Michael DeBakey⁴⁵ on August 7, 1953. A 53-year-old school bus driver gave a history of recurring episodes of transient right hemiparesis and dysphasia over a 2-year period. On examination, he had a mild residual right hemiparesis and a weak pulsation in his left carotid artery. No preoperative arteriogram was performed. During surgery, a severely stenotic atherosclerotic plaque with superimposed fresh clot completely occluding the left internal carotid artery was found. Thromboendarterectomy was carried out with good retrograde flow from both internal and external carotid arteries. An arteriogram performed postoperatively on the operating table showed the internal carotid to be patent in both its extracranial and intracranial portions. The patient made a good recovery and lived for 19 years without having further strokes. He died from complications of coronary artery disease on August 17, 1972.

The operation that gave the greatest impetus to the development of surgery for carotid occlusive disease was that of Eastcott, Pickering, and Rob,⁴⁶ performed on May 19, 1954, at St Mary's Hospital in London and reported in November 1954. In this case, a 66-year-old housewife, having suffered 33 transient episodes of right hemiparesis, aphasia, and left amaurosis over a 5-month period, was found to have a severe stenosis of the left carotid bifurcation after a percutaneous left carotid arteriogram. With the patient under general anesthesia with hypothermia to 28°C (82.4°F) by means of ice bags for cerebral protection, the bifurcation was resected and blood flow restored by end-to-end anastomosis between the common carotid and distal internal carotid arteries. The carotid was occluded for 28 minutes. The patient was completely relieved of her symptoms and was alive and well at the age of 86.

Following these landmark cases, a number of different methods of carotid reconstruction were reported. The Table⇓ lists in chronological order the early procedures performed for the treatment of extracranial cerebrovascular disease. With increasing experience, the various procedures listed were abandoned with the exception of endarterectomy, which has become the standard operation. I performed my first carotid endarterectomy on April 16, 1957.⁵²

The case described by Cooley et al⁵⁰ is of interest in that an external shunt was used for cerebral protection, the first reported use of a shunt for 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. Additional cerebral protection was attempted by immersing the patient's head in crushed ice for 30 minutes. Despite this the patient suffered an operation-related stroke from which he recovered rapidly over the course of several weeks.

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 selectively until October 14, 1960, when I first used an intraluminal inlying shunt. I have continued to use the inlying shunt, first selectively and then routinely, ever since. Austin and I⁵³ described our early experience with this type of shunt in 1962.

The use of a shunt is still provoking discussion. Some surgeons such as ourselves use it routinely, others use it selectively on the basis of an assessment of the collateral circulation, while some say they rarely or never use it. Methods to determine the adequacy of the cerebral circulation include determination of cerebral blood flow by the xenon method, temporary carotid occlusion under local anesthesia, determination of the stump pressure in the occluded distal internal carotid artery, electroencephalographic monitoring, transcranial Doppler monitoring, and sensory evoked potential monitoring.⁵⁴

In the early 1950s, we tested the patient's tolerance preoperatively by manually compressing the cervical carotid for up to 20 minutes and observing any untoward symptoms. This sometimes took place daily for up to 2 weeks or until the patient could tolerate the compression.⁵³

In the past, hypothermia, hypercarbia, and hypocarbia were used for cerebral protection. Today the temporary shunt remains the most effective means of providing cerebral protection when such is judged necessary. General anesthesia is also helpful.⁵⁴ Another controversy revolves around the use of patching the carotid arteriotomy after endarterectomy. It is useful for small arteries and reoperation but is probably not necessary as a routine maneuver.⁶ A variation of the standard carotid endarterectomy is eversion endarterectomy, used by some surgeons in an effort to reduce the incidence of postoperative neointimal hyperplasia.⁵⁵

As more and more vascular and neurosurgeons began to perform endarterectomy, it soon became clear that it was most effective for partially occlusive lesions rather than for total occlusions, in which restoration of flow was possible in only 40% of cases and in many of which operation was contraindicated because of the clinical presence of acute profound strokes, where operative mortality was reported to be from 20% to 60%.⁶

It was also gradually realized that the principal role of carotid endarterectomy was one of stroke prevention in patients with TIAs, mild deficits, and asymptomatic stenoses, rather than treatment for completed or profound strokes, as in the early days of endarterectomy. Although a few early reports gave unacceptable outcomes for endarterectomy, most reported results in general were satisfactory.⁶

The chief complication of carotid endarterectomy, apart from death, is the production or aggravation of neurological deficits. With proper selection of patients, arteriography by skilled radiologists, avoidance of surgery for those with acute profound and progressing strokes, meticulous operative techniques used by well-trained surgeons, and appropriate use of cerebral protection, results of operation have progressively improved.

In a survey of 15 960 carotid endarterectomies, Hertzer 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 is under 1% and the perioperative stroke rate less than 2%.⁶

Considerable controversy has arisen over the years as to the effectiveness of carotid endarterectomy compared with best medical therapy in preventing stroke. An early randomized study, the Joint Study of Extracranial Arterial Occlusion, between 1959 and 1976, provided a tremendous amount of important information but showed no statistically significant difference in stroke rates between surgical and medical groups.³

The surgeon's role in the treatment of cerebral ischemic syndromes by carotid endarterectomy has been substantiated by the recent reports of results of several multicenter randomized trials demonstrating the efficacy of surgery in preventing strokes in patients with high-grade carotid stenosis. In the NASCET study, the long-term stroke rate for surgical patients was 9% versus 26% for medical patients.⁵⁶ In the ECST, it was 2.8% for surgical patients (excluding perioperative mortality and morbidity of 7.5%) and 16.8% for medical patients.⁵⁷ In the VA symptomatic trial, stroke rate was 7.7% for the surgical group versus 19.4% for the medical patients.⁵⁸

In the VA asymptomatic trial, stroke plus TIA rate for surgery was 8% versus 20.6% for medical therapy.⁵⁹ In the ACAS trial, stroke only in the surgical group was 5.1% versus 11% in the medical arm.⁶⁰ Thus, endarterectomy is beneficial in certain groups of both symptomatic and asymptomatic patients with high-grade stenoses. Controversy now exists over the most appropriate method of measuring carotid stenosis.

It is difficult, however, to document significant prolongation of survival after carotid endarterectomy, largely because of the prevalence of concomitant coronary artery disease. The only way long-term survival can be substantially improved is by modification, by whatever means, of this major risk factor.⁶

Over the years the incidence of carotid endarterectomy rose steadily until 1985, when over 107 000 procedures were performed annually in the United States. Since serious concerns had been raised over the appropriateness and effectiveness of the operation, the incidence plummeted to around 70 000 operations per year. In 1991, the results of NASCET and ECST were reported, and the incidence of operation (one hopes for the right indications and with acceptable immediate and long-term results) has risen again to over 90 000.^{61 62 63}

Surgical treatment of occlusive lesions of the great vessels arising from the aortic arch did not lag far behind that of the carotid artery in the neck. Gordon Murray of Toronto in 1950 successfully restored circulation in a left common carotid artery totally occluded at the aortic arch by means of a probe and instrumentation.⁶⁴ On March 20, 1954, Davis, Grove, and Julian performed the first innominate endarterectomy. DeBakey and his group on January 4, 1957, constructed a bypass graft from the innominate to the distal subclavian and carotid arteries and shortly thereafter successfully performed subclavian endarterectomy. Bypass procedures including extrathoracic bypass and endarterectomy remain the usual standard operations today for lesions of the aortic arch vessels.^{3 39}

As a result of studies by Hutchinson and Yates⁶⁵ in 1956 directing attention to the importance of occlusive lesions in the cervical portion of the vertebral arteries as related to stroke syndromes, reconstructive operations on the vertebral vessels were developed. On September 7, 1957, Cate and Scott in Nashville carried out a successful endarterectomy of the left subclavian and left vertebral arteries. In 1958, Crawford, DeBakey, and Fields described treatment of vertebral-basilar insufficiency by means of vertebral endarterectomy in one case and bypass graft from the subclavian to the distal patent vertebral in another.^{3 39} Newer techniques have enlarged the scope of vertebral surgery. Edwards et al⁶⁶ have been foremost in promoting subclavian and vertebral transpositions into the common carotid artery. Berguer⁶⁷ has devised innovative procedures on the distal vertebral artery near the base of the skull. The only limiting factor here seems to be the imagination of the surgeon involved.

On the basis of microsurgical techniques developed in the 1960s, Jacobson, Yasargil, and Donaghy carried out extracranial to intracranial bypass procedures hoping for improvement in patients with strokes who had occluded cervical internal carotid arteries.⁶⁸ In 1977, a randomized trial was initiated. Unfortunately, the trial failed to demonstrate significant benefit from the surgery, and the operation is no longer performed except in occasional situations, where it may be quite beneficial.⁶⁹

A fascinating aspect of this subject is a study of famous people who have had strokes. Marcello Malpighi, one of the great early microscopists, suffered his first stroke at age 66, on July 25, 1694, and died of another “apoplexy” on November 29 of the same year.^{3 70} Louis Pasteur had a series of TIAs, affecting largely his speech area but also his left side, over a period of some 10 years before he finally died September 28, 1895, at the age of 73.^{3 70}

Several intriguing reports have speculated on how the fates of nations may have been affected by strokes occurring in their leaders. One world-famous figure who suffered from and eventually died of cerebrovascular deterioration was Marshal Paul von Hindenburg. Certainly his action in authorizing Hitler to form a cabinet in 1933 was a decision that altered the course of history. Whether anyone could have stopped Hitler at this time is subject to speculation, but in his senile and demented state Hindenburg refused or was unable to involve himself in trouble or controversy. He was so far gone mentally that his secretary of state actually had to write down for him, word for word, the questions put to any caller.⁷¹

In Russia, V.I. Lenin also suffered from cerebrovascular troubles. He experienced several transient ischemic episodes, finally had a complete right hemiplegia, and died of his third stroke at the early age of 54 years on January 21, 1924. Prior to his illness Lenin elevated Josef Stalin to several important positions in the government, but in the last years of his life Lenin had grave doubts about Stalin and wanted Leon Trotsky to assume the more important posts. Had Lenin lived to make Trotsky his heir apparent, instead of Stalin, who knows what the course of modern history might have been?^{3 71} Ironically, Josef Stalin, the Soviet dictator who succeeded Lenin, died of a stroke at age 73 on March 5, 1953, the cerebrovascular accident having occurred 4 days earlier.³

In our own country, no fewer than 10 American presidents have suffered from or died of cerebrovascular disease.^{3 72} A very dramatic example is the case of Woodrow Wilson. He had a stroke in September of 1919 with paralysis of his left arm and leg, which improved to some degree, but in October he suffered another episode. Again he improved but was almost totally incapacitated. Although unable to carry out the duties of the Presidency, he nevertheless did not step down from office. His term ended on March 4, 1921, when he was succeeded by Warren G. Harding. Woodrow Wilson died on February 3, 1924, of a massive cerebral infarction. It has been stated by those who have studied the President's illness in detail that Wilson's cerebrovascular disease significantly contributed to the defeat of support for the League of Nations by the United States.^{3 71 72}

The illness of Franklin Delano Roosevelt is well known. In 1943, he reportedly had severe symptoms of cerebrovascular insufficiency with multiple ischemic episodes. How this disease affected the Yalta agreements of 1945 and the subsequent Cold War is a matter of speculation. His sudden death at the Georgia Warm Springs on April 12, 1945, was said to be due to a massive cerebral hemorrhage, but no autopsy was performed.^{3 72 73}

President Eisenhower experienced several cerebrovascular episodes, which at that time were termed “little strokes” and were said to be due to intracranial disease. His death came ultimately, however, from complications of heart disease rather than stroke. The most recent cerebrovascular episode in an American President occurred April 22, 1994, when Richard Nixon had a massive stroke and died at the age of 81.

By contrast, the late Mayor Richard Daley of Chicago, Ill, after having transient cerebral ischemia, underwent carotid endarterectomy in 1974 performed by Dr Hushang Javid with complete success and restoration of brain function to normal.

In cerebrovascular insufficiency, morbidity at times may be more important than mortality. Thus the quality of survival is emphasized as a feature of this disease, more so perhaps than in coronary artery disease, and underlines the main role of carotid endarterectomy as one of stroke prevention.⁷⁴

But what of the future? What problems remain?

How can we best prevent atherosclerotic disease?

How can we best arrest or reverse atherosclerotic plaques?

While 20% to 30% of patients with tight stenoses have strokes, why do the remaining 70% to 80% of individuals with the same lesions not have strokes? What factors account for the difference? Will the study of plaque morphology help us?

How should carotid stenosis be measured, by the NASCET method or the ECST method? How will the differences best be reconciled?

How can we improve the outcome in acute profound strokes? Will thrombolysis be an answer?

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 noninvasive methods replace conventional invasive arteriography?

Will MR arteriography have a major role?

How can we eliminate white clot thrombosis in the endarterectomized carotid artery?

How can we prevent recurrent stenosis due to myointimal hyperplasia? What has cell biology taught us?

Are there better monitoring methods to detect cerebral ischemia during carotid endarterectomy?

Are there other ways to provide cerebral protection during carotid clamping?

Will carotid angioplasty with or without stenting have a role or even replace endarterectomy?

How are we going to refine the indications for endarterectomy to avoid unnecessary operations? There is still plenty of work to be done.

It has been a fascinating 40 years with widespread renewal of interest in strokes. All aspects of the field have been reexamined, including the role of the surgeon, and the interest continues unabated.

• Copyright © 1996 by American Heart Association