Cath Lab Digest

The transformation of the field of thoracic aortic surgery began with the performance of the first stent graft procedure for repair of a descending thoracic aortic aneurysm (TAA) by Dake et al in 1992.¹ It took place in the wake of the history-making first endovascular aneurysm repair (EVAR) procedure by Parodi et al in 1990, and Volodos’ first-ever stent graft aortic repair in 1986.²

The incipient thoracic endovascular aortic repair (TEVAR) field was slow to develop at first, lagging behind developments on the EVAR side for several years. Nonetheless, the emerging techniques for the thoracic aorta were received with wide enthusiasm and almost immediate embrace by specialists and the medical community at large because of the realities of surgical treatment that is viewed as maximally invasive, and often accompanied by a high rate of complication and even death. The perception of a poorly served patient population thus evolved over the years, providing great impetus for the creation of less invasive therapies.

Thoracic Aortic Aneurysm

TAA is a serious disease, and often fatal as patients face a rather limited 20% to 54% 5-year survival expectation (due to aneurysm rupture).^3,4 The incidence is reported in 10.4 per 100,000 people/year,⁵ or approximately 30,000 new cases each year in the U.S. alone. The corresponding number for abdominal aortic aneurysm (AAA) is 200,000, reflecting its significantly higher incidence. Like AAA, TAA is asymptomatic in 95% of cases or more.

Elective repair should be considered for all 5.5 cm TAA as they carry an annual rupture risk of 15%.^4,6,7 The rupture rate is reported to be 3.5 per 100,000 people/year, considerably lower than the rate of ruptured AAA. It is interesting and intriguing that the incidence of acute aortic dissection and ruptured TAA are almost identical.⁸ Overall, the total mortality for ruptured thoracic aneurysms approaches 97% among those reaching the hospital alive.⁹

Anatomic location and extent designate TAAs: ascending, arch, descending, and thoracoabdominal aortic aneurysms. Aneurysms of the descending thoracic aorta are most common (30%-40%). Aortic aneurysms have the same pathogenesis and essentially, the same risk factors: male gender, advanced age, cigarette smoking, atherosclerosis, hypertension, and genetic predisposition. Smoking is by far the most significant modifiable risk factor.¹⁰ Historically, the label atherosclerotic was applied to most thoracic and abdominal aneurysms, but today we know that the more appropriate term is degenerative. Loss of collagen and elastin in the wall of the aorta constitute the pathogenetic signatures of aneurysm formation. It is of interest that for unclear reasons there is an apparent cross-link between TAA disease and intracranial aneurysms, to the extent that some experts suggest screening and cerebrovascular imaging on thoracic aneurysm patients.

The Yale database (3,000+ patients) has produced invaluable information on the epidemiology and nature of TAA disease,¹¹ chiefly the following:

• Thoracic aneurysmal disease tends to be genetic in nature with a predominantly autosomal dominant inheritance;
• Matrix metalloproteinase enzymes are quite active;
• Aortic wall tension and diameter go hand-in-hand, approaching the tensile limits of aortic tissue at a 6.0 cm diameter;
• Extreme physical exertion (ie, heavy lifting) and emoting can precipitate occurrence of acute aortic dissection.

An increase in the true incidence of TAA has been suggested by recent evidence.^8,12,13 TAA growth can be described – generally – as slow and indolent at approximately 0.3 cm per year in the descending thoracic aorta and 0.1 cm per year in the ascending. Very rapid enlargement is often associated with an intercurrent dissection.¹⁴ Hinge points of aortic diameter progression (at which rupture or dissection are likely to occur) have emerged:¹¹ 6.0 cm in the ascending and 7.0 cm in the descending. They seem to represent the sizes where the wall tension approaches or exceeds the elastic limits of the aortic wall.¹⁴ Therefore, it is possible to prevent death from rupture of the thoracic aorta by undertaking repair before it reaches a dangerous size: the 5.5 cm diameter threshold emerges as most reasonable before intervention and repair can be performed in the majority of such patients.

More aggressive treatment guidelines can be justified in patients at greater risk such as those with Marfan syndrome, bicuspid aortic valve, and with a family history of aortic dissection. Naturally, patients with truly symptomatic aneurysms (5% or less of the TAA population) should be offered repair regardless of size.

Surgical treatment of TAA was reported as early as 1951.¹⁵ Improvements in surgical techniques and perioperative care over the past 3 decades have allowed skilled specialized aortic surgeons to perform complex thoracic aortic surgery with excellent results and safety. Remarkably, such capabilities are available in only a few centers around the world.¹⁶ Additionally, a considerable number of patients are unlikely surgical candidates because of medical reasons, all of which explain the rapid rise of TEVAR and its transformational influence.