The history of thoracic aortic surgery is short. Operations on the aortic root and ascending and transverse aorta were only made possible by the development of cardiopulmonary bypass in the 1950s. As in other areas of cardiovascular surgery, techniques in thoracic aortic replacement continue to improve. However, whereas surgical treatment of complex congenital cardiac anomalies, acquired valvular defects, and coronary occlusive disease have achieved very low levels of morbidity and mortality, operations on the thoracic aorta continue to be associated with significant risk. Factors contributing to surgical failure include delay in diagnosis and treatment, lack of familiarity with surgical methods due to relatively low patient numbers, and failure to define the optimum approach to individual problems. Causes of death or morbidity include haemorrhage, renal and pulmonary dysfunction, mesenteric vascular occlusion, and spinal cord ischaemia.

Although thoracic aneurysms show a greater tendency to rupture than abdominal aortic aneurysms, the threat of perioperative stroke, paraplegia, renal failure, or gut necrosis mitigate against early surgery in many centres. Inevitably an increasingly aged population will produce more patients with aneurysm formation due to medial or atheromatous degenerative disease. Improved techniques are consequently necessary to address an increasing number of patients with type A or type B dissection, and those with ascending, arch, descending thoracic, or thoracoabdominal aneurysms. Diagnostic methods, including CT and nuclear magnetic resonance imaging, have already advanced the non-invasive assessment and monitoring of thoracic aortic disease. Nevertheless thoracic aneurysm patients are at risk from acute coronary events during aortic cross-clamping and the need for coronary angiography is not yet obsolete.

Suturing of blood vessels was conceived more than two centuries ago, when an injured artery in the arm of a patient was successfully repaired. The concept lay dormant for more than a century until the impetus given to experimental surgery by the Listerian era. Czerny reported successful suture of an internal jugular vein and Postempski repaired a femoral arterial wound in the 1880s.

In 1881 Matas described the technique of endoaneurysmorrhaphy and in the early 1900s experimental surgery demonstrated the feasibility of excising arterial segments and restoring continuity by end-to-end anastomosis or arterial grafts. The feasibility of vascular anatomosis led to early experiments with renal and cardiac transplantation. However, except for individual efforts of a few surgeons, little consideration was given to the application of these principles to patients with arterial disease. This is perhaps understandable when one considers that ancillary measures such as general anaesthesia, blood transfusion, and antibiotics had not been developed, and the technique of arteriography has not been sufficiently refined for general and safe clinical use.

Roentgen announced the monumental discovery of X-rays in 1895 and within a year feasibility of radiographic visualization of blood vessels had been demonstrated by injecting contrast into the vessels of an amputated hand. In 1929 Swick reported the successful radiological use of organic iodide solutions. Thoracic aortic surgery began in 1944, with successful excision and end-to-end anastomosis in the repair of coarctation. A few years later human homograft tissue was first used to bridge the aortic defect resulting from excision of coarctation. In 1951 Oudot reported excision and homograft replacement for occlusive disease of the lower abdominal aorta. The following year Dubost performed the first resection and homograft replacement of an abdominal aortic aneurysm.

The use of homograft material represented a considerable advance in vascular surgery. However, accessibility to homograft material was limited and methods of sterilization and preservation inadequate. Observation of treated patients showed that tissue elements of the graft deteriorated, calcified, and often became aneurysmal. The need for more suitable arterial substitutes became increasingly apparent. In the meantime dos Santos observed that atheromatous occlusive disease in the femoral artery may be localized and accessible to thromboendarterectomy. The obstructive lesion could be peeled away inside the remaining wall of the artery by finding the appropriate plane of cleavage, thus restoring peripheral circulation in some patients without the need for graft replacement. An alternative approach was devised by Kunlin, who reasoned that it should be possible to support nature's collateralization of vascular obstruction by creating a vein bypass graft from above to below the lesion. The use of venous tissue for arterial reconstruction was extended by the technique of vein patch angioplasty. Although experiments with patch angioplasty had been performed as early as 1906, the procedure was thought to have limited clinical application. However, clinical experience with endarterectomy of small vessels such as the carotid, femoral, and popliteal arteries showed that luminal constriction resulting from longitudinal closure of a vascular wound could be avoided by repairing the defect with a vein patch.

Dubost's initial success with homograft replacement of the abdominal aorta was repeated by De Bakey and Cooley in 1953. This stimulated interest in replacement of descending thoracic aneurysms. The first patient to undergo this type of surgery was a 46-year-old man who had a large fusiform aneurysm of the lower descending thoracic aorta. This was replaced via a left thoracoabdominal approach, re-establishing aortic continuity with a homograft. Ten years later the patient returned with bronchogenic carcinoma of the left lung and underwent left pneumonectomy. The aortic graft was seen to be in good condition.

Apart from saccular aneurysms of the ascending aorta and aortic arch, where tangential excision with lateral aortography may be applied, ascending aortic surgery requires cardiopulmonary bypass. The first successful ascending aortic resection was performed in 1956 on a 50-year-old man. This was a remarkable achievement, considering that closure of an atrial septal defect on cardiopulmonary bypass had only been achieved the previous year. The aneurysm in this patient was extensive, originating just above the coronary ostia and involving the entire ascending aorta to the origin of the innominate artery. The distal occluding clamp was applied across the origin of this vessel into which a small perfusion cannula was inserted. The ascending aorta was replaced with an aortic homograft and the patient remained well until his death from lung cancer 14 years later. Homograft replacement of the aortic arch followed in 1957, using separate perfusion of the head vessels.

Initial successes provided substantial support for the growing conviction that excision and graft replacement was the optimum therapy for aneurysmal disease. This was the stimulus to explore technical resources to provide a synthetic vascular graft. One of the most significant developments in this regard was the observation that a fabric woven of Vinyon ‘N’ thread could function satisfactorily as an aortic substitute. Attention was then directed towards fabrics such as nylon, Orlon, Teflon, Ivalon, and Dacron, which were fashioned into tubes by sewing, braiding, heat sealing, knitting, and weaving. The Baylor group produced grafts from all these materials by sewing the edges of two sheets of fabric together and implanted them into laboratory animals: Dacron proved to be the best material.

In 1954 De Bakey implanted a Dacron aortic bifurcation graft made of two Y-shaped sheets of cloth with their edges machine-sewn together. The 54-year-old patient made an uneventful recovery and died from myocardial infarction 10 years later. A new knitting machine was designed to produce seamless Dacron tubes and bifurcation grafts. This work ultimately led to a highly satisfactory and effective arterial substitute for clinical use.

From a surgical standpoint, the aorta is divided into ascending, transverse, descending, thoracoabdominal, and abdominal parts (Fig. 1) 1831. The ascending aorta begins at the aortic valve and ends at the origin of the innominate artery. Immediately above the aortic valve are the three aortic sinuses, which correspond in position to the anteriorly situated right coronary cusp and the posteriorly situated left and non-coronary cusps (Fig. 2) 1832. From the left sinus arises the left main coronary artery and from the right sinus the right coronary artery. These arteries may have anomalous origins: for example, the right coronary may arise from the left coronary sinus taking an oblique passage through the wall of the aorta. There may be separate orifices for the left anterior descending and circumflex coronaries from the left coronary sinus. Similarly, it is not unusual for there to be a separate ostium for the conus branch of the right coronary artery. The left coronary artery, and very rarely the right or both coronary arteries may have anomalous origin from the pulmonary artery.

Integrity of the aortic sinuses is important for normal function of the aortic valve. Loss of the aortic sinuses may occur acutely in Type A aortic dissection or chronically in obliterative aortitis (e.g. Takyasu's disease), resulting in aortic reflux. For descriptive purposes in aortic surgery the left ventricular outflow tract, aortic valve, and aortic sinuses are known as the aortic root. Surgical techniques in this area depend on whether aneurysm formation involves the aortic sinuses and coronary ostia or begins above the aortic sinuses. In Marfan's syndrome (Fig. 3) 1833 both the aortic annulus and the sinuses have the propensity to dilate, and surgery of the ascending aorta in patients with this condition should always include root replacement. Congenital anomalies in this area include left or right aortoventricular tunnel, aortopulmonary window, and truncus arteriosus. The ascending aorta may bifurcate to give dual aortic arches and a vascular ring. The transverse thoracic aorta begins at the root of the innominate artery and ends just after the left subclavian artery. This part of the aorta gives rise to the great vessels of the head and upper limbs. The usual sequence for these vessels is the innominate artery, then the left common carotid artery, and last the left subclavian artery. The vessels rise sequentially as the transverse aorta passes from a central position behind the manubrium towards the left side of the vertebral column. The trachea and oesophagus are situated in the midline to the right of the transverse arch. The innominate artery passes anterior to the trachea before bifurcating into the right subclavian and right common carotid arteries at the thoracic inlet. Variations in origin of these vessels are unusual. The right subclavian and right common carotid arteries may rise separately from the transverse aorta. The right subclavian artery may rise distally from the arch and take a retro-oesophageal path to the thoracic inlet on the right. This anomaly can produce symptomatic oesophageal compression. Rarely, the descending thoracic aorta lies to the right side of the vertebral column in the thorax in association with intracardiac defects. Congenital anomalies of the great vessels may give rise to vascular rings which cause compression of the trachea and oesophagus. They are often symptomatic in infancy or childhood.

The descending thoracic aorta begins just distal to the left subclavian artery where the aorta reaches the fourth thoracic vertebra. Anteriorly is the ligamentum arteriosum, the fibrous remnant of the ductus arteriosus. The ductus arteriosus rarely persists into childhood or adult life. The left recurrent laryngeal nerve arises from the vagus nerve lateral to the aorta and passes around the ligamentum arteriosum or patent ductus to take a cranial course adjacent to the left side of the trachea and oesophagus. Damage to this structure during surgery of patent ductus arteriosus or the descending thoracic aorta may cause permanent left vocal cord paralysis. The descending part arbitrally meets the thoracoabdominal part at the lower end of the body of T10.

The descending thoracic aorta is fixed to the posterior wall of the chest by the segmental intercostal arteries; these in turn contribute to the vascular supply of the spinal cord (Fig. 4) 1834. Since the aorta meets the posterior chest wall at the level of T4, the upper intercostal vessels rise obliquely from the left and right sides of the aorta to reach their respective intercostal spaces. The junction of the transverse thoracic aorta with the fixed descending thoracic aorta has great strategic importance in traumatic injury. Deceleration road traffic injuries cause shearing forces at this site which cause the aorta to tear or rupture (Fig. 5) 1835. The descending thoracic aorta gives rise to the bronchial circulation and to multiple branches to the oesophagus. Certain pathological states may alter the size and nature of the intercostal and bronchial arteries. In patients with cyanotic congenital heart disease and impaired pulmonary blood flow the bronchial arteries enlarge to form aortopulmonary collateral vessels, which can reach the size of the native subclavian artery. In coarctation of the aorta (usually situated at the level of the ligamentum arteriosum just distal to the left subclavian artery) the intercostal circulation gives rise to multiple large collateral arteries in the chest wall which supply the distal aorta. In adult life these collaterals may become aneurysmal and may cause serious bleeding during thoracotomy.

The thoracoabdominal part of the descending aorta begins at the tenth intravertebral disc and is situated adjacent to the diaphragm both proximal and distal to its hiatus. The thoracic portion supplies intercostal and oesophageal branches. The abdominal portion supplies lumbar, diaphragmatic, and major visceral branches, including the coeliac axis, the superior mesenteric artery, and renal and adrenal vessels. The great radicular artery of Adamkiewicz arises from a left intercostal artery between T9 and L2 in 85 per cent of individuals. This vessel is usually visibly larger than corresponding branches. The number and importance of the branches of the thoracoabdominal aorta make its replacement complex.

The blood supply to the spinal cord has great importance in surgery of the descending thoracic and thoracoabdominal aorta. Though the causes of spinal cord injury are multifactorial, interruption of critical intercostal arteries plays an important part. One factor which clearly contributes to the varying incidence of neurological injury relates to the unpredictable anatomical variations of spinal cord blood flow. The majority of 62 radicular arteries present in the embryo ultimately regress: only two to five radicular arteries remain in the adult. The spinal cord has anterior and posterior spinal arteries running along its length. These vessels originate inside the skull as branches of the carotid circulation, but are fed by collateral arteries from the thoracic aorta. Seventy-five per cent of spinal cord blood supply is derived from the anterior spinal artery, which often becomes extremely narrow in calibre and distribution in the mid and lower portions of the spinal cord. This vessel is reinforced at various levels. In the neck the cervical radicular arteries arise as branches of the vertebral and subclavian arteries. In the chest the intercostals supply segmental branches, though the lower part of the spinal cord relies on the great radicular artery. This arises between T5 and 8 in 15 per cent of individuals, between T9 and 12 in 75 per cent, between L1 and L2 in 10 per cent and from L3 in 1 per cent. The vessel is large enough to be located by selective angiography when planning thoracic aortic surgery. Whenever possible it should be reimplanted into a vascular graft.

Inadequate blood flow through the lower segment of the anterior spinal artery or permanent interruption of the segmental blood supply to the dorsolumbosacral region by ligation of the critical intercostals, is likely to result in ischaemic injury to the cord. The dorsolumbosacral region extends from T8 to the conus terminalus of the spinal cord and generally derives its blood supply from the single radicular vessel of Adamkiewicz (arteria radicularis magna).

In a small proportion of individuals (approximately 15 per cent) the principal spinal radicular artery arises at a high level, between T5 and T8. This is generally associated with supplemental blood supply to the lower cord arising from additional vessels in the lower dorsolumbar region. In this case division or ligation of the intercostal arteries above T8 is unlikely to result in paraplegia; cord injury may only result from prolonged proximal aortic cross-clamping or interruption of the critical lower intercostal vessels. The critical importance of strategic intercostal arteries should not be underestimated, since their interruption results in a high incidence of paraplegia. High resistance is a characteristic of any blood supply based on small collateral vessels. Fluid pressure in the cerebrospinal canal represents a second barrier to blood flow: if this is higher than capillary perfusion pressure ischaemia can result despite patent and perfused anterior spinal collateral vessels. Distal blood pressure high enough to overcome these resistances is necessary to ensure spinal cord blood flow and maintain cord viability.

Coarctation of the aorta and patent ductus arteriosus are common anomalies which are amenable to surgical correction from the first few hours of life. Recently, innovative techniques such as balloon dilation of coarctation and percutaneous transvascular occlusion of patent ductus arteriosus have been developed, but as yet apply to small numbers of patients. Less common anomalies, such as ruptured aneurysm of the sinus of Valsalva, aortopulmonary window, and symptomatic vascular ring, usually warrant early surgical intervention. In adults most thoracic aortic surgery is undertaken for aneurysm repair. Congenital aneurysms do occur, though they are extremely rare. Conditions classified as congenital aortic aneurysms are more correctly identified as acquired dilations of the aorta due to a congenital structural abnormality in the vessel wall, or due to secondary deterioration of the aorta in association with other systemic disease processes. Post-stenotic dilation occurs in congenital aortic stenosis and coarctation of the aorta. Inherited disorders of connective tissue such as Marfan's syndrome, Ehlers-Danlos syndrome, or tuberous sclerosis may lead to aneurysm formation in childhood, though this occurs more commonly in early adult life. Rarely, bacterial invasion of the aortic wall, granulomatous inflammation, and trauma are responsible for aortic aneurysm in children. Disorders such as Takayasu's disease, syphilis, and cystic medial necrosis, which have been associated with the development of aortic aneurysms in adults, are rare causes in children.

Most acquired aneurysms (trauma excepted) present later in life. A true aneurysm always contains components of the aortic wall: aortic dissection is contained by the adventitia of the aorta and is therefore classified as a true aneurysm. A false aneurysm contains no component of the true aortic wall and occurs following penetrating injuries or traumatic transection, when haemorrhage is contained by overlying pleura and haematoma. Pathological processes which lead to thoracic aortic aneurysm formation are shown in Table 1 519. The most common of these are atherosclerosis, which affects predominantly those over the age of 60, and medial disorders, which usually require surgery at the age of 45 to 60. Clinically, medial disease is the more important, causing early cystic medial degeneration followed by aortoannular ectasia or acute aortic dissection.

The media of the aorta has four components, smooth muscle which provides tone, elastic fibres which determine the distensibility of the vessel, collagen fibres which give strength to the media, and a mucopolysaccharide connective tissue base. The collagen network, particularly types 1 and 3 collagen, are primarily responsible for the tensile strength of the aorta. When deficiencies exist in the construction of this collagen, as may occur in some varieties of Ehlers-Danlos syndrome and in some families with a history of familial aortic aneurysms, it is assumed that the genetic factor predisposes to an acquired dilation. Degeneration of the media occurs with age, predominantly affecting the elastic fibres and smooth muscle cells. Medial cystic necrosis occurs as part of the ageing process but may be accelerated in certain types of disease.

Special staining techniques allow medial degeneration to be graded. Severe degeneration (grades 3 and 4) is found in 21 per cent of patients with Type A acute aortic dissection, 10 per cent of patients with Type B dissection, and 43 per cent of patients with Marfan's syndrome, where the elastic component of the media suffers accelerated degeneration.

Marfan's syndrome is a hereditary disorder of the connective tissue producing well known ocular, skeletal, and cardiovascular manifestations (Fig. 3) 1833. Ninety-five per cent of patients with Marfan's syndrome have cardiovascular abnormalities, including fusiform aneurysm and dissection of the aorta, aneurysm of the aortic branches, and disease of aortic and mitral valves. The most common manifestations are dilation of the aortic root and mitral valve abnormalities. Aortic root dilation begins in utero, and invariably progresses. Cardiac events are rare before the age of 15, but aneurysm formation and dissection, rupture, cardiac tamponade, and sudden death occur with increasing frequency later in life as the aortic root diameter increases to 5 or 6 cm (Fig. 7) 1837,1838. Aortic valve insufficiency usually begins when the annulus becomes dilated to 6.0 cm. Dissection or rupture of the aorta tends to occur before cardiac failure from aortic insufficiency ( Fig. 8 1839; Table 3 521). The principal indication for operation is increase in the diameter of the aortic root to greater than 5 cm. Mitral valve prolapse ultimately occurs in 80 per cent of patients with Marfan's syndrome. The cardiovascular manifestations of Marfan's syndrome cause death in over one-third of patients by the age of 32, and in two-thirds by the age of 50.

Thoracic aortic aneurysms occur predominantly three times more often in men than in women. Important pathophysiological correlates in atherosclerotic aortic aneurysm formation are the ageing process, hypertension, smoking, hyperlipidaemia, and diabetes mellitus. The susceptibility of the aorta is variable: the thoracic aorta rarely develops obstructive atherosclerotic lesions, whereas the abdominal aorta commonly develops clinically significant stenotic and ulcerating plaques. A number of haemodynamic factors have been identified as important in the formation and localization of atherosclerotic plaques. These include wall shear stress, flow patterns and velocities, and flow disturbances. In the thoracic aorta and the suprarenal abdominal aorta, the flow directional vector is forward throughout the cardiac cycle. The infrarenal abdominal aorta, on the other hand, experiences directional oscillation of the shear stress vector during the cardiac cycle, with forward and reverse flow. This flow characteristic may predispose the abdominal aorta and lower extremity vessels to increased plaque deposition. Atherosclerotic plaques preferentially form in regions of low wall shear stress and not in regions of high wall shear stress. Low shear rates may retard the transport of atherogenic substances away from the arterial wall, resulting in an increased accumulation of lipids. The differing susceptibilities of the thoracic and abdominal aorta to atherosclerosis may also be due to differences in the architecture, composition, and nutrition of the arterial wall. The thoracic aorta is thicker and has a greater number of medial lamellar units than the abdominal aorta, reflecting its greater diameter and tangential wall tension. The thoracic aorta contains a larger proportion of elastin and a lower proportion of collagen than the abdominal aorta or peripheral vessels. This results in greater distensibility and pulse propagation in the thoracic segment. The outer two-thirds of the thoracic aortic media is well perfused by intramural vasa vasorum, whereas the inner lamellar units are nourished by diffusion from the lumen. In comparison, the abdominal aorta is nourished only from the lumen and lacks medial vasa vasorum. This may place the outer medial smooth muscle cells in a relatively ischaemic zone and may alter metabolic function. Thus the composition and microarchitecture of the aortic media and the metabolic state of the medial smooth muscle cells may be important factors in determining susceptibilities of different segments of the aorta to atherosclerosis. A number of haemodynamic factors act to inhibit plaque formation in the thoracic aorta, including high wall shear stress, short near wall particle diffusion time, and unidirectional, non-oscillating flow.

Observations on the natural history of thoracic aortic aneurysm have led to the abnormal proteolysis theory of aneurysm formation (Table 3) 521. Increased levels of the enzyme elastase have been demonstrated in the aortic wall of aneurysm patients and in the circulating leucocytes of smokers. The serum of smokers with abdominal aortic aneurysms contains decreased levels of natural protease inhibitors but unique elastolytic serum enzymes. This combination of factors leads to weakening of the medial component of the aortic wall and aneurysm formation.

Tobacco abuse is common among aortic aneurysm patients, but the presence of chronic obstructive pulmonary disease, irrespective of tobacco exposure, is the single best actuarial predictor of risk of rupture. Obviously the interplay of environmental factors needs to be studied against a background of defined genetic risk. It is likely that the risk of smoking in addition to an underlying deficiency of an antiprotease system may be particularly deleterious, for example, in individuals who smoke, and who have &agr;&sub1;-antitripsin deficiency and emphysema. That cigarette smoking has an effect on atherosclerosis is supported by results from a retrospective necropsy survey in which smoking histories were obtained from relatives of deceased patients to evaluate the strength of association between cigarette smoking and atherosclerosis in 1320 males aged between 25 and 64 years. Atherosclerosis in the aorta and coronary arteries was greatest in heavy smokers and least in non-smokers. Animal studies have shown that both acute and subacute exposure to cigarette smoke results in striking morphological changes in aortic endothelium. Smoking also promotes platelet adhesion to endothelium, together with higher levels of plasma fibrinogen, lower levels of plasminogen and plasminogen activator, and increased levels of factor VII. Diabetes, atherosclerosis, and hyperlipidaemia are also closely linked: arterial disease now accounts for more than 70 per cent of deaths from diabetes.

Aortic aneurysms are occasionally caused by other localized phenomena or systemic conditions. Aneurysms associated with bacterial infection occur sporadically. Certain varieties of infected aneurysm develop as a consequence of bacterial colonization of prosthetic grafts. The normal arterial wall is very resistant to bacterial infection, and bacterial colonization is rare unless structural disruption has occurred, either acutely through penetrating trauma or chronically in an atherosclerotic or aneurysmal area. The single exception to this rule is the predilection for infection of normal arterial wall of Salmonella species. Salmonella aortitis without aneurysm formation may lead to weakening of the aortic wall, and absence of aneurysm formation does not preclude rupture. Syphilitic aneurysms still occur sporadically (Fig. 9) 1840,1841. Spirochaetal infection of the vasa vasorum of the large arteries, especially in the thoracic aorta, leads to destruction of the aortic media and marked saccular dilation of the aorta. Such aneurysms erode into the mediastinal structures, bronchial tree, or even through the chest wall. The ascending aorta and arch are sites of predilection.

Fibromuscular dysplasia or the hormonal changes associated with pregnancy may lead to aneurysm formation in young and middle-aged women, though this usually occurs in visceral arteries. The standard inflammatory aortic aneurysm seen usually in the elderly occurs more frequently in the abdominal aorta than in the thoracic aorta. Takayasu's aortitis, though generally presenting with aortic occlusion, occasionally presents with thoracic aortic aneurysm (Fig. 10) 1842.

Surgery of the thoracic aorta relies heavily on accurate diagnosis. Recent developments in angiography, ultrasound, and magnetic resonance imaging (MRI) now allow thorough evaluation of the aorta with minimal invasion. Aortography has long been the standard against which other imaging techniques are compared. Advances in catheterization technique, together with a decrease in contrast toxicity, have lowered the risks of angiography. Digital subtraction angiography, particularly using intra-arterial injection, provides increased contrast sensitivity with excellent resolution. This method uses fluoroscopy to collect intensified images which are converted to a digital form, stored in a computer, and processed to extract extraneous detail and amplify contrast.

Angiography delineates luminal anatomy but will not demonstrate the aortic wall and periaortic tissues. Aortic and branch vessel lumen size and contour are shown best. Aortography is used to define occlusive lesions and luminal defects but will not clearly delineate aneurysms associated with occlusive disease. Accurate delineations of the dimensions of an aneurysm may be obscured by intraluminal thrombosis. Complicated aortic aneurysms, particularly contained ruptures and inflammatory aneurysms, are notoriously difficult to define by aortography. Dissecting aortic aneurysms are identified by narrowing or distortion of the contrast column or by the presence of an intimal flap between a double lumen. In many patients with disease of the thoracic aorta coronary angiograms are desirable to determine the extent of coronary occlusive disease.

Aortography is an invasive technique and therefore has complications. Digital subtraction angiography does offer some advantages over conventional aortography: less contrast is necessary to visualize vessels, thereby reducing risk in renal failure patients requiring aortic evaluation. In practice complications occur in fewer than 4 per cent of patients. Catheter-related complications include haemorrhage, thrombosis, pseudoaneurysm, and arteriovenous fistula formation.

Ultrasound imaging is derived from echo-ranging devices which are capable of measuring the distance to an object from the time required by an emitted pulse of sound to be reflected back to the source. In the chest, ultrasonography is used to assess the ascending aorta and aortic valve. Ultrasound can quickly differentiate aortic aneurysm from aortic tortuosity or mediastinal lymphadenopathy. Dissecting aneurysms with extramural haematoma or pericardial fluid are well visualized by two-dimensional echocardiography, and ultrasound imaging has not been shown to cause any deleterious effects. Transoesophageal echocardiography is now the investigation of choice for suspected aortic dissection.

The introduction of computerized tomography revolutionized thoracic vascular imaging. The CT scan uses a computer to process circumferentially acquired radiographic data in order to create a cross-sectional image. The image obtained actually represents a tissue slice of selected thickness between 2 mm and 1.0 cm: the thinner the slice the better the spatial resolution. Infusion of contrast can be used to depict vascular images and sequential analysis of CT sections can provide a three-dimensional study of the aorta. The CT scan is capable of delineating accurately images of the thoracic aorta, mediastinum, and pleural and peritoneal cavities. With contrast infusion the aortic lumen can be differentiated from wall thrombus, calcification, and aneurysm formation (Fig. 11(a–c)) 1843,1844,1845. Contained aneurysm rupture is identified by loss of periaortic soft tissue planes. Dissecting aortic aneurysms are easily identified when the true and false lumens are both patent (Fig. 12) 1846. If the false lumen is already occluded by thrombosis it may be impossible to differentiate a dissection from a thrombosis-lined aneurysm. Postoperative graft complications such as pseudoaneurysms, infection, and graft–enteric fistula formation can be well defined by this technique. There are few complications of CT scanning. The level of radiation exposure is less than that for a barium enema, and contrast-related problems may be decreased by the use of a non-ionic type of contrast medium.

MRI is a non-invasive technique that uses a radiofrequency pulse directed at a substance within a large magnetic field, inducing a transition between energy states of certain atoms. The time required for localized nuclei to return to the baseline energy state, called the relaxation time, is measured and translated by computer into an image. Various radiofrequency pulse sequences are used in combination with gradient magnetic fields to create an optimal image. MRI does not require ionizing radiation or contrast infusion to visualize vasculature in multiple planes. Spatial resolution is similar to that obtained with CT scanning, but the MRI offers better soft tissue resolution and is not limited by air, bone, excess fat, or operator skill. The aortic lumen and wall branch vessels and adjacent structures are all well defined by MRI. Aortic congenital abnormalities, thoracic aneurysms, and aortic dissection are well visualized in multiple planes (Fig. 13) 1847. Congenital anomalies such as double aortic arch, coarctation of the aorta, and anomalous vessel origin can be clearly defined. Use of oblique sections may delineate vascular anatomy even better than aortography by providing images along the long axis of the vessel (Fig. 14) 1848. Resolution is such that a contained rupture can be differentiated from inflammatory fibrosis around an aneurysm (Fig. 15) 1849. Graft complications such as haematoma, pseudoaneurysm, or infection are reliably defined, though the patency of small grafts and aortoenteric fistula are not.

MRI studies are contraindicated in unco-operative, haemodynamically unstable, or claustrophobic patients, and in those dependent on devices with ferromagnetic properties such as pacemakers, cerebral aneurysm clips, and ventilators. A relatively long scan time is required within the strong magnetic field.

Surgical procedures on the thoracic aorta require cross-clamping of the vessel with interruption of distal flow. With the exception of saccular aneurysm, where a side clamp can be applied and distal flow maintained, the success of thoracic aortic surgery depends on preservation of function in dependent organs. The methods adopted depend on the site of cross-clamping and associated risks. The abdominal viscera, including the liver and kidneys, may tolerate 30 min of normothermic interruption of blood supply, but the brain will tolerate little more than 4 min of unprotected circulatory arrest. In addition, aortic cross-clamping performed with the heart supporting the circulation causes hypertension proximal to the clamp, increased stroke work, and subendocardial myocardial ischaemia, particularly in patients with coronary occlusive disease. For coronary patients with impaired left ventricular function unprotected aortic cross-clamping even of the abdominal segment may have serious adverse consequences. Perfusion techniques vary widely according to the site of the aortic operation. Surgery of the aortic root and ascending aorta requires whole body perfusion with moderate or profound hypothermia while the heart and lungs are out of circuit. Full cardiopulmonary bypass with a pump oxygenator and cardiotomy suction apparatus are required. To ensure continuous cerebral perfusion during resection and graft replacement of the ascending aorta most patients require placement of the distal occluding clamp just proximal to the origin of the innominate artery. Often, however, the pathological process extends into the arch or beyond, and may involve the origin of the innominate, left carotid, and left subclavian arteries. With an aortic cross-clamp in place it is impossible to ensure perfusion to arch vessels and clamping may promote aortic rupture in aortic dissection or cerebral embolization from atherosclerotic debris. Cooley suggested the use of circulatory arrest in these patients in order to perform the distal anastomosis by an open technique (Fig. 16) 1850. Arterial return from the pump oxygenator is via a common femoral artery. Siting for the venous outflow cannula depends on the anatomical findings, but is usually in the right atrium. The systemic temperature is reduced by cardiopulmonary bypass and heat exchange to 20°C. During this interval the arch vessels are mobilized and, at an appropriate time, the vessels are cross-clamped. The arterial return pump is discontinued and the venous outflow occluded. The aorta can then be opened widely and the pathological condition of the interior of the transverse arch and origin of the arch vessels appraised. In patients with aortic dissection the relationship of the true and dissected false lumen must be established. The anastomosis with the aorta wide open and bloodless facilitates proper management of the aortic arch by resection and accurate anastomosis of the graft to the underside of the aorta. At the end of the procedure arterial return is re-established to fill the aorta gradually and eliminate entrapped air from the roots of the head vessels. This open-ended technique has greatly facilitated extended resection of the ascending aorta. Meanwhile, cold potassium cardioplegic myocardial arrest together with profound systemic hypothermia protects the heart, the brain, and the abdominal viscera.

Whereas surgery of the ascending aorta and aortic arch requires hypothermic bypass in order to provide a bloodless field and protect the brain and myocardium, most operations on the descending aorta can be performed by simple cross-clamping. Shunt bypass and hypothermic cardiopulmonary bypass techniques were introduced to provide perfusion to the abdominal viscera during normothermic cross-clamping and to off-load the myocardium against an acute increase in afterload. It was hoped that the spinal cord might be protected by perfusion of the distal thoracic aorta and, consequently, the principal spinal radicular vessels between T10 and L2. Table 4 522 summarizes the passive shunt, pump bypass, and hypothermic cardiopulmonary bypass techniques employed in descending aortic surgery. None can convincingly be said to protect the spinal cord if the spinal vascular anatomy is unfavourable. Hypothermic cardiopulmonary bypass methods, discussed later, require heparinization and can be used with or without total circulatory arrest. Of the passive shunt bypass methods the ascending aorta to distal aorta is preferable and can be performed with a heparin-bonded shunt, making systemic heparinization unnecessary. Shunts between the aortic arch and iliac artery, left subclavian and the distal aorta, and left ventricle to distal aorta are less reliable with unpredictable flow. For pump bypass methods a roller or centrifugal pump may be employed. Centrifugal pumps can be used without heparin, in particular for aorto-aortic bypass. Left atriofemoral bypass can be performed with either a centrifugal or a roller pump: the former does not require systemic heparinization. When a roller pump is used heparin and a blood reservoir are necessary. Various methods of venoarterial pump bypass have been employed, including from the superior vena cava to the femoral artery and from the right atrium and femoral vein to the femoral artery. Both of these methods have been used with or without an oxygenator, reservoir, and systemic heparinization. For straightforward operations such as repair of coarctation in an adult or repair of traumatic aortic laceration we use simple normothermic aortic cross-clamping without bypass techniques. This type of repair can almost always be achieved in less than 30 min, the arbitrary period for alleged safe cross-clamping. ‘Safe’ applies more to the medicolegal aspects than to the spinal cord. For complicated excision and replacement of extensive descending thoracic and thoracoabdominal aneurysms and in certain patients with Type B dissection we employ our own hypothermic cardiopulmonary bypass technique as described later.

Bleeding problems remain an important cause of morbidity and mortality in thoracic aortic surgery, particularly for aortic dissection. Operative methods have long been influenced by the relatively porous nature of proprietary vascular prostheses. Indeed the classical wraparound techniques for aortic root replacement as described by Bentall and De Bono with modifications by Cabrol, were designed specifically to cope with oozing through porous grafts. Most commonly used grafts are made from either Dacron or Teflon (polytetrafluoroethylene, PTFE). Teflon is a smooth, non-adherent, non-wettable surface that may inhibit the sticking of platelets and fibrinous material to the surface. This allows the use of smaller diameter grafts for peripheral vessels or for modified Blalock shunts in infants (Gore-Tex or Impra). Teflon is non-porous to blood, and bleeding through the graft itself does not occur. However, Teflon grafts are relatively non-compliant and kink easily: external ribbing has been applied to help prevent this problem. Bleeding occurs through suture holes and gaps between sutures, and these grafts are not normally used in patients requiring systemic heparinization.

Dacron grafts are available as knitted and woven varieties (Fig. 17) 1851. Knitted grafts are of high porosity and are easier to sew, but leak when the vascular clamps are removed until clot forms in the graft interstices. Woven grafts are of low porosity and are more difficult to sew but bleeding through the graft is minimized or eliminated. As a general rule, the lower the porosity of a graft the greater the stiffness and poorer the handling characteristics. Knitted grafts are designed for abdominal and peripheral vascular reconstruction in non-heparinized patients. In general they are easily sewn to pathological vessels because of their soft compliant nature. Their deformability allows a snug fit and minimizes bleeding at the anastomotic site. Ease of suture passage is particularly helpful when the native vessel wall is heavily calcified, resulting in needle blunting or deflection from the intended suture path. However, when the aortic clamps are removed bleeding through the graft interstices can sometimes be considerable. Knitted grafts are therefore contraindicated in heparinized patients due to the risk of uncontrollable haemorrhage. The standard knitted graft has been modified by the incorporation of a velour inner and outer pile to enhance the incorporation of clots in the graft interstices (Meadox double velour graft). Knitted grafts less than 5 mm in diameter should not be used because of the high rate of thrombosis.

It was originally thought that high porosity knitted grafts were necessary to allow endothelial cells and their subendothelial matrix to invade and adhere to the inner surface of the vascular prosthesis, reducing thromboembolism and maintaining patency. However, although prosthetic grafts may develop a neoendothelium in canine and non-human primate models, re-endothelialization occurs only sporadically or not at all in man. For practical purposes, re-endothelialization is, therefore, not a consideration when implanting prosthetic grafts in patients.

The tight weave of woven grafts was designed specifically for use in patients undergoing thoracic aortic replacement with systemic heparinization. These grafts are stiffer, and eventually blunt fine needles during suture passage. Graft stiffness is not usually a problem when anastomosing to the margins of thickened aorta after resection of fusiform or saccular aneurysms, where the tissues are thick, fibrous, and hold sutures. When the aorta is thin or dissected, or in paediatric patients, attempts to sew a stiff non-compliant graft may be fraught with further tearing, sometimes to the point of suture line avulsion.

There have been recent improvements in woven Dacron grafts. The Meadox low porosity Veri-Soft graft is made of Dacron yarn that is soft enough to allow good flexibility but has a tight enough weave to prevent significant haemorrhage through the interstices. However, preclotting is advisable, even for low porosity grafts, and this further impairs handling characteristics. The object of preclotting is to seal the interstices of the woven or knitted material so that bleeding does not occur when the clamps are removed. The patient's own non-heparinized fresh blood is most effective for this purpose, but this does not apply when cardiopulmonary bypass is already established. Since it is impossible to size the native aorta accurately until the patient is systemically heparinized with the vessel open, complicated and tedious graft preparation is necessary. We have used coating with autologous or heterologous plasma followed by microwave coagulation. This certainly seals the graft, but it also impairs handling characteristics and suture passage. Fresh donor blood of the same group from a volunteer in the operating theatre is feasible but we abandoned this method when a patient contracted postoperative hepatitis for a completely different reason. Bleeding through the suture holes in Gore-Tex grafts can be limited by using small diameter needles and Gore-Tex suture material that expands when wet.

Experimental work has demonstrated no difference in the long-term patency of woven versus Dacron grafts. An aortic bifurcation graft in which one limb was knitted and the other woven was implanted into 143 consecutive patients with atherosclerotic aortoiliac occlusion or abdominal aortic aneurysm. There was no difference in patency at periods of 1 month to 2 years.

For aortic root replacement, proprietary composite grafts of a Carbomedics, Medtronic, or St Jude valve sewn into a woven Dacron graft are available (Fig. 18) 1852. In this case the valve annulus size determines selection of the prosthesis: this can only be judged accurately with the patient heparinized and the aorta open. Preclotting with fresh frozen plasma followed by autoclaving is therefore required and wastes time. Porcine valved conduits are commonly used for right ventricular outflow reconstruction in children. Unfortunately the incidence of porcine valve degradation is extremely high, making aortic homograft material far superior (Fig. 19) 1853. Aortic root homografts are particularly useful when enlargement is required or for the treatment of infective conditions such as prosthetic valve endocarditis with root abscesses. They are less applicable in very large aortic roots because of size mismatch. A non-suturable ring of Dacron felt can be incorporated into the suture line to avoid homograft dilation in patients with Marfan's syndrome. Recently, the availability of the completely impervious collagen impregnated woven Dacron prosthesis (Hemashield, Meadox) has eliminated the need for preclotting and provided a graft with excellent handling and suturing characteristics. Hemashield is low porosity woven Dacron which is impregnated with type 1 collagen derived from fresh young calf skin. The collagen for Hemashield is prepared from calf skin by a sequence of steps including mechanical cleansing, washing, and chemical treatment. The processed skin is then homogenized to produce a paste composed of 90 per cent collagen microfibres. This is used to coat a woven double velour Dacron polyester graft. Electron microscopy shows that the collagen layer completely covers the fibres and interstices of the fabric. The graft is biocompatible in terms of pyrogenicity, cytotoxicity, and antigenicity. It is soft and pliable, with excellent handling characteristics. The collagen is absorbable and rendered non-antigenic by cross-linking on the graft surface. The resulting vascular prosthesis is therefore blood compatible and does not induce platelet aggregation or intravascular clotting. Less than 10 per cent of the bovine collagen remains on the graft after 30 days and less than 2 per cent of the graft surface remains covered with collagen after 90 days.

Successful surgery of the thoracic aorta depends on the ability to prevent both surgical and abnormal bleeding. The tenuous nature of diseased or dissected arterial wall presents a major operative risk. Medial necrosis, collagen cross-linking deficiencies, or atheroma are present in most abnormal aortic tissues, lowering the tensile strength and suture holding capacity. This, together with high wall tension, weak adventitia, and absence of reinforcing pleura in the ascending thoracic aorta increases the likelihood of suture line tearing and haemorrhage that may be difficult to control by standard methods. Surgical bleeding prolongs cardiopulmonary bypass, which in turn leads to coagulation problems and the potential for multisystem organ failure. Operative techniques have therefore been designed specifically to combat bleeding. These include wraparound techniques, including the fistula method of Cabrol, and insertion of a graft with rigid ends inside the pathological aorta and fixing this with external ties to avoid an aortic suture line. Although the introduction of completely impervious vascular grafts has greatly reduced operative haemorrhage and transfused blood requirements, bleeding through suture holes in the native pathological aorta can cause problems. The use of thrombogenic materials such as oxidized cellulose and gelatin sponges are rarely effective in this situation. We routinely use Teflon strips to buttress dissected aorta, though this does not entirely eliminate the bleeding. In patients with dissection, poor tissues, or detachment of the adventitia we use Teflon O rings for reimplantation of the coronaries in aortic root replacement. Hammond described tanning of dissected aorta with glutaraldehyde prior to anastomosis. The dilute glutaraldehyde solution is carefully applied to the native aorta on cotton wool balls which are kept in apposition to the tissue for 4 to 5 min. This greatly strengthens the weakened tissues and promotes their suture holding ability. Care must be taken not to allow glutaraldehyde to drip within the aortic lumen or contaminate adjacent tissue.

For the past 5 years we have used acrylic blue glue (Braun) to seal suture lines in patients with aortic dissection. Cyanoacrylate adhesives were first used as topical haemostats during the late 1960s, but were not adopted widely because of their lack of adhesion to moist surfaces and the potential histotoxic side-effects. Undoubtedly the profound exothermic reaction that occurs when large amounts of glue are applied has the potential to cause damage, but in practice we have not experienced any adverse reaction. When the glue is applied prophylactically before blood is admitted into the repair site there is little danger of adverse effects (Fig. 20) 1854. The glue is supplied in a plastic vial with a long narrow sealed vent. When the tip is removed it can be applied accurately to the native aorta and sets rapidly. If glue fails to stop bleeding from an uncontrolled tear in the native aorta wall, it can be peeled away from the surface to allow secondary suture placement. Acrylic glue can be used to occlude the path of blood loss from inaccessible areas and tamponade the bleeding area.

Bachet advocates the use of gelatin resorcin formol glue for patients with acute dissection. Carpentier's group have successfully used this agent to stick the dissected layers together, avoiding resection of the aorta with its attendant risks of bleeding. We have found this glue to be excellent for reconstitution of the dissected aortic wall in conventional repair of acute type A or B dissection.

Fibrin sealant is an alternative haemostatic agent which consists of completely biodegradable components. The underlying principle is local imitation of the last stages of the physiological coagulation process by the use of highly concentrated human fibrinogen and bovine thrombin. All components of fibrin sealant are completely biodegradable within 6 weeks and cause no foreign body reaction. Fibrin sealant requires about 20 min of preparation and is applied through a needle for accurate placement. We and others have found this agent to be particularly useful in children when Dacron grafts are anastomosed to myocardium, and for bleeding surfaces at reoperation. Topical infusion of human cryoprecipitate is particularly useful for stopping diffuse oozing in patients with acute aortic dissection, disseminated intravascular coagulation, or undergoing reoperation with diffuse bleeding. The concentrated solution is poured into the pericardium over raw surfaces. The cryoprecipitate assumes a gelatinous form and deposits fibrin strands over the surfaces. On several occasions, this method has allowed us to close patients with diffuse abnormal bleeding. Usually we combine topical and intravenous application, together with administration of fresh frozen plasma and platelets. The risks are those associated with the use of a multidonor plasma pool, but in Britain transmission of hepatitis or AIDS is extremely rare.

Bleeding from a cut blood vessel ceases because of a combination of vasoconstriction and the formation of a platelet plug, followed by the development of a fibrin network. In the abnormal thoracic aorta vasoconstriction does not occur, and adhesion of platelets to puncture sites and small tears is the first and crucial step in the haemostatic process. Plug formation occurs only when platelets have first been deposited on the subendothelium. Platelets possess receptors for various adhesive proteins present on the blood vessel wall or in the plasma. The high shear forces associated with cardiopulmonary bypass mean that binding of the platelets to endothelium is through the receptor glycoprotein 1b, which binds to Von Willebrand factor. This in turn binds to the exposed subendothelium. Platelets are activated as they aggregate together by expression of glycoproteins IIb and IIIa, which link platelets together through fibrinogen molecules. During cardiopulmonary bypass heparin is used to bind antithrombin III, preventing propagation of the clotting cascade. However, the fibrinolytic system and platelets are activated by exposure to the foreign materials of the perfusion circuit. Harker showed that the bleeding problems associated with cardiopulmonary bypass were commonly related to a defect in platelet function and that the degree of functional impairment was proportional to the duration of cardiopulmonary bypass and level of hypothermia. There is also evidence that fibrinolytic activity may be responsible for excessive bleeding. Increased fibrinolytic activity is primarily the result of an increase in tissue plasminogen activator initiated before cardiopulmonary bypass. This reaches a maximum 1 h after the start of perfusion. Fibrinolytic activity is also caused to a lesser extent by the production of free plasmin at the beginning of cardiopulmonary bypass induced by activation of factor XIIa, probably by the first cycle through the bypass equipment. The mechanisms underlying an increase in tissue plasminogen activator release during surgery are not clearly defined but include venous occlusion, hypoxia, thrombin, and adrenaline. A hyperadrenergic state induced by surgical stimulation may prove responsible for the initial increase in tissue plasminogen activator before bypass.

In 1984 Westaby et al. suggested the use of aprotinin, a non-specific protease inhibitor, to inhibit elastase release following complement and white cell activation in the extracorporal circuit. As early as 1964 Trasylol had been shown to reduce fibrinolytic activity during cardiovascular operations, but this aspect had been essentially forgotten. During the clinical trial of aprotinin in coronary bypass patients bleeding was seen to be considerably reduced and the operative field appeared abnormally dry after reversal of heparin by protamine. Further trials confirmed substantial reductions in perioperative blood loss following aprotinin infusion. In low concentrations aprotinin is a powerful inhibitor of plasmin; in high doses it also inhibits kallikrein, which is formed during activation of coagulation by negatively charged surfaces such as those in cardiopulmonary bypass equipment and exposed subendothelial layers. Kallikrein has a central role in the activation of the inflammatory response, complement, the angiotensin system, fibrinolysis, and coagulation. Consequently if kallikrein is inhibited there is a decreased inflammatory response and less tendency to activate coagulation and fibrinolysis.

During cardiopulmonary bypass aprotinin directly inhibits kallikrein production, and probably release of tissue plasminogen activator, as shown during liver transplantation. Aprotinin preserves platelet function through its antifibrinolytic effect. Free plasmin removes the Von Willebrand receptor glycoprotein Ib from the platelet membrane; thus there is inhibition of platelet adhesion to subendothelial structures and a platelet plug is formed. This occurs during cardiopulmonary bypass and has been shown to be inhibited by aprotinin. In addition, aprotinin inhibits the coagulation pathway and prolongs the activated clotting time. When heparin therapy is monitored by activated coagulation during cardiopulmonary bypass the activated clotting timer should run at a higher level than normal to ensure that adequate levels of heparin are used.

We have been cautious in the clinical use of aprotinin, since it is a prothrombotic agent: early in its use we suspected that it may promote coronary graft occlusion. We therefore restrict its use to patients undergoing surgery for acute aortic dissection or ruptured thoracic aneurysms who present with substantial blood loss and require transfusion of large volumes of blood. In profoundly hypothermic circulatory arrest states aprotinin may promote bleeding by inhibiting the protein C and tissue plasminogen activator systems which maintain the fluid status of static blood. Platelet microaggregates may form and produce a disseminated intravascular coagulation effect.

Other agents have been used to reduce perioperative bleeding. Desmopressin increases the plasma concentrations and activity of Von Willebrand factor, probably by inducing release of this agent from the endothelium. Clinical trials of this agent during cardiopulmonary bypass have demonstrated shortened bleeding time postoperatively and reduced blood loss. Plasminogen and plasmin combine to fibrin through their lysine binding sites. This binding can be reduced by the lysine analogues, &egr;-aminocaproic acid and tranexamic acid, thereby delaying fibrinolysis. However, these agents are rarely used clinically and have not yet been shown to produce significant benefit in the treatment of established and excessive postoperative bleeding. Dipyridamole limits platelet aggregation and granular release by inhibiting platelet phosphodiesterase activity. This agent is used to preserve vein graft patency, but in one study of perioperative bleeding during cardiac surgery patients receiving dipyridamole had higher platelet counts at the end of operation and less blood loss than controls.

Since bleeding remains a particularly important complication in thoracic aortic surgery, particularly for acute aortic dissection, pharmacological methods for inhibition of abnormal bleeding play an important role. Aprotinin currently appears to be the most promising agent to reduce bleeding.

Acute aortic dissection occurs when an intimal tear allows blood to enter the media. A combination of factors, including hypertension and cystic medial degeneration, allow the tear to propagate longitudinally through the aortic wall (Fig. 22) 1856. Tears occur at the site of maximum stress on the aortic wall: 66 per cent occur in the anterior aortic wall above the aortic valve (Fig. 23) 1857, and 33 per cent occur on the posterior wall of the proximal descending thoracic aorta. The classification of acute aortic dissection is shown in Fig. 24 1858. Hypertension is an important aetiological factor: dilated aortas tend to dissect more readily. Flexion of the ascending aorta and stress at the site of tethering of the descending aorta to the posterior thoracic wall may account for the site of intimal tear, which often occurs through an atherosclerotic plaque. Rigid or calcified atherosclerotic plaques alter the distensibility of the aorta. &bgr;-Blockers prescribed for patients with hypertension can increase the risk of aortic dissection by increasing systemic vascular resistance. Vasodilators reduce this effect.

Ninety per cent of patients with acute aortic dissection present with sudden excruciating chest pain which migrates anteroposteriorly. There are no prodromal symptoms and the pain is distinctly different in character and mode of onset to that of acute myocardial infarction. The patient with aortic dissection can usually recall precisely his activities at the time of onset, unless stroke is the presenting feature. Seventy-five per cent of patients have systemic hypertension on admission to hospital and 25 per cent have acute aortic regurgitation with an audible murmur (Fig. 25) 1859. Ten per cent suffer an associated acute myocardial infarction, usually from occlusion of the right coronary artery by retrograde dissection down to the aortic annulus. The classical absent limb pulse or stroke occurs in relatively few patients (Fig. 26) 1860. Rupture of the aorta with sudden death from haemorrhage or cardiac tamponade occurs frequently. At presentation the chest radiograph shows mediastinal widening in at least 65 per cent of patients, often with a left pleural effusion (Fig. 27) 1861.

These clinical features are emphasized for two important reasons. First, the outlook for patients with aortic dissection worsens with time because of the development of critical events such as stroke, renal failure, ischaemic bowel, and cardiac tamponade. Surgery provides good long-term results in patients operated upon before irreversible injury to vital organs has occurred. However, initial diagnostic error is a major problem: up to 50 per cent of patients are referred more than 36 h after the original event, often with established bowel infarction or renal failure. In our experience of 54 patients in 4.5 years, operation within 24 h of acute dissection using modern techniques carries a very low in-hospital mortality risk. Hospital deaths occurred in patients who presented late with established pulmonary and renal failure, ischaemic gut, or coagulopathy. The second reason for emphasizing diagnostic accuracy is that a number of patients are mistakenly treated with streptokinase for suspected acute myocardial infarction. This perpetuates the tear by preventing clotting in the false lumen and creates difficulties during early operation through gross derangement of clotting and platelet function. We have operated on patients with acute dissection within 24 h of streptokinase administration by giving considerable amounts of fresh frozen plasma, platelets, and cryoprecipitate. CT of the thorax has been acclaimed as the diagnostic method of choice in aortic dissection but is not always immediately available. CT scan may not demonstrate details of the aortic root and valve, or left ventricular function; it may even fail to demonstrate the dissection. Magnetic resonance imaging is even less likely to be immediately available, but when it is patient monitoring is more difficult than for CT. Modern echocardiography may show the dissection flap in the ascending aorta, the anatomy of the aortic valve, and the presence of aortic regurgitation, as well as left ventricular function and regional wall motion abnormalities. The use of the transoesophageal window raises the sensitivity and specificity to nearly 100 per cent. This technique is already available with colour-flow Doppler and biplane transducers, and satisfactory imaging is guaranteed and obtained very quickly.

Coronary angiography is desirable for patients with a history of ischaemic heart disease or previous coronary grafts, but this should not delay rapid transfer to the operating theatre. In patients with previous coronary bypass grafts the problem is addressed by excising the top ends in a single aortic button and reimplanting this into the new ascending aortic graft.

Careful medical management is imperative both pre- and postoperatively (Table 5) 523. The aim of systemic pressure control is to reduce the mean blood pressure and dp/dt. Sodium nitroprusside alone does not reduce dp/dt. Arfonad effectively reduces wall tension and is probably superior to most other drugs. Early presentation with stroke does not contraindicate surgery, as long as the patient is not clinically brain dead. Cerebral deficits usually resolve after prompt repair which reopens the arch vessels and reperfuses ischaemic brain. All patients with Type A dissection should be submitted for surgical repair as soon as possible (Table 6) 524. Currently, medical management is advocated for the majority of patients with Type B dissection, though improvements in surgical technique, including hypothermic spinal cord protection, make this more controversial. Certainly patients with leak into the left pleural cavity or persistent pain over 2 to 3 days should be considered for operation. Surgery is the only option when dissection occludes vessels to the kidneys and gut.

Patients with cardiac tamponade often deteriorate in the anaesthetic room, and urgent intervention is required. We routinely cannulate the femoral artery for arterial return and have the cannula in place before the pericardium is opened. Relief of tamponade often results in a blood pressure surge which may precipitate rupture of the false lumen. With established arterial return bypass can be commenced using suckers while a two-stage cannula is quickly inserted into the right atrial appendage.

It is important to check the efficacy of perfusion soon after commencing bypass. The temperature of the head should be assessed: in a small proportion of patients femoral arterial perfusion will not reach the head. It is therefore useful to have a second arterial line which can be inserted through the apex of the left ventricle, thereby perfusing the head through the true lumen via the aortic valve (Fig. 28) 1862. We routinely use a cerebral protection cocktail consisting of the calcium channel blocker nimodipine, the barbiturate thiopentone, and the free radical scavenger mannitol. In one of our patients where the aortic cross-clamp had already been applied and cardioplegia administered the anaesthetist reported failure to cool the head after 10 min of cardiopulmonary bypass. The lower body temperature had already fallen to 27°C. For this patient the cannula was urgently switched to the aortic arch, which restored cerebral perfusion after 15 min. The patient made a full neurological recovery and returned to his occupation as an accountant. We consider that pharmacological cerebral protection contributed to his recovery.

It is important to establish the extent of surgery required at an early stage. Aortic valve replacement is rarely required: the great majority are repairable by resuspension, even in patients with non-stenotic bicuspid valves. Patients with Marfan's syndrome should always undergo aortic root replacement since their aortic sinuses will eventually expand with aortic regurgitation or rupture if left (Table 7) 525. We frequently use total circulatory arrest with open hemiarch repair. However, in a small proportion of patients the tear can be completely excised with an aortic cross-clamp in place. In these patients it is possible to perform ascending aortic replacement quickly at temperatures between 27 and 32°C, thereby avoiding the coagulation problems associated with profound hypothermia. Even with impervious vascular grafts we consider this to be an advantage.

If the tear cannot be found in the ascending aorta we employ total circulatory arrest at 18°C and aim to excise the tear. This sometimes requires replacement of the underside of the arch. The potential for cross-clamp damage is addressed by excising the site of cross-clamp application. On several occasions we have employed Hammond's technique of glutaraldehyde tanning of dissected tissue. We buttress the suture lines with Teflon and use the Hemashield graft. A thin layer of Histoacryl glue seals the repair. Using these methods our hospital mortality rate for Type A dissection in 54 patients in 5 years has been 9 per cent, with no deaths from haemorrhage.

The Carpentier group now advocate dissection repair without graft replacement. They have reported a series of carefully selected patients where the intimal tear was directly sutured with the extensive use of gelatin resorcin formaldehyde glue to close the false lumen. There were no hospital deaths in 15 patients. We now use GRF glue routinely but always in combination with ascending aortic replacement.

We have recently performed nuclear magnetic resonance imaging on patients who had previously undergone ascending aortic replacement for Type A dissection. More than 50 per cent of the patients had a persistently patent false lumen with blood flow. In two patients aneurysm formation within the affected aorta required aortic root and aortic arch replacement, respectively.

Reluctance to operate on patients with Type B dissection stems not from the surgical difficulties of graft insertion but from a comparatively high incidence of major complications, including paraplegia and acute renal tubular necrosis. The natural history of Type B dissection is for the descending aorta to become progressively enlarged and aneurysmal, with the risk of rupture and sudden death (Fig. 29) 1863. Despite this the Mayo clinics report satisfactory long-term results for conservative treatment. Indications for surgery in Type B dissection include compromise of a major aortic branch, formation of an acute saccular type aneurysm, haemorrhage into the pleural cavity, inability to relieve or control pain within 4 h, and progressive increase in size of the dissecting haematoma on serial chest radiographs or CT scan.

Cross-clamping of the descending thoracic aorta cuts off segmental spinal collateral vessels from the intercostal arteries. Occlusion of the left subclavian artery causes a steal phenomenon and further reduces spinal cord blood supply. When the descending thoracic aorta is open, intercostal steal takes blood away from the spinal cord arteries particularly in the face of increased cerebrospinal fluid pressure (Fig. 30) 1864. Hypertension proximal to the aortic cross-clamp decreases the perfusion gradient, but the use of sodium nitroprusside to reduce hypertension causes an adverse rise in cerebrospinal fluid pressure from less than 10 mmHg to 20 mmHg, possibly by vasodilation in the intrathecal space. Nitroprusside also reduces the distal aortic pressure and may paralyse distal autonomic function. The combination of a reduced distal aortic pressure and increased intrathecal pressure decreases spinal cord perfusion pressure. Nitroprusside should therefore not be used to reduce afterload during aortic cross-clamping.

In experimental studies, spinal fluid drainage prevents the increase of spinal fluid pressure during cross-clamping, and steroids appear to increase the protective effect. In clinical practice, regardless of protective efforts, the incidence of paraplegia following operations on the descending thoracic aorta ranges from 5 to 7 per cent in patients with coarctation or traumatic transection to 15 to 20 per cent in patients with extensive thoracoabdominal aneurysms. The highest rates of paraplegia (>40 per cent) occur in patients with chronic type B dissection.

The descending thoracic aorta is exposed through the left chest with a large posterolateral incision in the fourth or fifth intercostal space. Thoracoabdominal aneurysms are exposed through a double incision, one in the fourth and one in the seventh intercostal space (Fig. 31) 1865. We are not aware of any definite evidence that normothermic shunt techniques protect against paraplegia, and consider that they prolong and complicate operative repair. At least eight different techniques have been described: this suggests that none has been entirely successful. The sites of cannulation for passive shunt bypass and roller or centrifugal pump bypass are shown in Table 4 522. These include left atrial to femoral bypass with or without an oxygenator, or non-pump bypass methods with a heparin-bonded shunt providing perfusion to the lower half of the body beneath the cross-clamp. For patients with extensive descending thoracic or thoracoabdominal aneurysms brought electively to the operating theatre we use hypothermic cardiopulmonary bypass with a central cannulation technique (Fig. 32) 1866.

Hypothermic perfusion is used only when prolonged cross-clamp times are expected for reimplantation of intercostal, renal, and visceral vessels, and for emergency situations such as leaking Type B dissection where control of pressure, flow, and temperature are important (Fig. 33) 1867. Cross-clamping of the dissected descending aorta while the heart supports the circulation is particularly hazardous. Hypertension proximal to the cross-clamps causes subendocardial ischaemia and left ventricular failure. In ideal circumstances the same conditions of controlled flow, pressure reduction, and hypothermic organ protection used for ascending aortic surgery should provide similar benefits for the descending thoracic and abdominal aorta. In particular, hypothermia and reimplantation of the critical spinal radicular vessels might protect against paraplegia.

Hypothermic cardiopulmonary bypass techniques, with or without periods of circulatory arrest, have recently been described for major thoracic and thoracoabdominal resection. These were applied clinically after animal experiments showed profound hypothermia to have a marked protective effect on spinal cord function during prolonged periods of aortic occlusion. However, established methods have distinct disadvantages. Femoral bypass cannot provide blood flow to the cerebral and coronary circulation when the cross-clamps are applied, and in some patients with small femoral vessels flow rates may be limited. Although retrograde femoral arterial perfusion is used routinely for Type A dissection patients it can be hazardous in patients with Type B dissection or severe aortoiliac disease and cannot be used safely in an emergency when a descending thoracic aneurysm has ruptured. Central cannulation is therefore desirable. The recently described Kouchoukos technique is effective but requires dual cannulation of the femoral vein and right ventricle for venous return. Arterial return is by the femoral artery followed by secondary central arterial cannulation when the proximal descending aortic anastomosis is completed. The Westaby technique uses central venous cannulation using a two-stage cannula inserted through the right internal jugular vein (Fig. 32) 1866. Venous drainage is established with the patient lying supine before positioning for left thoracotomy. Arterial return is then established with a cannula in the proximal aortic arch. This allows continuous hypothermic perfusion of the coronary and brachiocephalic vessels while affording hypothermic protection for the spinal cord and abdominal organs during aortic cross-clamping. Circulatory arrest can be used intermittently to reduce bleeding through collateral vessels or for open anastomosis techniques. The method described evolved during emergency operations for ruptured thoracic and thoracoabdominal aneurysms. During cooling the heart fibrillates and care is taken to check for left ventricular distension. The method is not suitable for patients with significant aortic regurgitation. When profound hypothermia is secure the aortic cross-clamps are applied and the rate of perfusion reduced to approximately 0.8 l/min.m² to supply continued blood flow to the coronary and brachiocephalic vessels. With the aorta open blood is retrieved from the operative site using a cell saver, since the depth of blood in the chest is seldom sufficient for cardiotomy suction. Short periods of low flow or circulatory arrest can be employed to control collateral intercostal bleeding. The diseased aorta is opened and those vessels requiring reimplantation are identified and mobilized. For Type B dissection, the cross-clamps are usually applied between the left carotid and subclavian vessels and at the level of the 5th or 6th thoracic vertebra. The intimal tear is usually located distal to the left subclavian artery. This part of the aorta is resected and replaced with an impervious Dacron graft. Bleeding intercostal vessels must be controlled from within the aortic lumen. If the operation is performed at normothermia without bypass techniques the procedure should be completed so that the aortic cross-clamps can be released within 30 min to minimize the risk of spinal cord ischaemia. For thoracoabdominal aneurysm the aorta is replaced with appropriate lengths of Hemashield into which the visceral vessels are reimplanted. Attempts are made to identify and reimplant the principal spinal radicular artery and selected large proximal intercostal vessels. Profound hypothermia is extremely useful for protection of the myocardium, brain, and visceral vessels during extensive thoracoabdominal replacement. However, two of eight patients undergoing extensive thoracoabdominal replacement have suffered paraplegia despite profound hypothermia and reimplantation of the principal spinal radicular vessels. This suggests that the spinal cord anatomy is the key factor in paraplegia and that hypothermic protection may not be as effective as we had hoped.

These occur predominantly through atherosclerosis, previous aortic dissection or syphilis. Because of the site and extent of these aneurysms, there is a high incidence of paraplegia following their repair. The methods described for Type B aortic dissection apply directly to well-defined aneurysms of the descending aortic segment. However, few surgeons can replace the thoracoabdominal aorta with implantation of all visceral vessels into the graft within the safe duration of simple aortic cross clamping (Fig. 33) 1867. Profound hypothermia with total circulatory arrest affords spinal cord protection and minimizes blood loss. In order to reduce the risk of paraplegia it is important to identify and reimplant the principal spinal radicular artery. In atherosclerotic disease it is often necessary to endarterectomize the coeliac axis, mesenteric artery, or renal vessels. Where the origins of two branch arteries are in close proximity a button of aorta encompassing both may be sutured into the main graft. This technique is commonly used for the right renal artery, together with the coeliac axis or superior mesenteric artery. The left renal artery is reimplanted separately. Care must be taken not to damage the renal veins or inferior vena cava during these extensive operations. The general operative approach to suprarenal and thoracoabdominal aneurysms must be highly individualized, depending on the local anatomical circumstances. The overall morbidity and mortality associated with elective thoracoabdominal aneurysm resection has substantially diminished with improved techniques and vascular grafts. The operative mortality is related to the age of the patient and other underlying problems such as ischaemic heart disease, carotid occlusion, chronic obstructive airways disease, and pre-existing renal failure. Infection, paraplegia, and anastomotic aneurysms have been the primary postoperative complications. The long-term prognosis after successful resection is surprisingly favourable, and depends substantially on the overall condition of the patient, many of whom have concomitant coronary, carotid, and obstructive lung disease.

Coarctation of the aorta is a congenital narrowing of the upper descending thoracic aorta adjacent to the ligamentum arteriosum. Sometimes it is combined with more proximal aortic narrowing. Uncommonly, coarctation occurs more proximally between the left common carotid and subclavian arteries or distally in the descending thoracic aorta. Occasionally, the adult aorta may be redundant and severely kinked opposite the ligamentum arteriosum without any pressure gradient (so-called pseudocoarctation lesion). The lesion of classical coarctation is a shelf or enfolding of the aortic media into the lumen. The shelf is usually marked externally by a localized indentation or wasting of the aortic wall. The aorta beyond the narrowing usually shows post-stenotic dilatation. Collateral circulation develops between the aorta proximal to the narrowing and the distal vessel. When well developed this is responsible for some of the signs, such as parascapular pulsations and rib notching. The enlarged tortuous third and fourth intercostal arteries may become aneurysmal in adults. A bicuspid aortic valve occurs in association in one-third of patients. Many adolescent and young adult patients remain asymptomatic, but often have short legs. They are diagnosed when delayed or absent femoral pulses and systemic hypertension are detected on routine examination. Heart failure appears at about 30 years of age and is preceded by effort dyspnoea, cardiomegaly, and left ventricular hypertrophy on the electrocardiogram. The radiographic findings include a ‘figure 3’ sign in the left upper mediastinal shadow, and almost always rib notching. There is a known association between Turner's syndrome and coarctation of the aorta. The diagnosis can be confirmed by MRI, echocardiography, or invasively by catheterization and aortography. If left untreated, 35 per cent of patients die before the third decade and a further 25 per cent die during both the fourth and fifth decades. Ninety-eight per cent are dead by the age of 60 years. Causes of mortality include heart failure, bacterial endocarditis, aortic dissection, or rupture of associated intracranial aneurysms. Surgery is usually undertaken without perfusion techniques since the surgical options of resection with end-to-end anastomosis, diamond patch aortoplasty, or Dacron graft bypass can usually be carried out in less than 30 min. However, in adults the intercostal arteries are large and friable, and surgical dissection is hazardous. The use of controlled hypotension by the anaesthetist is important but once the aortic clamps are in place, upper body blood pressure is allowed to rise moderately (90–100 mmHg) to promote collateral blood flow to the spinal cord. When an aneurysm of the aorta or intercostal vessels is present resection of the segment of the aorta along with the coarctation is required, and continuity is re-established with an interposed woven Dacron graft. Sacrifice of intercostal arteries increases the likelihood of paraplegia. Nevertheless, paraplegia occurs in less than 5 per cent of adult patients with coarctation, probably because the blood pressure in the distal aorta is maintained by collateral vessels during cross-clamping. Postoperatively systemic hypertension persists in 50 per cent of patients and requires prolonged treatment.

Known risk factors for spinal cord injury include prolonged cross-clamp time (>30 min), increased CSF pressure which may impair cord perfusion, low distal aortic pressure, loss of critical intercostal or lumbar arteries, and the use of nitrate vasodilators. Spinal cord perfusion pressure below the cross-clamps depends on the distal aortic pressure minus the intrathecal pressure. Theoretically, shunt techniques could protect the cord by maintaining distal aortic pressure. Spinal fluid drainage may also prevent an increase in intrathecal pressure during cross-clamping. Spinal cord blood flow is partly dependent on regional vascular resistance and partly on blood pressure. Perfusion pressure can be increased by either raising diastolic blood pressure or reducing the CSF pressure. Nevertheless Crawford and colleagues have shown a high incidence of paraplegia in patients with a high mean distal aortic pressure (80–110 mmHg) during bypass for descending thoracic aortic replacement.

Somatosensory evoked potential recording can be used to monitor spinal cord conduction during aortic cross-clamping. This technique uses an electrical stimulus applied to the leg or foot to evoke cerebral potential tracings which are analysed by computer to determine the brain's electrical response (Fig. 34) 1868. This varies from conventional EEG tracings, in which spontaneous rather than provoked electrical activity is recorded from the cerebral cortex. The evoked potentials are only sensitive to dorsal (posterior) or spinal cord function; the ventral or anterior portion of the cord is at greatest risk of developing ischaemia. Although the use of motor evoked potentials has been proposed as a warning sign for paraplegia during clinical surgery, the awareness of an impending cord problem is unlikely to expedite cross-clamp removal. In dogs, however, the method has been used to demonstrate that spinal cord function can be maintained for up to 1 h of normothermic cross-clamping, provided the mean distal aortic pressure is above 60 mmHg.

Failure to reattach important spinal cord blood vessels after extensive thoracic or thoracoabdominal resection may cause paraplegia. The principal spinal radicular artery can sometimes be identified at operation because of its size. Methods of intraoperative identification would be of great value but those currently available are complex and not applicable to emergency operations in patients with Type B dissection or ruptured thoracic aneurysms. Currently, hypothermic techniques possibly combined with pharmacological protection with an appropriate calcium channel blocker and barbiturate combination offer the best methods of cord protection. Attempts should be made to preserve the principal spinal radicular artery: this is sometimes possible by creating a long oblique distal anastomosis to protect the intercostal and lumbar vessels between T10 and L2.

In 1981 Carpentier's group described a thoracic aortic bypass technique for treatment of Type B aortic dissection (Fig. 35) 1869. The method was designed to reduce morbidity and mortality by reducing blood loss and the risk of paraplegia. As originally described the method did not require cardiopulmonary bypass and is not subject to the problems of proximal hypertension and distal hypoperfusion through unprotected aortic cross-clamping. The operation does not involve a direct attack on the descending thoracic aorta. A median sternotomy incision extended down into the abdomen allows the descending aorta to be bypassed with a graft from the ascending to the infrarenal abdominal aorta. The native aortic lumen is then occluded just distal to the left subclavian artery. When the aorta is interrupted there is a reversal of blood flow in the descending thoracic aorta (Fig. 36) 1870. This results in retrograde flow into the aneurysm, causing considerable turbulence and progressive thrombosis of the descending thoracic aorta down to the first major abdominal branch, the coeliac axis. Thromboexclusion firstly protects the diseased aortic segment from rupture and then gradually occludes it by thrombosis. In the meantime, because the process is slow, collaterals develop and protect the spinal cord. Apart from Carpentier's initial report there has been radiological documentation of this thrombotic process in only two other patients. In general the method has not been adopted and its usefulness is underestimated.

We have recently used thromboexclusion combined with coronary artery bypass surgery in a 62-year-old Jehovah's witness who was restricted to a wheelchair by pain from a progressively expanding Type B dissection (Fig. 37) 1871. Additionally he had also suffered previous myocardial infarction with impairment of left ventricular function. On cardiopulmonary bypass the left anterior descending coronary was grafted and then, using reduced pressure and flow, a 30 cm Hemashield graft was anastomosed to the infrarenal abdominal aorta and brought through the diagphram to the right side of the ascending aorta. The operation was completed by stapling the distal aortic arch. There was no significant bleeding in this patient and the postoperative haemoglobin level was 10.6 g. He made an uneventful recovery. Encouraged by this success we then applied the method to a 60-year-old woman with a massive syphilitic descending thoracic aneurysm who had previously undergone ascending aortic replacement for a ruptured aneurysm. In this patient the proximal end of the bypass graft was anastomosed to the Hemashield ascending aortic graft. In addition to its application for patients with acute Type B dissection as advocated by Carpentier the process for thromboexclusion may well prove applicable to patients with massive descending thoracic aneurysms where the risks of paraplegia are considered prohibitive.

These patients usually present with aortic regurgitation due to dilatation of the aortic annulus and are found to have an ascending aortic aneurysm involving the aortic sinuses (Fig. 38) 1872 (Table 7) 525. Non-invasive diagnostic techniques such as two-dimensional echocardiography, CT, and nuclear magnetic scanning provide excellent imaging of size and extent of the aneurysm and of left ventricular function. Coronary angiography is usually used to rule out the presence of occlusive disease in patients over 40 years of age. Combined replacement of the aortic valve and ascending aorta is required with reimplantation of the coronary ostia into the graft (Bentall procedure; Fig. 39 1873,1874,1875,1876). Composite proprietary valve conduits and antibiotic sterilized aortic homografts are used for this procedure and with improvements in myocardial protection the operative mortality is now between 5 and 10 per cent. In Oxford the wrap-around inclusion technique has been superseded by excision of the pathological aorta and mobilization of the coronary arteries before reimplantation into the graft. Bleeding has largely been eliminated by electively sealing the suture lines with acrylic (Histoacryl Braun) or resorcinol-based glues.

Nuclear magnetic resonance imaging and three-dimensional reconstruction of CT scan images has improved our understanding of the natural history of thoracic aneurysm. The second technique is able to define specific irregularities in the aortic wall which may predict rupture. Ascending aortic aneurysms are known to increase in diameter by 1.5 cm/year, three times faster than an infrarenal aortic aneurysm. Descending aortic aneurysms also increase in size faster than abdominal aortic aneurysms, but in addition expand by elongation. Risk factors for rupture of a thoracic aneurysm include size, elevated diastolic blood pressure, and presence of obstructive pulmonary disease. Indications for surgery in thoracic aneurysms are pain, an ascending aortic dilation to more than 5 cm in patients with Marfan's syndrome, a diameter above 8 cm in patients with other pathology, and for all saccular aneurysms, where the nature of the defect implies significant wall weakness. Aneurysms between 6 and 8 cm (twice normal size) can be managed conservatively with 3- to 6-monthly CT or MRI scanning. Surgery is advised if the aneurysm reaches 8 cm.

Aneurysms which do not involve the aortic sinuses can be replaced with a straight tube graft, using cardiopulmonary bypass with or without total circulatory arrest, according to the site of the distal anastomosis. When the graft involves only the ascending aorta the surgical mortality is between 5 and 10 per cent. For operations involving the ascending aorta together with the aortic arch the mortality increases to more than 20 per cent.

Surgery of the aortic arch has been greatly simplified by the techniques of profound hypothermia and total circulatory arrest. Separate cannulation and continuous perfusion of the cerebral vessels were previously required. Using median sternotomy and total circulatory arrest without aortic cross-clamps, the arch can be replaced with a tube graft. Implantation of the innominate, left carotid, and left subclavian vessels is performed en bloc on an oval button of aorta. With the circulation arrested, the distal anastomosis to the descending thoracic aorta is performed first, followed by implantation of the brachiocephalic vessels. An aortic cross-clamp can then be applied to the graft and perfusion to the head and body recommenced. The proximal anastomosis to the ascending aorta is undertaken during the rewarming phase of perfusion. Care must be taken to remove air from the cerebral vessels. During the procedure the myocardium is protected by cold potassium cardioplegia.

Despite improvements in technique, the mortality rate associated with aortic arch replacement in most centres remains between 20 and 30 per cent. This may be due to the rarity with which the operation is performed.

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