**2. Anatomy and physiology of the aortic root**

Improved imaging and computer simulation has increased our understanding of the aortic root anatomy, structure and function. Aortic root had been described as the vascular tube supporting the aortic valve leaflets and connecting the left ventricular outflow tract inferiorly to the sinotubular junction superiorly [1]. Two thirds of the lower segment (aortic annulus) of the aortic root is attached to the interventricular septum while the remainder is attached to the fibrous part of the anterior mitral valve leaflet [2]. This tubular structure (**Figure 1**) encompasses the aortic valve leaflets, coronary ostia, commissures, interleaflet triangles and the sinuses [1]. All these components link together to act as a single unit. It is now clear, that this is much more than just a passive unit governed by pressure changes across the valve [3, 4]. The geometric relationship of the valve leaflets as well as individual lengths are important for it to work as a single efficient hemodynamic unit [5].

#### **Figure 1.**

*Opened aortic root section. Sinotubular junction is indicated by the open arrows, small arrows indicating the coronary ostia (left and right), broken lines indicating the fibrous skeleton between the aortic and mitral valves. L, R, and N mark the left, right and the non-coronary cusps, respectively [6].*

The dilated portion of the aortic wall between the aortic annulus and sino-tubular junction is known as the sinus of Valsalva. These sinuses are named according to the relationship of the origin of the coronary ostia from the root that is left, right or non-coronary sinuses. The sinuses are labelled corresponding to their coronary ostia. One of the important roles provided by these sinuses is preventing obstruction of the coronary ostia during movement of the aortic valve leaflets against the aortic wall, so that coronary blood flow is maintained [5]. An important function is prevention of ostial obstruction during systole when the aortic valve is open [7]. Generation of Eddy currents during early systole prevents the aortic leaflets from touching the aortic wall [8].

The aortic valve leaflets which are inserted at their bases in a semilunar fashion to the aortic annulus. They allow uni-directional flow of blood from the left ventricle to the aorta. Aortic valve leaflets are variable in size and number, the noncoronary cusp being the largest compared to the left or right aortic valve cusps. The most common variation is the bicuspid aortic valve, which consists of a semi-lunar opening due to the presence of two leaflets, and the commonest deviation from the normal tri-leaflet pattern is the known congenital anomaly called bicuspid aortic valve [9]. The attachment of the curved aortic valve leaflets form the triangular space named as the interleaflet triangles, the apices of these triangles is known as the valve commissures which are at the level of the sinotubular junction [10]. Aortic valve competence depends on the overlap between these adjacent free margins of the leaflets.

The aortic valve annulus represents the ventriculo-aortic junction which is a complex structure and universally accepted term as aortic annulus [9]. The basic attachments of the aortic valve leaflets at the aortic annulus comprise muscular and fibrous parts [5]. The right aortic valve leaflet attaches to both the membranous and the interventricular septa, while the non-coronary leaflet attaches to the membranous septum and the fibrous skeleton of the anterior mitral valve leaflet, and the left aortic valve leaflet attaches to the fibrous skeleton of the anterior mitral valve leaflet and partly to the interventricular septum [9]. Connective tissue disorders that involve the fibrous skeleton of the aortic root lead to alteration in normal geometry. Damage begets further damage leading to significant valve distortion and subsequent clinical sequelae [9].

**37**

*Aortic Root Reconstruction*

than 45 mm [15].

**3.2 Bicuspid aortic valve**

**3.3 Inflammatory etiology**

**3.4 Cystic medial necrosis**

**4. Aortic root aneurysm**

tion of basophilic substances [26].

aorta) is 55 mm or more.

regarding surgery for the ascending aorta [27]:

**3. Aortic root pathology**

**3.1 Connective tissue disorders**

*DOI: http://dx.doi.org/10.5772/intechopen.86034*

Connective tissue disorder is among the most common non-infective etiology of aortic root pathology. Marfan's syndrome, Ehlers-Danlos syndrome and Loeys-Dietz syndrome predominantly involve the elastic aortic root [11–13]. Marfan's syndrome is an autosomal dominant disorder characterized by mutation in the gene encoding for fibrillin-1. It leads to cystic medial necrosis and involves all connective tissue containing high percentages of elastin. Disease is multi-systemic; however aortic dissection remains an important cause of mortality [14]. The probability of aortic emergencies increases significantly when transverse aortic diameters is more

Patients with vascular type of the Ehlers-Danlos syndrome are prone to aortic dissection rather than aneurysm, while patients with Loeys-Dietz syndrome are

Bicuspid aortic valve (BAV) is present in 1–2% of the population; almost 40%

While the inheritance of BAV is not clearly defined, gene sequence defects leading to aortopathy is more prevalent in this population [19]. Degenerative changes in the tunica media with reduced elastin increases risk of dissection these patients [20, 21].

Giant cell arteritis and Takayasu arteritis are rarer causes of aneurysmal dilatation/aortic dissection [22, 23]. While temporal artery involvement is the hallmark of giant cell arteritis, at least 0.15% also had aortic dissection in an autopsy series [22]. Takayasu arteritis on the other hand is an inflammatory disorder that leads to large vessel inflammation characterized by fibrosis and narrowing, which may lead to aneurysmal formation and possible rupture [23]. Corticosteroids are used for acute therapy and surgery is performed once active inflammation subsides [24, 25].

Cystic medial necrosis (CMN) is a pathological term that is characterized by the formation of cyst like lesions in the medial layer of the large arteries with accumula-

The American Association of Thoracic Surgeons present following guidelines

a.Surgical repair should be performed when aortic diameter (root or ascending

b.Surgical repair should be performed when aortic diameter (root or ascending aorta) is 50 mm or more in the presence of certain risk factors such as: root

liable to have aortic aneurysm and dissection at younger age [11, 16, 17].

also have thoracic aortic dilatation at the time of presentation [18].
