**Abstract**

The modern approach to the correction of aortic dissection involves the most complete reconstruction of the entire pathologically altered segment of the vessel, which is often impossible due to the vastness of the lesion and the associated severity of surgery. Reduction of intraoperative trauma can improve survival in the immediate postoperative period, and the completeness of reconstruction to reduce the number of complications and relapses in the long term. In this chapter, the methods of reconstruction of the aorta in case of distal dissection from a conventional open surgery to endovascular techniques, or usage of their combination for minimization of surgical trauma, are reviewed.

**Keywords:** aortic dissection, hemodynamic, surgical approach, aortic surgery, EVAR, hybrid

## **1. Introduction**

Aortic dissection is defined as the penetration of blood masses between the inner and middle layers of the aortic wall, with the formation of a rupture of the inner layer of the aortic wall, intima. In this case, a flap is formed that divides the aortic lumen into true and false [1, 2].

The aortic wall consists of three layers: the inner tunica intima, the middle tunica media, and the outer tunic of adventitia. Despite the fact that different components and special types of cells form each of these layers, they all represent a single structure that can withstand high variable loads. The inner layer, tunica intima, has a thickness of 130 microns. Its first shell is the endothelium, a singlerow layer of cells that directly contact the blood. Endothelial cells are oriented in accordance with the direction of blood flow [3]. The endothelium prevents thrombosis, has selective permeability to liquids and nutrients, participates in maintaining vascular tone, regulates blood pressure, has immunomodulatory and barrier functions, and plays an important role in regulating vasculoangiogenesis and remodeling the cardiovascular system [4]. A thin subendothelial shell, consisting of a small number of collagen-synthesizing fibroblasts and collagen fibers, attaches to the endothelium. The processes of endothelial cells connect the intima with the middle layer.

Tunica media is the thickest and most durable layer of the aortic wall that converts the pulsating blood flow, so it is most susceptible to variable loads. The average thickness of the media is up to 1.2 mm. Elastic plates separated by thin layers of connective tissue, collagen fibers, and smooth muscle cells form the structure of the media tunic. Elastic and collagen fibers make up 20–30% of the total volume of the

aortic wall separately, and smooth muscle cells make up 5% [5]. Elastic plates are concentrically arranged fenestrated membranes (lamellae), the fibers of which are intertwined. The media tunic has 45–60 elastic plates covering 1/3–3/4 of the circumference of the aortic diameter. As a rule, these are oppositely twisted, cross-linked spiral structures arranged in a staggered order, which are held together by interlamellar connecting fibers. A network of fine collagen fibers surrounds both lamellar and connective elastic fibers. In addition, the elastic plates are supported by muscle fibers connected through points of contact with the mucoid membrane of the elastic plates. Interstitium contains colloidal mixtures of proteoglycans. The outermost elastic lamellar plates separate the aortic media from the thin adventitial layer [6, 7].

The adventitia tunic consists of loose connective tissue with a small number of elastic fibers, muscle cells, and macrophages. Through it from the outside, the vessels that feed the wall of the aorta vasa vasorum and nerve endings pass. Vasa vasorum, originated from the network of vessels located in adventitia, penetrate the outer third of the media and branch between the outer and middle layers, penetrating no deeper than the inner third of the media of the aorta. Thus, the outer third of the aorta receives nutrition through the vasa vasorum, while the inner layers are fed by diffusion from its lumen, which will support the structure of the aortic flow [8] (**Figure 1**).

Despite a long history of studying the pathogenesis of aortic dissection, it is still not clear enough. When studying the morphology of the aortic wall in patients with dissection, changes in the middle tunic of the media were most often detected. Gsell (1928) described damage to smooth muscle fibers during aortic dissection, Erdheim (1929) described damage to elastic fibers, and Cellina (1931) described a combination of these processes [6]. Currently, the media damage is, described as damage and loss of smooth muscle fibers, destruction and fragmentation of elastic plates, and filling of the resulting voids with proteoglycans [9] (**Figures 2** and **3**).

Such changes may occur in patients with inherited syndromes accompanied by connective tissue dysplasia, such as Marfan, Loeys-Dietz, Ehlers-Danlos, Turner, and others, or in their absence.

The same changes along with atherosclerosis are found in the aortic wall in elderly patients and with increased variable loads, in particular with arterial hypertension. It is, believed that due to the loss of elastic properties of the aortic wall, the vasa vasorum network is traumatized, which leads to the formation of lacunae

#### **Figure 1.**

*Aortic sections from a normal subject. Panel is oriented with the intima at the top and the adventitia at the bottom; hematoxylin and eosin (H&E) staining.*

**279**

**Figure 3.**

**Figure 2.**

the proximal dissection.

*Methods of Reconstruction for Distal Aortic Dissection DOI: http://dx.doi.org/10.5772/intechopen.93339*

*and accumulation of proteoglycans (stained blue) in the medial layer.*

filled with blood, and subsequently an intramural hematoma. The beginning of the stratification is the rupture of the intima due to the impact of the peak load [6, 7] (**Figures 4** and **5**). However, this concept does not explain the mechanism of dissection in acute trauma in young patients with noncompromised aortic wall. In all likelihood, with excessive loads or due to degenerative changes within it, the aortic wall ceases to function as a whole and is divided into separate fragments with

*Necrosis of the aortic media tunic, chaotic arrangement of smooth muscle and elastic fibers.*

*Aortic sections from a patient with aortic dissection. Fragmentation of elastic fibers, loss of smooth muscle cells,* 

The exact number of cases of distal aortic dissection is very difficult to determine, since this disease refers to various conditions due to different causes. It is important to divide the distal dissection into primary and secondary. Primary dissection is a firstly appeared dissection, and secondary distal dissection can be called the presence of active false lumen of the descending aorta, after correction of

different mechanical properties (**Figure 6**).

*Methods of Reconstruction for Distal Aortic Dissection DOI: http://dx.doi.org/10.5772/intechopen.93339*

#### **Figure 2.**

*Aortic sections from a patient with aortic dissection. Fragmentation of elastic fibers, loss of smooth muscle cells, and accumulation of proteoglycans (stained blue) in the medial layer.*

#### **Figure 3.**

*Necrosis of the aortic media tunic, chaotic arrangement of smooth muscle and elastic fibers.*

filled with blood, and subsequently an intramural hematoma. The beginning of the stratification is the rupture of the intima due to the impact of the peak load [6, 7] (**Figures 4** and **5**). However, this concept does not explain the mechanism of dissection in acute trauma in young patients with noncompromised aortic wall. In all likelihood, with excessive loads or due to degenerative changes within it, the aortic wall ceases to function as a whole and is divided into separate fragments with different mechanical properties (**Figure 6**).

The exact number of cases of distal aortic dissection is very difficult to determine, since this disease refers to various conditions due to different causes. It is important to divide the distal dissection into primary and secondary. Primary dissection is a firstly appeared dissection, and secondary distal dissection can be called the presence of active false lumen of the descending aorta, after correction of the proximal dissection.

**Figure 4.** *Dissection in the middle layer of the aorta, tunic media. On the left are the nuclei of single erythrocytes.*

#### **Figure 5.**

*Extensive acute aortic dissection. Areas of tearing are localized in the distal third of the media tunic closer to the adventitia. A large number of red blood cells are observed inside the false lumen.*

Primary dissection may be associated with dysplasia of connective tissue due to congenital genetic syndromes such as Marfan, Loeys-Dietz, Ehlers-Danlos, Turner, and others. Connective tissue dysplasia in distal dissection can also occur without the presence of hereditary syndromes. Distal dissection occurs in patients without connective tissue dysplasia, for example, after trauma.

Recently, acute aortic syndrome has been isolated, which, in addition to aortic dissection, includes a penetrating ulcer and an intramural hematoma; these conditions are predictors of dissection and require exactly the same approach as the dissection itself.

**281**

**Figure 6.**

*Methods of Reconstruction for Distal Aortic Dissection DOI: http://dx.doi.org/10.5772/intechopen.93339*

Distal dissection or aortic dissection of type B most often affects male patients and has an incidence between 2.9 and 4.0 per 100,000 people per year [10]. The number of cases of distal dissection is increasing, with improved diagnostic capabilities and an aging population being put forward as reasons. A recent prospective analysis of 30,412 middle-aged men and women over a 20-year follow-up period showed the incidence of acute aortic dissection in 15 patients per 100,000 population per year [11]. The number of penetrating aortic ulcers has also increased. In symptomatic patients considered as candidates for invasive intervention, the prevalence of penetrating ulcer is from 2.3 to 7.6%, while in 90% of patients, the lesion is localized in the descending thoracic aorta [12]. The prevalence of intramural hematoma is from 5 to 20% of patients with acute aortic syndrome;, in 60% of cases, the descending thoracic aorta is involved in the process [13]. Blunt aortic trauma occurs in less than 1% of all road accidents. However, it is the second most common cause of death among trauma patients and accounts for 16% of all traumatic deaths [14]. Rupture of an aneurysm of the descending thoracic aorta occurs in 5 persons per 100,000 population per year. The average age of patients in this cohort is 70 years for men and 72 years for women [15]. Mortality in aneurysms and aortic dissection has recently increased from 2.49 per 100,000 to 2.78 per 100,000 of the population

*Chronic aortic dissection. The formation of a pseudo-intima is observed along the edges of the false lumen.*

per year from 1990 to 2010, with a predominance of males [16].

Most clinical classifications of aortic dissection, including the first and most common, proposed by DeBakey, are based on the identification of the localization of the initial rupture of intima, since most of this largely depends on the severity of the patient's condition, further treatment tactics, and prognosis of his life. According to DeBakey, the aortic dissection is divided into three types: type I—primary rupture of intima is localized in the ascending aorta, and the dissection extends below the source of the left subclavian artery; type II—primary rupture of intima is localized in the ascending aorta, and the dissection extends no further than the source of the brachycephalic trunk; and type III—primary rupture of intima is localized below the source of the left subclavian artery and extends to the distal aorta, up to its bifurcation [17]. Subsequently, types I and II were combined into one type A, and type III

was separated into type B, and this classification was called Standford [18].

**Figure 6.** *Chronic aortic dissection. The formation of a pseudo-intima is observed along the edges of the false lumen.*

Distal dissection or aortic dissection of type B most often affects male patients and has an incidence between 2.9 and 4.0 per 100,000 people per year [10]. The number of cases of distal dissection is increasing, with improved diagnostic capabilities and an aging population being put forward as reasons. A recent prospective analysis of 30,412 middle-aged men and women over a 20-year follow-up period showed the incidence of acute aortic dissection in 15 patients per 100,000 population per year [11]. The number of penetrating aortic ulcers has also increased. In symptomatic patients considered as candidates for invasive intervention, the prevalence of penetrating ulcer is from 2.3 to 7.6%, while in 90% of patients, the lesion is localized in the descending thoracic aorta [12]. The prevalence of intramural hematoma is from 5 to 20% of patients with acute aortic syndrome;, in 60% of cases, the descending thoracic aorta is involved in the process [13]. Blunt aortic trauma occurs in less than 1% of all road accidents. However, it is the second most common cause of death among trauma patients and accounts for 16% of all traumatic deaths [14]. Rupture of an aneurysm of the descending thoracic aorta occurs in 5 persons per 100,000 population per year. The average age of patients in this cohort is 70 years for men and 72 years for women [15]. Mortality in aneurysms and aortic dissection has recently increased from 2.49 per 100,000 to 2.78 per 100,000 of the population per year from 1990 to 2010, with a predominance of males [16].

Most clinical classifications of aortic dissection, including the first and most common, proposed by DeBakey, are based on the identification of the localization of the initial rupture of intima, since most of this largely depends on the severity of the patient's condition, further treatment tactics, and prognosis of his life. According to DeBakey, the aortic dissection is divided into three types: type I—primary rupture of intima is localized in the ascending aorta, and the dissection extends below the source of the left subclavian artery; type II—primary rupture of intima is localized in the ascending aorta, and the dissection extends no further than the source of the brachycephalic trunk; and type III—primary rupture of intima is localized below the source of the left subclavian artery and extends to the distal aorta, up to its bifurcation [17]. Subsequently, types I and II were combined into one type A, and type III was separated into type B, and this classification was called Standford [18].

Some authors began to call the type A dissection (types I and II by DeBakey) proximal, and type B (type III by DeBakey) distal, since apparently these terms most fully reflect the essence of pathological processes occurring inside the aorta [19, 20]. For forms where the dissection is limited to the aortic arch or extends retrograde from the descending aorta to the arch and ends before the ascending aorta, the term "non A non B" is proposed [21, 22].

Currently, new classifications that are more modern are proposed, in particular DISSECT classification, which considers six key parameters: duration of the disease, localization of intimal rupture, size of the stratified aorta, length of the affected area of the aorta, clinical complications of stratification, and the presence of false lumen thrombosis [23]. In the surgical treatment of distal dissection (type III DeBakey) within 30 days mortality surgery ranges from 10 to 24%, while at carrying out of conservative therapy, this index varies within 10%. Therefore, the distal dissection (type III DeBakey) is adopted a conservative wait-and-see tactic. Long-term results demonstrate the need for intervention in 20% of patients treated conservatively within 3 years from the beginning symptoms of the dissection [24].

The strategy and tactics of treatment of distal widespread aortic dissection are still the subject of discussion [25]. A majority of authors agree that invasive intervention is indicated by increasing the diameter of the aorta to 5.5 cm, with the combined diameter of the true and false lumen to 4.5 cm, or with complicated forms of dissection [22]. Complicated forms of aortic dissection type B are considered to be a rapid increase in the diameter of the aorta; rupture of the aorta and/or hypotension or shock; ischemia of internal organs, kidneys or lower limbs; paraplegia/paraparesis; periaortic hematoma; re-emerged or untreatable pain syndrome; and refractory to drug therapy hypertension. At the same time, with conservative treatment of complicated forms of distal aortic dissection, mortality is about 50% [26–29].

Consequently, most interventions in distal aortic dissection are carried out for emergency indications. Methods of reconstruction in distal aortic dissection can be divided into traditional open, video-assisted, X-ray endovascular, and hybrid.
