ETIOLOGY AND MECHANISMS OF AORTIC REGURGITATION
The physiologic functioning of the aortic valve in diastole is dependent on the interplay of several components forming a complex that includes the aortic valve, aortic annulus, sinuses of Valsalva, and the sinotubular junction. The aortic annulus is formed by the basal insertions of the leaflets into the muscle of the left ventricular outflow tract (LVOT) and the fibrosa of the anterior mitral leaflet. The aortic valve leaflets then extend as semilunar structures along the sinuses of Valsalva to end at the sinotubular junction where the commissures are formed and whose diameter is normally 10% to 15% smaller than the diameter of the true aortic annulus (2
). A delineation of the mechanisms of AR is of increasing clinical importance as the mechanism impacts on the surgical approach including determination of suitability for valve repair. A proposed classification system (Table 11.1
) has been advanced that involves three functional mechanisms (Fig. 11.1
AR is due to the enlargement of any of the components of the aortic root or ascending aorta with normal aortic cusp motion, as seen in idiopathic annuloaortic ectasia, ascending aortic aneurysm, Marfan syndrome, aortitis, or Ehlers-Danlos syndrome
(Videos 11.1 and 11.2). Aortic enlargement results in
outward displacement of the commissures and leaflet tethering which leads to incomplete leaflet closure in diastole generally resulting in a central regurgitant orifice and jet. Type 1 AR has been subdivided into sub-types depending on the location of enlargement: type 1A (ascending aorta and sinotubular junction), type 1B (sinuses of Valsalva and sinotubular junction), and type 1C (aortic annulus). Type 1 AR also includes regurgitation due to aortic cusp perforation (type 1D).
TABLE 11.1 Etiology and Mechanisms of Aortic Regurgitation
Type 1: Normal cusp motion
dilatation of ascending aorta and sinotubular junction (STJ) (1A)
dilatation of aortic root at sinus of Valsalva (SOV) and STJ (1B)
dilatation of aortic annulus (1C)
leaflet perforation (1D)
Congenital aortic root abnormalities
Connective tissue disease (Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome)
Bicuspid valve-associated aortopathy
Acquired aortic root abnormalities
Autoimmune disease (systemic lupus erythematosus, ankylosing spondylitis)
Aortitis (syphilitic, Takayasu’s)
Endocarditis (leaflet perforation)
Type 2: Excessive cusp motion (cusp prolapse or flail)
Bicuspid aortic valve disease
Acute aortic dissection
Ventricular septal defect
Type 3: Restricted cusp motion
Bicuspid aortic valve disease
FIGURE 11.1 Examples of the various mechanisms of aortic regurgitation. Type 1: Severe dilatation of the aortic root at the sinuses of Valsalva resulting in incomplete leaflet closure and severe, central aortic regurgitation (top). Type 2: Complete prolapse of the right coronary cusp of a trileaflet aortic valve resulting in highly eccentric, severe aortic regurgitation (middle). Type 3: Severe restriction of heavily calcified aortic valve leaflets in a patient with both severe aortic stenosis and severe aortic regurgitation (bottom).
AR is due to excessive cusp motion from complete or partial prolapse or flail aortic cusp resulting in below the annular non-coaptation plane
(Videos 11.3 and 11.4). Prolapse or flail cusps can occur in the setting of excessive cusp tissue (e.g., bicuspid aortic valve or congenitally elongated cusp), disruption of aortic commissures (e.g., acute aortic dissection), or in the setting of a ventricular septal defect. Type 2 AR results in an eccentric regurgitant jet.
AR is due to restricted leaflet motion and primary cusp damage resulting in poor leaflet coaptation (e.g., calcific degenerative, rheumatic, radiation, or bicuspid valve disease)
(Videos 11.5 and 11.6). Regurgitant jets in type 3 AR may be eccentric or central. The mechanism of AR may also be multifactorial with a single etiology causing AR from more than one mechanism (6
). TEE evaluation has been shown to correlate very highly with surgical findings, and the evaluation of the potential mechanisms of AR should be part of the preoperative echocardiographic evaluation along with AR severity assessment (4
). Lastly, the assessment of the sizes of the components of the aortic root complex should be performed prior to aortic valve surgery (Fig. 11.2
FIGURE 11.2 Mid-esophageal aortic valve long-axis view (top) demonstrating appropriate locations for measuring the aortic annulus (a), sinus of Valsalva (b), sinotubular junction (c), and proximal ascending aorta (d). Three-dimensional multiplanar reconstruction (bottom) demonstrating appropriate way to perform “sinus-to-commissure” aortic root measurements in the aortic root long- and short-axis views. Ao, aorta; LVOT, left ventricular outflow tract; RVOT, right ventricular outflow tract.
HEMODYNAMICS OF AORTIC REGURGITATION
AR represents both an increase in preload and afterload to the left ventricle. The increase in preload is a result of the increased end-diastolic volume resulting from the added regurgitant volume. The increase in afterload is a function of the increased radius of the ventricle. Increase in the end-diastolic radius of a ventricle at any wall thickness increases the wall stress and the force needed to eject blood (law of Laplace). The general response of the ventricle to chronic AR is to dilate and become more compliant to accommodate the extra volume and to hypertrophy to reduce wall stress. The hypertrophy occurs both longitudinally as the heart enlarges (so-called eccentric hypertrophy) and concentrically, as evidenced by its maintaining a “normal” wall thickness as it enlarges. Accordingly, the size of the ventricle is an index of the severity and duration of the regurgitation and should be factored into the assessment of the severity of the lesion.
Acute AR, most commonly due to a tear in the valve secondary to endocarditis, deceleration injury in a motor vehicle accident, or an acute aortic dissection offers a contrasting clinical presentation. Acute AR is one of the least well-tolerated valvular lesions because of the limited ability of the heart to compensate for an acute increase in volume load by the mechanisms mentioned in the preceding text. Consequently, the LV diastolic pressure rises rapidly and is transmitted to the lungs resulting in severe pulmonary congestion. Therefore, in acute AR the chamber is often normal in size but with catastrophic hemodynamic consequences. Diagnosis of significant AR in the setting of heart failure is essential as intra-aortic balloon counterpulsation is contraindicated because diastolic pressure augmentation worsens the regurgitation.
The assessment of the severity of valvular insufficiency is complicated by the potentially dramatic effects of even transient changes in loading conditions and peripheral vascular resistance on Doppler indices of AR severity. Because the operating room environment is one in which a multitude of factors affect both the preload and afterload of the ventricle, the potential impact of these changes must be borne in mind when the severity of a valvular lesion is evaluated. Acute increases in peripheral vascular resistance (e.g., following surgical stimulation or the administration of vasopressors) can increase the apparent degree of valvular
insufficiency by increasing systemic vascular resistance and impeding peripheral runoff. Conversely, vasodilators (e.g., volatile anesthetics, angiotensin-converting enzyme inhibitors and receptor blockers, or calcium channel blockers) reduce peripheral vascular resistance and decrease the apparent degree of insufficiency, both clinically and by Doppler interrogation. The physical properties (e.g., distensibility, elasticity, compliance) of the source (aorta) and recipient (the left ventricle) of regurgitant flow, in addition to the size of the regurgitant orifice and the physical properties of the involved valve, are other dynamic variables that further complicate intraoperative assessment. In fact, some clinicians feel that it is not possible to definitively assess regurgitant lesions in the operating room environment. As a result of the multitude of factors influencing any assessment of the severity of AR, the estimate should be based on an integration of the results of all Doppler approaches providing technically adequate data in any given patient.
ECHOCARDIOGRAPHIC EVALUATION OF THE AORTIC VALVE
The aortic valve can be evaluated by M-mode, two-dimensional (2D), Doppler, and three-dimensional (3D) echocardiographic techniques. Transesophageal 2D echocardiographic imaging of the aortic valve is generally superior to transthoracic imaging because of the improved resolution of the higher frequency TEE probe which makes it possible to delineate the size of regurgitant jets more accurately than with transthoracic techniques. Three-dimensional TEE is playing an emerging role in the assessment of AR and reference is made to current observations utilizing 3D imaging for the assessment of regurgitant severity. Three-dimensional imaging, like 2D imaging, however, shares the limits inherent to all ultrasound techniques determined by the interrelation of sector (volume) size, frame (volume) rate, and depth on image resolution.
When imaging the regurgitant aortic valve and aortic root complex, it is, first, essential to determine the etiology of regurgitation by assessing leaflet structure, motion, and function. Two- and three-dimensional imaging of the aortic root complex should also be performed for precise measurement of dimensions of the aortic annulus, aortic root (at the sinuses of Valsalva), sinotubular junction, and ascending aorta (Fig. 11.2
). Following this structural assessment, a comprehensive Doppler echocardiographic assessment of the aortic valve should follow. In general, the assessment of AR severity involves an integrative approach which utilizes both qualitative and quantitative Doppler techniques. The various approaches to assessing the severity of AR with TEE will be presented in the order of their relative clinical applicability. The American Society of Echocardiography has also published detailed recommendations for the echocardiographic assessment of AR which should be utilized as an important reference (5
The most useful views are generally obtained by starting from the standard mid-esophageal (ME) four-chamber view and changing the angle of interrogation to approximately 45° to obtain the aortic valve short-axis view. In this view, the individual aortic cusps and sinuses are visualized in exquisite detail. Occasionally, the probe may need to be withdrawn or anteflexed to improve the image in this view. The angle of interrogation is then further advanced to 120 to 150° to produce the ME long-axis view of the LVOT, aortic valve, and proximal aorta. Further withdrawal from this position and, occasionally, slight anteflexion with or without rotation can be used to visualize the proximal ascending aorta, while the angle of interrogation can be decreased to 100 or 110° to better visualize the distal tubular ascending aorta. Biplane imaging of the aortic valve is also very useful for simultaneous short- and long-axis imaging of the aortic valve and root. In addition, 3D imaging of the aortic valve can be performed either in the short-axis or long-axis view for the creating of unique en face volume renderings of the aortic valve complex and for multiplanar reconstruction of the regurgitant jet’s vena contracta (VC) area.
Alternatively, but less frequently, good views can be obtained from a deep transgastric (TG) position at an angle close to 0° or greater, subject to individual variation, or from a standard midpapillary TG view at an angle of approximately 120° (TG long-axis view). These approaches have the advantage of aligning the ultrasound beam nearly parallel to the direction of blood flow, which is essential for accurate quantitative Doppler analysis of both the pressure half-time of the regurgitant jet as well as stroke volume. However, far-field beam widening and the greater distances traveled reduces spatial resolution in these views making them a poor choice for visualizing the cross-sectional area of an AR jet immediately below the valve plane. However, they may be the only means of assessing the outflow tract in the presence of a prosthetic mitral valve (MV), which frequently causes acoustic shadowing of the aortic annulus in more standard views, and occasionally, of an aortic prosthesis when its ring obscures the outflow tract image by acoustic shadowing.
The pressure gradient between the regurgitant and recipient chambers in regurgitant valvular lesions is always high and in AR corresponds to the diastolic gradient between the aortic root and the left ventricle. By
the simplified Bernoulli equation, the gradient equals four times the square of the peak jet velocity. In aortic regurgitant lesions, it is the rate of change in pressure gradients that provides clinically useful information unlike the peak velocity measurement used to assess stenotic lesions. While these data are best obtained in the TG views where the Doppler beam is most parallel to flow, fortunately, color Doppler techniques for the assessment of AR can also provide clinically useful information that is, to a significant degree, independent of the beam angle in relation to the regurgitant flow.