The Aortic Valve, Ascending Aorta, Aortic Arch, Descending Thoracic and Abdominal Aortas

The Aortic Valve, Ascending Aorta, Aortic Arch, Descending Thoracic and Abdominal Aortas


The aortic valve region includes the subvalvular area or the left ventricular outflow tract, the aortic annulus, and the attached leaflets and their attachments or commissures. The aortic annulus and the sinus of Valsalva area up to the sinotubular junction constitute the “aortic root.” The aorta from the sinotubular junction to the innominate artery is termed the ascending aorta.

The aortic valve has three leaflets each attached to the aortic annulus and suspended by commissures. The leaflets themselves consist of a more basal area that is thicker than the upper portion of the leaflets and a more superior portion of the leaflets that is thinner than the basal areas. The crescent-shaped areas on the three leaflets define the junction between the stiffer base and the thin coaptation area. This crescent area is called the “lunula” probably because of the half-moon-like shape. The central portion of the leaflets has a small nodular area named the nodes of Arantius. At coaptation, all three of these nodular areas come together in the center of the aorta along with the thin lunular areas to form a tight area of coaptation that does not leak.1

All of these areas are subject to various abnormalities. The subvalvular area can have a thick membranelike area that involves the interventricular septum and also reflects onto the anterior mitral valve leaflet offering obstruction to the left ventricular outflow. The aortic annular area is joined with the mitral annular area forming the mitral aortic curtain. The leaflets are subject to thickening, thinning and disruption all of which have associated functional abnormalities. The aortic root itself can become ectatic, as, for example, in Marfan syndrome,
which distorts the commissural areas and results in dysfunction of the valve. The ascending aorta can become ectatic in association with bicuspid aortic valve or dissected in association with cystic medial necrosis. Congenital abnormalities of the aortic valve include the unicuspid aortic valve, the bicuspid aortic valve, and even the quadricuspid aortic valve. The valve leaflets can become thickened, and stenosis can result. Stenosis of the aorta itself can occur at or just above the sinotubular junction as is seen in Williams syndrome.

Endocarditis can occur and involve the leaflet areas or the annulus or the valve leaflet areas, and function abnormalities follow.

Prosthetic valves offer relief from regurgitation and stenosis. They have their own unique appearance and set of abnormalities.


Understanding the gross anatomy of the aortic valves makes understanding of imaging techniques easier. Several different anatomic abnormalities are illustrated in the following page. The unicuspid valve has no defined cusp regions and little in the way of raphes. The bicuspid valve has two cusps but usually has some identifiable raphe. The trileaflet calcified aortic valve has dense calcification at the base and less calcification at the tips of the leaflets. The leaflets are not fused as they might be in rheumatic disease. The rare quadricuspid aortic valve is illustrated in live 3D stop frame. The following page illustrates some of these valves.

FIGURE 4.1 Calcified unicuspid aortic valve.

FIGURE 4.2 Bicuspid aortic valve with fusion of the LCC and RCC.

FIGURE 4.3 Calcific aortic stenosis in a tricuspid aortic valve.

FIGURE 4.4 Quadricuspid aortic valve.



Aortic stenosis is a common abnormality in older individuals. The leaflets become sclerotic at their bases and progress to calcification and immobility in the basal portions and thickening above the coaptation line to form a stiff, stenotic valve with a high gradient. Valves with this configuration are usually seen in the seventh decade and higher in contrast to stenosis from a congenital bicuspid valve, which presents in general a decade earlier. Once flow through these trileaflet valves is abnormal, a progressive process develops such that the thickening and calcification begets more of the same.

Symptoms fall onto three categories. Syncope, angina pectoris, and dyspnea are cardinal symptoms that signal a poor prognosis. Symptoms may be subtle in that instead of frank congestive heart failure, simple fatigue or mild shortness of breath may be present. Instead of classic angina pectoris, a complaint of slight chest tightness on exertion may be present. Syncope is never a good sign and may have several causes from atrioventricular block to power failure.2

Once symptoms develop, intervention is needed since the prognosis is poor after this point. Intervention is indicated either by surgical replacement or by percutaneous technique. Currently, many different options are available for intervention, and each should be considered carefully in every clinical situation.

Consideration of anatomy and quantification of functional abnormality are key determinants that imaging techniques can define. Cardiac catheterization offers additional information along with definition of the coronary anatomy. Illustrations of these techniques will follow.


In individuals who have abnormal left ventricular function and significant aortic stenosis, the question is often asked as to whether the left ventricle can respond by increasing the stroke volume and the cardiac output. In the echo laboratory, flow reserve is assessed by giving dobutamine and measuring surrogates of cardiac output. The velocity time integral (VTI) of the left ventricular outflow tract can be measured, and increase in this parameter suggests that some degree of flow reserve is present. This concept is used for risk stratification in individuals undergoing surgery. Those with low flow reserve do less well than do those who had flow reserve.4 Flow reserve is defined as an increase in stroke volume (or VTI of the LVOT) by 20% or greater in response to 5 to 20 µg/k/min of dobutamine.

In individuals who have low ejection fraction (<50%) and low mean gradients (<40 mm Hg) and calculated low valve area (<1.0 cm2, <0.6 cm2/m2), evaluation of flow reserve is indicated. In this setting, if an increase in flow is associated with an increase in gradient and the valve area that stays generally the same, severe aortic stenosis is present and flow reserve is present. If stroke volume (VTI of the LVOT) increases by 20%, then flow reserve is present. If an increase flow is associated with only slight increase in gradient and the calculated valve area increases above 1.0 cm2, then pseudostenosis is present, the problem is low flow reserve, and intervention has high risk and less potential benefit.5,6

In addition, there are a group of individuals in whom there is low flow, low gradient, and low valve area and who have normal or preserved EF. These individuals are typically older age, female gender, and associated with systemic arterial hypertension, metabolic syndrome, or diabetes. Concentric remodeling, small cavity size and diastolic dysfunction are also associated with this syndrome. Although the ejection fraction is normal, longitudinal function of the ventricle is abnormal as has been demonstrated by global longitudinal strain.7

Much information is available in the literature concerning these issues including recommendations from the guidelines.8,9


There is a group of individuals who have low flow, low gradient, and preserved ejection fraction that has been puzzling. They have calculated aortic valve areas that are <1.0 cm2 with AVA index <0.6 cm2/m2, low-gradient <40 mm Hg peak and low stroke volume index <35 mL/m2 and EF ≥ 50%. When these findings are present, they often are in older individuals of female gender who have a history of systemic arterial hypertension, diabetes, and metabolic syndrome.11 Often, centric remodeling is present with left ventricular hypertrophy. It has been shown that although circumferential wall motion is normal, the global longitudinal strain values are not normal.12,13 Dobutamine stress echo may be helpful in determining whether pseudo-severe aortic stenosis is present.14,15 The response to intervention is good but may not be great, and transcatheter valve replacement may be a better alternative than surgical treatment.

ACC/AHA Guidelines for Aortic Valve Replacement

The ACC/AHA guidelines are available for application to individuals who have aortic valve stenosis and provide recommendations along with the level of evidence for the recommendation. In addition, information is given concerning the risk/benefit of the indication in various categories. The pathways that lead to the recommendations are in the following figure.

FIGURE 4.13 Currently in the United States, TAVR is approved for use in individuals with high and intermediate risk, and low-risk individuals are under investigation in clinical trial. (Source: Nishimura RA, Otto CM, Bonow RO, et al. 2014 ACC/AHA Guideline for management of patients with valvular heart disease. A report of the ACC/AHA association task force on practice guidelines. J Am Coll Cardiol. 2014;63(22):e57-e185.)


Aortic regurgitation (AR) has a number of etiologies. In contrast to aortic stenosis, the etiologies are not as easily determined. They may be congenital or from other processes such as degeneration from aging, myxomatous changes, infection, trauma, or toxicity from drugs. In addition, they may be associated with abnormalities of the aortic root as seen with Marfan syndrome, aortic dissection, and infectious and inflammatory changes.9,16

AR may be acute or chronic. Acute AR is not tolerated well and might be seen in the setting of dissection, endocarditis, and trauma. In this setting, the left ventricle does not have time to compensate, end-diastolic pressures are high, early mitral valve closure is present sometimes with late diastolic mitral
regurgitation, and pulmonary edema follows. The murmur of AR may be difficult to identify or may be early, low pitched, and rapidly tapering as the diastolic pressures quickly equilibrate. Surgical intervention is needed early in the course of acute AR.

Slowly developing AR allows time for adjustments to be made. The left ventricle remodels by enlarging, a state of compensation occurs with low diastolic pressures and long murmurs, and symptoms may be minimal. Exercise results in shortening of diastole and less aortic regurgitation and therefore may be tolerated better than expected. The murmur of aortic regurgitation is high pitched and long and usually lasts throughout diastole. An Austin Flint rumble may accompany the high-pitched diastolic blow when listening at the apex with the bell of the stethoscope. The timing of surgery is often difficult and requires choosing a time that avoids having a postoperative state in which the valve does not leak yet the myocardium is irreversibly damaged. Guidelines offer recommendations for the timing of surgical intervention.


When the jet of aortic regurgitation is identified, thoughts about etiology should be considered. A quick survey of the adjacent areas should be undertaken. The subvalvular area should be inspected for size and the presence of a membrane or a hypertrophic septum. The aortic annulus should be assessed looking for calcium that might extend up upon the leaflets. The thickness of the leaflets and their mobility should be noted. The size of the sinuses of Valsalva and how they relate to the sinotubular junction have important information as does the size of the ascending aorta above the sinotubular junction. Effacement of the sinotubular junction usually means that it is dilated. In the case of dissecting aortic aneurysm, a dilated ascending aorta is a clue, and searching for extra echoes in the lumen of the aorta that might be oscillating makes the diagnosis of dissection. Focusing on this area when seeing a jet of aortic regurgitation on 2D echocardiography usually makes the correct diagnosis as to etiology. Determination of severity of the aortic regurgitation follows.

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May 5, 2019 | Posted by in CARDIOLOGY | Comments Off on The Aortic Valve, Ascending Aorta, Aortic Arch, Descending Thoracic and Abdominal Aortas
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