Thoracic Aortic Surgery

Thoracic Aortic Surgery

Yuki Ikeno

Akiko Tanaka

Anthony L. Estrera


The aorta is the conduit that carries almost 200 million L of blood to the body in a lifetime. Yet despite its critical role, it is subject to a variety of disease processes that can have serious health consequences. This chapter describes the anatomy of the aorta, the classification and pathogenesis of aortic diseases, and the epidemiology and risk factors associated with specific aortic conditions. As the principal treatment of serious aortic disease is surgery, surgical strategies, including organ protection during aortic repair, will also be reviewed.


The aorta is anatomically divided into the aortic root, ascending aorta, transverse aortic arch, descending thoracic aorta, and abdominal aorta (Figure 89.1). The aortic wall is composed of three layers: intima, media, and adventitia. The intima is the innermost layer and made of a single layer of endothelium. The media lies between intima and adventitia and is made of smooth muscle cells, elastic tissue, and collagen. The adventitia is the outmost layer, mainly composed of collagen, lymphatics, and a network of small blood vessels (vasa vasorum). The intima and inner one-third of media are directly nourished by blood from the aortic lumen, whereas the vasa vasorum feeds the outer two-thirds of media and adventitia.


Aortic diseases can be classified into the following categories: true aneurysm, false aneurysm (pseudoaneurysm), aortic dissection, and penetrating aortic ulcer.1 A true aortic aneurysm is a dilatation of the aorta, involving all three layers of the aortic wall. An aneurysm is defined by a diameter of 50% or greater than the normal. The aneurysm location is described using the anatomy mentioned earlier, and the descending thoracic aortic aneurysm is further divided into three extents (ie, A, B, and C) and the thoracoabdominal aneurysm is subdivided into five extents (ie, I-V)2,3 (Figure 89.2). In a false aneurysm, the aneurysmal wall consists of adventitia or periaortic tissue.

Aortic dissection occurs when blood enters through an intimal tear and rapidly separates the media, forming a false lumen. Two classifications of aortic dissection based on the extent of the dissection are widely used: the DeBakey and Stanford classifications.4 In DeBakey type I or Stanford type A dissection, the dissection involves the ascending aorta. In DeBakey type II, only the ascending aorta is involved. In DeBakey type III, or Stanford type B, spares the ascending aorta and involves the descending/thoracoabdominal aorta (Figure 89.3A,B). However, these classifications are confusing when the dissection flap extends from the transverse arch without the ascending aorta involved, the so-called non-A and non-B. Thus, recently, the Society of Vascular Surgery and Society of Thoracic Surgeons described a new classification system, focusing on the location of the entry tear: Any dissection with the entry tear in the ascending aorta is named type A; tear in the arch or dissection is type B, regardless of the proximal extension; and type I is defined as unidentified tear but dissection involving the ascending aorta.5 This classification is useful when evaluating the indication for thoracic endovascular aortic repair (TEVAR).

Aortic dissection is also classified based on the time elapsed since initial clinical presentation (hyperacute: <24 hours,
acute: 2-7 days, subacute: >7-30 days, chronic: >30 days).6 Chronic aortic dissection may develop aneurysmal dilatation of the aortic wall.

Penetrating arteriosclerotic ulcer is an aortic disorder, which penetrates and ulcerates the internal elastic lamina of the aortic wall. It is a form of diffuse arteriosclerotic disease with sessile, mobile, or pedunculated atheroma composed of lipid deposition in the intimal layer of the aorta.


Thoracic Aortic Aneurysms

A variety of conditions involve the development of aortic disease: congenital, degenerative, traumatic, inflammatory, infectious, and anastomotic. Genetic/congenital conditions—such as Marfan syndrome, Loeys-Dietz syndrome, Ehlers-Danlos syndrome, Turner syndrome, Noonan syndrome, and autosomal dominant polycystic kidney disease—carry higher risks for aortic dissection and rupture.7,8 Aneurysmal changes can also occur in the aorta distal to stenotic aortic valves or coarctation. Patients with a bicuspid aortic valve are at risk for developing ascending aortic dilatation from structural aortic wall abnormalities and turbulent flow.9 Cystic medial degeneration and atherosclerosis are the common causes of a degenerative aneurysm. Cystic medial degeneration, the loss of elastic tissue and smooth muscle cells because of the inflammation and apoptosis, is most frequently observed in the ascending aorta,10 while atherosclerosis mainly affects the descending thoracic and abdominal aortic segments. Blunt aortic trauma can also cause aortic disease, most frequently occurring at the isthmus.11 Inflammatory diseases are rare but can also cause aortic disease. These include Takayasu arteritis, Behçet disease, and giant cell arteritis.12 Infection from bacteria and fungus can cause aneurysmal degeneration.

Incidence and Survival

The incidence of thoracic aortic aneurysms is 5.9 new aneurysms per 100,000 person-years in the United States.13 The major causes of deaths in people with these aneurysms are aortic rupture and dissection. Joyce and colleagues14 reported a survival rate of 50% at 5 years and 30% at 10 years in 107 patients with a thoracic aortic aneurysm. Of those, 32% died of rupture. Aneurysm diameter correlates with the survival: patients whose aortic diameter was more than 6 cm showed significantly lower survival than patients with an aortic diameter of less than 6 cm (36.6% vs 61.1%, at 5 years, respectively).

Aortic Growth Rate and Aortic Events

Elefteriades and colleagues reported in a retrospective study that the mean growth rate of the ascending aorta was 0.14 cm per year, and that of the descending/thoracoabdominal aortic aneurysm was 0.19 cm per year, with an incremental increase in growth rate as the diameter continues to enlarge. In addition,
the aortic diameter following aortic dissection grew at a faster rate of 0.37 cm per year.15,16 In the ascending aorta, the yearly incidence of adverse aortic events (ie, a composite of rupture, dissection, and death) was significantly associated with aortic size (3.5-3.9 cm, 2.2%; 4.0-4.4 cm, 4.3%; 4.5-4.9 cm, 4.0%; 5.0-5.4 cm, 5.8%; 5.5-5.9 cm, 6.8%; >6.0 cm, 15.0%). The rate of adverse events increased sharply at the size of 5.25 and 5.5 cm and then again between 5.75 and 6 cm. Likewise, the yearly rate of adverse aortic events in the descending/thoracoabdominal aorta increased markedly at a size of 6 cm and 6.5 cm (3.0-3.4 cm, 0.6%; 3.5-4.0 cm, 4.1%; 4.0-4.4 cm, 7.3%; 4.5-4.9 cm, 10.2%; 5.0-5.4 cm, 3.0%; 5.5-5.9 cm, 7.8%; 6.0-6.4 cm, 18.7%; 6.5-6.9 cm, 21.0%; >7 cm, 18.9%). Connective tissue disease is also known as an independent risk factor for aortic events.

Aortic Dissection

Epidemiology and Risk Factors

In population-based studies, the incidence of acute aortic dissection is estimated at 2 to 6 per 100,000 person-years.17,18 The incidence is higher in men than in women and increases with age. In the International Registry of Acute Aortic Dissection (IRAD), the mean age was 63 years, 65% of which were men. Other risk factors for aortic dissection include preexisting aortic disease, aortic valve disease, a family history of aortic diseases, a history of cardiac surgery, cigarette smoking, blunt chest trauma, and use of drugs, such as cocaine and amphetamines.19

Clinical Presentation: Acute Aortic Dissection

Abrupt onset of chest/back pain is the most frequent symptom of acute aortic dissection. Other symptoms and presentations are aortic rupture, aortic valve regurgitation, cardiac tamponade, myocardial ischemia, congestive heart failure, and end-organ malperfusion (ie, neurological deficit, spinal cord injury, mesenteric ischemia, renal failure, and limb ischemia). P pulse deficits may be observed in as many as 30%. Because of these lethal complications, the prognosis of the disease without prompt treatment is devastating. Hirst and colleagues reported that 3% of patients with acute type A dissection died immediately after the onset, 21% within 24 hours, 74% within 2 weeks, 80% within a month, and 93% within a year.20 Thus, the acute phase (2 weeks within onset) is considered a critical time with high mortality.21

However, the prognosis of acute aortic dissection highly depends on its extension. In the autopsy study of acute aortic
dissection, patients with Stanford type A dissection emerged as a cause of sudden cardiovascular death more frequently than Stanford type B (65.0% vs 6.5%),22 and most deaths occurred in the acute phase. The mortality rate for Stanford type B dissection in the acute phase is approximately 50% in patients with end-organ ischemia or rupture and 10% in patients without complications.23


The history of aortic surgery has been a series of challenges against the lethal natural history of aortic disease and complexity of the procedures. A vital contribution to the modern aortic surgery was made by Rudolph Matas in 1902, when he first performed the endoaneurysmorrhaphy with controlling proximal and distal artery.1 Throughout the first half of the 20th century, sporadic attempts were made to treat aortic aneurysms, almost all in the abdominal aorta. In 1944, Alexander and Byron successfully resected a thoracic aortic aneurysm secondary to coarctation without reconstruction of aortic continuity.24 In 1948, Gross and colleagues replaced the coarctation with an aortic allograft, although the result was unsatisfactory. In 1950, Swan and colleagues reported a successful series for treating coarctations and aneurysms using an allograft replacement. In 1953, DeBakey and Cooley reported the first successful application of resection and grafting to a descending thoracic aortic aneurysm.25 Three years later, they reported the first successful modern operation for ascending aortic aneurysm by graft replacement under cardiopulmonary bypass (CPB). In 1964, Wheat and colleagues reported a simultaneous but separate replacement of the ascending aorta and aortic valve, with reimplantation of the coronary ostia into the graft. Bentall and De Bono, in 1968, accomplished a root replacement with a composite of a valve and polyester tube graft.

Transverse arch repair, a more complicated surgical challenge, saw technical advances, and improved outcomes with the development of strategies for brain protection. In 1957, DeBakey and colleagues reported the first successful aortic arch aneurysm with allograft replacement under CPB and antegrade cerebral perfusion. Morris and colleagues reported the first acute type A dissection repair in 1963. In 1975, Griepp and colleagues established the hypothermic circulatory arrest for aortic arch repair,26 which pioneered subsequent brain protection strategies.

The thoracoabdominal aneurysm also remained a challenge, not only because of the magnitude of the operation but also due to the potential for multiorgan dysfunction after repair, including in the intestinal, renal, and spinal cord ischemic complications. In 1955, Ellis and colleagues reported a repair of an aneurysm involving a renal artery by graft replacement. In the same year, Etheredge and colleagues reported a successful repair of the thoracoabdominal aneurysm, including the celiac and superior mesenteric arteries. Finally, in 1956, DeBakey and colleagues reported a successful repair of thoracoabdominal aneurysm involving all the visceral arteries.

The development of devices also has contributed to the improvement of surgical outcomes. Instead of an allograft, the first satisfactory synthetic aortic substitute was a fabric tube made of polyvinyl chloride cloth in 1954. Since Deterling and colleagues reported the utility of polyester, it has been widely used. Impregnating the polyester graft with collagen, gelatin, or albumin has demonstrated a considerable reduction in blood loss through the grafts. Guilmet and colleagues described the use of gelatin-resorcinol-formaldehyde glue to reinforce the dissected aortic wall before anastomoses in 1979.27 An albumin and glutaraldehyde-based adhesive, the BioGlue (CryoLife Inc, Kennesaw, GA, USA), has been approved for use in the United States.

Endovascular stent grafting—thoracic endovascular aortic repair (TEVAR)—was introduced by Dake and colleagues in the early 1990s, using a custom-designed graft.28 Currently, a variety of off-the-shelf grafts have become available for clinical use.


The surgical indications of chronic thoracic aortic disease are determined by the balance of surgical risks and the expected adverse events due to the aortic disease. Guidelines suggest optimal treatment options for each condition.18,19,29 Patients who have an acute aortic syndrome (ie, ruptured aneurysm, acute aortic dissection, intimal hematoma, and symptomatic aortic ulcer) are indicated for emergent/urgent surgical repair, due to their highly lethal nature. In patients with acute type B dissection, interventions should be recommended when patients have organ malperfusion syndrome, progression of dissection, aneurysm expansion, or uncontrolled hypertension (complicated type B dissection). Medical management had been preferred when patients do not have these features (uncomplicated type B dissection), but endovascular options may be considered to prevent late complications.30 The Investigation of Stent Grafts in Aortic Dissection (INSTEAD) trial compared TEVAR and optimal medical therapy (OMT) for patients with subacute and chronic uncomplicated type B dissection (2-52 weeks after initial diagnosis). At early follow-up, patients treated with TEVAR were found to have improved aortic remodeling but no difference in mortality. However, after 5 years, TEVAR significantly reduced the incidence of aneurysm formation, and aortic-related mortality compared with OMT.30 As a result, some surgical teams recommend a more aggressive approach, advocating TEVAR for treatment of patients with uncomplicated type B dissection.

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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Thoracic Aortic Surgery
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