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Tirone E. David, M.D.
The aortic root is the anatomic segment between the left ventricle and the ascending aorta. The aortic annulus, the aortic cusps, the aortic sinuses, and the sinotubular junction are the components of the aortic root and they function as a unit. The aortic annulus is a fibrous structure that attaches the aortic root to the left ventricle. It is attached directly to the myocardium in approximately 45% of its circumference and to fibrous structures in the remaining 55%. The aortic annulus has a scalloped shape. Histological examination of the aortic annulus reveals that the aortic root has a fibrous continuity with the anterior leaflet of the mitral valve and membranous septum, and it is attached to muscular septum through fibrous strands. The fibrous tissue that separates the mitral valve from the aortic valve is called intervalvular fibrous body. An important structure immediately below the membranous septum is the bundle of His. The atrioventricular node lies in the floor of the right atrium between the tricuspid annulus and the coronary sinus orifice. This node gives origin to the bundle of His, which travels through the right fibrous trigone along the posterior edge of the membranous septum to the muscular septum. At this point the bundle of His divides into left and right bundle branches, which run sub-endocardially along both sides of the muscular septum.
The normal aortic valve has three cusps. Each cusp has a semilunar shape and has a base and a free margin. The base is attached to the aortic annulus in a crescent fashion. The point where the free margin of a cusp joins its base is the commissure, and the ridge in the aortic wall that lies immediately above the commissures is the sinotubular junction. The spaces contained between the aortic annulus and the sinotubular junction are the aortic sinuses or sinuses of Valsalva. There are three cusps and three sinuses: left cusp and sinus, right cusp and sinus, and non-coronary cusp and sinus. The left main coronary artery arises from the left aortic sinus and the right coronary artery from the right aortic sinus.
The triangular spaces underneath two aortic cusps are part of the left ventricular outflow tract but they are important for aortic valve function. The sub-commissural triangle beneath the right and left aortic cusps is muscular whereas the other two sub-commissural triangles are fibrous.
The normal aortic root has a fairly consistent shape and the sizes of the cusps, the aortic annulus, the aortic sinuses and the sinotubular junction are interdependent. Thus, large cusps have proportionally large annulus, aortic sinus and sinotubular junction. The three aortic cusps often have different sizes in a person, and the right and non-coronary cusps are usually larger than the left cusp. There are, however, certain geometric parameters that are fairly constant among the various components of the aortic root.
The free margin of an aortic cusp extends from one commissure to the other. The length of the free margin of an aortic cusp is approximately 1.5 times the length of its base.
During diastole, the free margins and part of the body of the three cusps touch each other approximately in the center of the aortic root to seal the aortic orifice. Thus, the average length of the free margins of three aortic cusps must exceed the diameter of the sinotubular junction to allow the cusps to coapt centrally and render the aortic valve competent. If a pathological process causes shortening of the length of the free margin of a cusp or if the sinotubular junction dilates, the cusps cannot coapt centrally resulting in aortic insufficiency. If the length of a free margin is elongated, the cusp prolapses, and depending of the degree of prolapse, aortic insufficiency ensues.
The diameter of the aortic annulus is 10% to 20% larger than the diameter of the sinotubular junction of the aortic root in young patients. As the number of elastic fibers in the arterial wall decreases with age, the sinotubular junction dilates, and its diameter tends to become equal to that of the aortic annulus in older patients. Dilation of the aortic annulus pulls the belly of the aortic cusps apart decreasing the coaptation area and eventually causes aortic insufficiency. With dilation of the aortic annulus, the sub-commissural triangles of the non-coronary cusp tend to become more obtuse as the crescent shape of the aortic annulus along its fibrous insertion flattens. The subcommisural triangle beneath the right and left cusps does not change much in patients with annuloaortic ectasia because it is part of the muscular interventricular septum and it is not affected by the connective tissue disorder that causes dilation of the fibrous skeleton of the heart.
The aortic sinuses facilitate closure of the aortic valve by creating eddies currents between the cusps and arterial wall. They also prevent the cusps from occluding the coronary artery orifices during systole, thus guaranteeing myocardial perfusion during the entire cardiac cycle. Isolated dilation of the aortic sinuses does not cause aortic insufficiency. That is why patients with congenital aortic sinus aneurysm can have a competent aortic valve.
The aortic root of young individuals is elastic and very compliant. It expands and contracts during the cardiac cycle. Expansion and contraction of the aortic annulus is heterogeneous probably because of its attachments to contractile myocardium and to fibrous structure such as the membranous septum and intervalvular fibrous body. On the other hand, the expansion and contraction of the sinotubular junction is more uniform. The aortic root also displays some degree of torsion during isovolumic contraction and ejection of the left ventricle. Compliance decreases with aging due to loss of elastic fibers, and the movements of the aortic annulus, cusps, sinuses and sinotubular junction also change.
Pathology
Anatomically normal tricuspid aortic valve may become calcified late in life and cause aortic stenosis (AS). This lesion is referred as dystrophic calcification, senile calcification, or degenerative calcification. The pathogenesis is this lesion is complex and poorly understood, but it appears to be related to inflammation, infiltration of lipoproteins, and ossification. Statins (3-hydroxy-3-methyl-glutamyl coenzyme A reductase inhibitors) may be effective in retarding this process.
Bicuspid aortic valve (BAV) occurs in approximately 1% to 2% of the population, and is the most common aortic valve pathology. BAV may function well and cause no hemodynamic problems until late in life when it becomes calcified and stenotic. Bicuspid aortic valve can also cause AI, AS, and mixed lesions in younger patients. Most BAV have 3 aortic sinuses and the larger one of the two cusps has a raphe instead of a commissure. The right coronary artery is usually non-dominant and small. Patients with BAV and other congenital anomalies of the aortic valve frequently have premature degenerative changes of the media of the aortic root and ascending aorta. These patients are at risk of developing aneurysm and aortic dissection.
Rheumatic aortic valve is still seen in the Western World but largely in immigrants. This disease causes fibrosis, commissural fusion, thickening and contraction of the aortic cusps. It may also calcify in the later stages.
Infective endocarditis of the aortic valve usually occurs in patients with preexisting aortic valve disease, particularly BAV, but it may also occur in patients with normal valves. Infection in the native valve may destroy one or more cusps with consequent AI.
An increasingly more common cause of aortic valve disease is prosthetic and biological valve disease. Mechanical aortic valve may become stenotic because of pannus or thrombosis. Bioprosthetic valves and aortic valve homograft may become stenotic or incompetent because of calcification and/or cusp tear. AI is the usual mode of failure of currently used porcine valves and AS of pericardial valves. Pulmonary autograft (Ross procedure) may become incompetent because of cusp prolapse and/or dilation of the root.
From 1990 to 2004 aortic valve replacement was performed in 5,198 patients at Toronto General Hospital. Table 1 shows the pathology of the aortic valve. Aortic stenosis was present in 2,699 (52%), insufficiency in 1,356 (26%), mixed in 1,065 ((20%) and unrecorded 142 (2,7%). Isolated aortic valve replacement was performed in 4077 (82%) patients and combined with replacement of the ascending aorta in 1124 (18%).
Table 1: Pathology of the aortic valve in operated patients
| Pathology |
Number |
(%) |
| Tricuspid calcific |
1,736 |
(33.4) |
| Bicuspid |
1,547 |
(29.7) |
| Other congenital |
97 |
(1.8) |
| Rheumatic |
570 |
(10.9) |
| Annuloaortic ectasia |
183 |
(3.5) |
| Dissection |
31 |
(0.6) |
| Prosthetic valve disease |
503 |
(9.6) |
| Miscellaneous |
248 |
(4.7) |
| Not recorded |
283 |
(5.4) |
