Chapter 7. Mitral Valve

The evaluation of valvular heart disease has become increasingly dependent on echocardiography. Since its introduction to the operating room, transesophageal echocardiography (TEE) has played a major role in surgical decision making and anesthetic management of patients undergoing mitral valve surgery. Mitral valve replacement has its own implications and is not free of risk, leading surgeons to develop techniques for mitral valve repair, which are becoming more and more intricate as our understanding of valve function expands. Recent outcome literature indicates strong support for repair relative to replacement in patients with organic, nonischemic mitral valve pathology,1 and the role of intraoperative TEE in mitral valve repair2 and replacement surgery3 is well established. A good knowledge of mitral valve anatomy and its assessment by TEE is therefore vital to any successful intraoperative echocardiographer.

The mitral valve is located between the left atrium and the left ventricle and allows unidirectional flow of blood towards the left ventricle, prevents backward flow of blood into the left atrium during left ventricular systole, and allows unobstructed flow of blood to the left ventricle during diastole, maintaining low left atrial pressures. The anterior mitral valve leaflet also forms part of the left ventricular outflow tract and allows for unimpeded left ventricular ejection during systole. For the mitral valve to function normally, it relies on the integrated function of a number of structures, which are collectively referred to as the mitral valvar complex. This complex consists of the anterior (aortic) and posterior (mural) leaflets, together with the annulus, chordae tendineae, papillary muscles, and left ventricle. Abnormalities of any of these structures can result in valvular dysfunction, and should therefore be included in the comprehensive evaluation of the mitral valve.4

Mitral Valve Leaflets and Commissures

Two leaflets separated by two commissural areas cover the mitral valve area during systole. The anterior or aortic leaflet is situated anteriorly and to the right, adjacent to and in continuum with the aortic valve, and occupies approximately one-third of the annular circumference. Both the aortic and mitral valves contribute to the so-called fibrous skeleton of the heart, and the connection between the two is sometimes described as the aortomitral continuity. The posterior or mural leaflet occupies the remaining two-thirds of the annular circumference and is much narrower than the anterior leaflet. Although the posterior leaflet appears to have less height than the anterior leaflet, they are similar in surface area. The posterior leaflet is subdivided into three scallops by clefts. The scallop adjacent the anterolateral commissure is named P1, with P3 situated on the other end of the posterior leaflet in close relation to the posteromedial commissure. P2 is the middle scallop in between P1 and P3. Even though the anterior leaflet is not anatomically divided into scallops, the areas opposing the posterior leaflet are correspondingly referred to as the A1, A2, and A3 segments (Figure 7–1).5 Closure of the valve requires apposition and coaptation of the two leaflets, and this occurs along a single semilunar coaptation line. The ends of this coaptation line do not extend all the way to the annulus and are known as commissures. These commissural areas are situated anterolaterally and posteromedially, in relation to their papillary muscles.

Mitral Annulus

Anatomically, the annulus is formed by lateral extensions of fibroelastic tissue, originating from the left and right fibrous trigones. The amount of fibrous tissue decreases towards the inferolateral aspect of the annulus until only myocardium is present, making the inferolateral annulus most susceptible to dilatation. The aortomitral fibrous continuity, another area where the annulus is not well defined, is situated between the two trigones. Left atrial implantation serves as an indicator of the mitral annulus in this region. Undulations in the mitral annulus results in a saddle shape, with the commissural areas located more towards the ventricle and the intertrigonal and posterolateral areas located more towards the left atrium. The annulus is oval shaped, with the intercommissural (intertrough) distance greater than the aortic to mural (interpeak) distance. The valve is slightly tilted in the chest, with the anterior part superior to the more inferiorly positioned inferolateral part.

Papillary Muscles and Chordae Tendineae

The subvalvular apparatus consists of two papillary muscles supporting the mitral valve leaflets by means of multiple chordae tendineae. The posteromedial papillary muscle is found in close relation to the posteromedial commissure and the interventricular septum. In the case of the mitral valve, there is no direct leaflet connection to the interventricular septum as occurs with the tricuspid valve septal leaflet. This is a distinguishing feature allowing identification of the tricuspid or mitral valve where transposition is suspected. Blood supply to the posteromedial papillary muscle is usually provided by a single coronary artery. Depending on dominance of the circulation, it can be either a branch from the posterior descending artery, or a branch from the obtuse marginal artery. The anterolateral papillary muscle is found in relation to the anterolateral commissure and receives blood supply from both the left anterior descending artery via the first marginal artery, and from the circumflex artery via the first obtuse marginal artery. This dual supply makes dysfunction of the anterolateral papillary muscle less likely.6

Primary chordae tendineae stretch from the papillary muscles and attach to the tips of the mitral valve leaflets. Secondary and tertiary chordae also attach to the body and base of the leaflets, respectively. Separate chordae also originate from the left ventricular free wall and attach to the ventricular surface of the posterior leaflet, in particular. During ventricular systole, contraction of the papillary muscles and left ventricular free wall therefore prevents the mitral valve leaflets from prolapsing into the left atrium. Dysfunction of the papillary muscles or chordae can cause mitral valve dysfunction by either allowing excessive motion of the leaflets or by restricting movement of the leaflets and thus preventing proper coaptation.

Left Ventricular Myocardium

The left ventricular myocardium determines the position of the papillary muscles relative to the mitral coaptation point. Left ventricular dilatation alters the spatial relation of the papillary muscles and attachment of tertiary chordae to the leaflets, thus moving the coaptation point deeper into the ventricle. The result is tethering of the leaflets with inadequate coaptation and valvular dysfunction.

Left Atrium

The role of the left atrium in normal mitral valve function is not clearly defined. However, left atrial tissue is continuous with the mural leaflet and may potentially interfere with normal leaflet motion when left atrial dilatation occurs.7 The atrial attachment to the aortomitral fibrous continuity is also the hinge point of the aortic leaflet, and atrial dilatation may therefore affect the function of the aortic leaflet.

Complete and accurate two-dimensional (2D) echocardiographic assessment of mitral valve morphology requires the examiner to obtain multiple tomographic two-dimensional views and mentally reconstruct a three-dimensional interpretation (Figure 7–2). Three-dimensional imaging, when it is available on all ultrasound systems, will make such mental reconstruction unnecessary (Figure 7–3). The following views, included in the American Society of Echocardiography (ASE)/Society of Cardiovascular Anesthesiologists (SCA) guidelines for performing a comprehensive intraoperative TEE exam, allow systematic assessment of the mitral valve.8

Midesophageal Four-Chamber View (ME 4 CH)

This view is achieved by gently retroflexing the probe in the midesophageal position, directing the imaging sector towards the cardiac apex through the mitral valve. In the classical ME 4 CH view, which is obtained at 20° to 30°, the imaging plane transects the mitral valve in an oblique plane relative to the valve commissures, thus showing the A3 segment of the aortic leaflet to the left of the display and the P1 scallop of the posterior leaflet to the right of the display (see Figures 7–2 and 7–3). By withdrawing or anteflexing the probe slightly, the tomographic plane will transect the valve closer to the anterolateral commissure, bringing the left ventricular outflow tract (LVOT) into view, while advancing or retroflexing the probe slightly transects the valve more toward the posteromedial commissure. When the ME 4 CH imaging plane is at 0° (often the five-chamber rather than four-chamber view), the middle part of the aortic leaflet (A2 segment) and the more anterior part of P2 are seen. Any subvalvular or LVOT pathology can be visualized in this view.

Midesophageal Mitral Commissural View (ME COMM)

From the ME 4 CH view, the multiplane angle of the probe is electronically rotated forward to approximately 60°, aligning the tomographic sector with the mitral valvar commissures. In this view, the P1 scallop is viewed to the right of the screen, and the P3 scallop to the left of the image. In the middle will be the A2 segment moving in and out of view as the valve opens and closes (see Figures 7–2 and 7–3). P2 will be behind A2 (into the screen), but is usually not visible unless it is prolapsing. Applying color Doppler imaging to the valve and rotating the probe in small increments allows one to accurately identify the origin of any mitral regurgitation jet.

Midesophageal Two-Chamber View (ME 2 CH)

Further rotation of the multiplane angle to approximately 90° displays this view. Once again, the imaging sector cuts through the mitral valve at an oblique angle relative to the commissures, showing the more anterior parts of the aortic leaflet (A2, A1) to the right of the image and the more posterior parts of the mural leaflet (P3) to the left of the image (see Figures 7–2 and 7–3).

Midesophageal Long-Axis View (ME LAX)

With the multiplane angle between 120° and 140°, the aortic valve should appear in its long axis together with the mitral valve. This imaging plane cuts through the mitral valve perpendicular to the coaptation line, and in diastole clearly demonstrates the aortomitral continuity and the unfolded length/height of A2, together with P2 (see Figures 7–2 and 7–3). Turning the probe to the right will show the more posterior part of the mitral valve (A3/P3), and leftwards the more anterior parts of the mitral valve (A1/P1). Since the midesophageal long-axis view intersects the mitral valve perpendicular to the coaptation line, it is the best view to measure the interpeak distance of the annulus (Figure 7–4) or the diameter of a mitral regurgitant jet vena contracta in systole (Figure 7–5). The left ventricular outflow tract is also clearly visualized to assess any subaortic valve or outflow tract pathology.

Transgastric Two-Chamber View (TG 2 CH)

Advancing the probe into the stomach and rotating the multiplane angle forward to approximately 90° demonstrates this view (Figure 7–6). Here, the subvalvar apparatus can be assessed, with the posteromedial papillary muscle in the near field and the anterolateral papillary muscle in the far field. Chordal pathology can also be identified and located.

Transgastric Basal Short-Axis View

From the transgastric two-chamber view, the probe is slowly withdrawn until the mitral valve is in the middle of the image and perpendicular to the tip of the probe. The multiplane angle is reduced to 0°, and the mitral valve will now be seen in short axis. The anterolateral commissure together with A1/P1 will be in the far field and to the right of the image, while the posteromedial commissure and A3/P3 are in the near field and to the left of the image (Figure 7–7). Although quantification of mitral valve pathology with color Doppler is not possible in this view, it is helpful to identify the origin of mitral regurgitation. One should be careful not to confuse the color jet of aortic regurgitation with a color jet originating from mitral regurgitation.

It is important to complete a 2D evaluation of the mitral valve before color Doppler is applied in order to establish mechanisms of mitral valve disease as well as its hemodynamic consequences. Chamber enlargement and indirect signs of pulmonary hypertension are indicators of severe degrees of mitral valve disease, as well as long-standing pathology.

Doppler Assessment

After a comprehensive 2D examination of the valve, color Doppler is applied to all of the midesophageal views. In order to achieve good temporal resolution, it is necessary to keep the two-dimensional and color Doppler sectors as small as possible, but still big enough to include the whole mitral valve area of interrogation. A frame rate of at least 15 frames per second is considered adequate. With color Doppler the presence of mitral regurgitation (in systole) or mitral stenosis (in diastole) can be demonstrated. Pulsed-wave and continuous-wave Doppler should be applied across the valve to quantify the degree of mitral valve disease severity, and will be discussed below under specific headings.

Three-Dimensional Echocardiography

Considerable experience is usually required to mentally integrate a number of two-dimensional views of the mitral valve into a three-dimensional structure and then present a clear description to the surgeon. The recent introduction of real-time three-dimensional (3D) transesophageal echocardiography into clinical practice is proving to add incremental value in localizing and demonstrating mitral valve pathology during repair procedures.9,10 The spatial and temporal resolution of the currently available matrix array transesophageal transducer allows three-dimensional views of unparalleled quality at acceptable frame rates (see Figure 7–3). A single 3D volume acquisition allows a comprehensive 2D evaluation in any plane extracted from the dataset. It significantly reduces the number of steps required to complete a comprehensive examination of the mitral valve, thus reducing the examination time.11 The feasibility of intraoperative geometric analysis using integrated 3D mitral valve assessment software has been confirmed, providing much greater quantitative assessment of the mitral valve within the operative environment than has ever been possible.12 Postoperatively, it also provides excellent views of both bioprosthetic and mechanical valves and annuloplasty rings or bands (see Chapter 24).13 It is expected that a combined 2D and 3D transesophageal echocardiography examination will in the foreseeable future become routine for preoperative surgical planning and guidance during mitral valve procedures.

Mitral valve prolapse (MVP) is characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. Thickening of the mitral leaflets greater than 5 mm and leaflet displacement greater than 2 mm indicates classic MVP. In severe cases of classic MVP, complications include mitral regurgitation, infective endocarditis, congestive heart failure, and in rare circumstances, cardiac arrest, usually resulting in sudden death. Early studies estimated a prevalence of 38% among healthy teenaged males, but with improved echocardiographic techniques and clear diagnostic criteria, the true prevalence of MVP is estimated at 2% to 3% of the population.14

Mitral regurgitation results from the incomplete closure of the mitral valve leaflets during left ventricular systole, resulting in backflow of blood into the left atrium. The amount of backflow will determine the hemodynamic consequences of the mitral regurgitation and appears to be mostly affected by the area of the regurgitant orifice. Other factors that influence the amount of regurgitation include the duration of systole and the pressure gradient between the left ventricle and atrium.

Normal size and function of the left atrium, left ventricle, mitral annulus, and leaflets is required to ensure a competent mitral valve complex. Dysfunction of any of these components can result in mitral regurgitation. Typically, leaflet motion will be altered in a way to prevent adequate coaptation and apposition. A functional classification of mitral regurgitation was proposed by Carpentier in the 1980s,15 whereby valvular pathology is described in terms of the opening and closing motion of the leaflet (Figure 7–8). This allows a better understanding of the etiology and type of valvular dysfunction. In mitral valve repair, this classification also helps in deciding whether repair is feasible or not and which type of surgical procedure will be best suited for the specific lesion.

Type I lesions are characterized by normal leaflet motion, and mitral regurgitation is caused by annular dilatation or leaflet perforation. The resultant mitral regurgitation jet is usually centrally directed (Figure 7–9A).

Type II lesions result from increased leaflet motion. This results from elongated or ruptured chordae allowing the affected leaflet to move beyond the coaptation point and level of the annulus. The direction of the mitral regurgitation jet is directed away from the pathological leaflet (Figure 7–9B).

Type III lesions are the result of restricted leaflet motion. This category is differentiated into type IIIa and type IIIb lesions. In type IIIa lesions, leaflet motion is restricted during systole and diastole and is usually the consequence of rheumatic heart disease. This type of mitral regurgitation is seldom seen in isolation as the diastolic restriction causes varying degrees of stenosis as well. The usually eccentric mitral regurgitation jet is more likely to be in the direction of the pathological restricted leaflet (Figure 7–9C). When both leaflets are equally involved in the disease process, the jet may be centrally directed. In type IIIb lesions, leaflet motion is restricted during systole and is the result of displacement of either one or both of the papillary muscles, or any segment of the ventricular wall, as found in ischemic mitral regurgitation. The posterior leaflet is typically involved, and the regurgitant jet is directed towards the restricted leaflet. It can also be due to a global ventricular dysfunction as found in dilated cardiomyopathy. In this condition both leaflets are tethered and pulled out of position by the chordae and dilated ventricle, leading to tenting and poor coaptation, with the coaptation point displaced into the ventricle (Figure 7–9D). A type IIIb lesion is a ventricular problem and the leaflets themselves are not abnormal. Type IIIb is also usually accompanied by a dilated annulus.

Abnormalities of the Leaflets

Rheumatic heart disease results in thickening and deformation of the mitral leaflets (Figure 7–10) with subsequent insufficient coaptation (almost always associated with mitral stenosis). Infective endocarditis can result in direct destruction of valvar tissue, preventing closure, or even perforation, of the leaflets. Furthermore, the presence of large vegetations can also interfere with proper closure of the valve.

Abnormalities of the Mitral Annulus

The intercommissural annular dimension (intertrough distance) is greater than the dimension measured perpendicular to the mitral coaptation surface (interpeak distance), resulting in an oval-shaped mitral annulus. Furthermore, the inferolateral mitral annulus is almost devoid of fibrous support and is the area most likely to be involved in annular dilatation. Thus, when annular dilatation occurs, the ratio of interpeak to intertrough distance is altered. The result is an inability of the mitral leaflets to coapt sufficiently to prevent the backflow of blood to the left atrium during systole.

Annular calcification can also result in improper leaflet motion and subsequent mitral regurgitation. Degenerative calcification is accelerated by conditions such as systemic hypertension, aortic stenosis, and diabetes. Intrinsic abnormalities of the fibrous skeleton of the heart, such as is found in patients with Marfan and Hurler syndromes, as well as other connective tissue diseases, may result in accelerated calcification as well as annular dilatation. Patients with hyperparathyroidism secondary to renal disease may suffer from early calcification of the mitral annulus. Annular calcification can also result in mitral stenosis, and mixed valvular disease is common.

The presence of mitral regurgitation of hemodynamic significance results in a volume overload of the left ventricle with subsequent dilatation. During systole this ventricle offloads into the left atrium and therefore experiences a falsely low afterload, resulting in apparent hyperdynamic ventricular function. Ventricular dilatation is often accompanied by mitral annular dilatation, which is a compounding factor in other mechanisms of mitral regurgitation.16 For this reason one will often hear that “mitral valve regurgitation begets mitral valve regurgitation.”

Abnormalities of the Chordae Tendineae

Disruption of chordae leads to excessive motion of the involved mitral leaflet and subsequent regurgitation. This typically presents as a flail leaflet with rather sudden onset of symptoms. Ruptured chordae can result from infective endocarditis, chest trauma, and fibroelastic deficiency of mitral valve tissue. Mitral regurgitation secondary to chord rupture is more likely to be severe (Figure 7–11). Prolongation of the chordae, as occurs in myxomatous degeneration of the mitral valve, results in prolapse of the affected leaflet (Figure 7–12). The onset of symptoms in these patients is typically gradual over time. Certain diseases can result in fibrosis and shortening of the chordae. The result is retraction of the mitral valve leaflets from the coaptation point and restricted motion of leaflets. This typically occurs in rheumatic heart disease where the chordal involvement can be severe.

Abnormalities of the Papillary Muscles

The posteromedial papillary muscle is more prone to ischemic events, as blood is supplied by the terminal part of a single coronary artery in the majority of patients.6 Necrosis of the papillary muscle after myocardial infarction is not uncommon, but acute rupture is a rare occurrence. Ischemic dysfunction of the papillary muscle can result in inadequate leaflet coaptation with mitral regurgitation. Alteration in the papillary muscle structure or its spatial relation to the rest of the mitral valve apparatus, such as occurs in ventricular dilation and remodeling, can also result in restricted motion of especially the posterior leaflet.

Abnormal Left Ventricular Function and Structure

Ventricular dilatation alters the orientation of the papillary muscle relative to the valvular apparatus (Figure 7–13). The chordae arising from the inferolateral free wall to the posterior mitral leaflet is also pulled down, and subsequent tethering of especially the posterior leaflet occurs. This commonly occurs in ventricular dilation secondary to ischemia or dilated cardiomyopathy. Asymmetric hypertrophy of the left ventricle with dynamic left ventricular outflow tract obstruction can also result in mitral regurgitation. Flow phenomena caused by forceful left ventricular ejection through a narrowed left ventricular outflow tract results in systolic anterior motion of the anterior mitral valve leaflet with inadequate coaptation (Figure 7–14).

As evident from the mechanisms discussed above, it is important to assess all parts of the mitral valvar apparatus as more than one mechanism of regurgitation can be present at the same time.

Two-Dimensional Imaging

Dysfunction of any of the components of the mitral valve apparatus can result in mitral regurgitation and should prompt a comprehensive 2D evaluation of the valve. When mitral valve disease is to be addressed by means of surgery, the 2D evaluation of the mechanism of pathology plays an important role in deciding whether either valve repair or replacement is indicated, and in the case of repair, which technique will be more appropriate.17 Mitral regurgitation results in volume overload of the left-sided cardiac chambers with subsequent dilatation.18 The right ventricle and atrium may also be affected secondary to the development of pulmonary hypertension. Chamber dilatation is usually seen in long-standing hemodynamic significant mitral regurgitation, but might not be present in the case of sudden-onset severe mitral regurgitation. When mitral valve morphology is abnormal on 2D examination, the chances of dealing with a more severe degree of mitral regurgitation are much greater than when the valve appears normal. Indications of more severe mitral regurgitation on 2D evaluation include flail leaflets such as in chordal or papillary muscle rupture, severe prolapse as in myxomatous degeneration of the valve, leaflet perforation, or the presence of leaflet tenting with a large coaptation defect.

Doppler Imaging

Color-Flow Doppler

With the aliasing velocity set to between 50 and 60 cm/s and the color gain settings adjusted to eliminate noise, a midesophageal four-chamber view is obtained. Position the color Doppler sector to include the whole of the mitral valve. If mitral regurgitation appears to be present, reduce the size of the Doppler sector to the smallest size that still includes the entire mitral regurgitation jet. This will help to improve temporal resolution by increasing frame rate. After recording a number of cardiac cycles, scroll back and forth and identify the frame where the jet area appears at its biggest. Using the trace function, planimeter the surface area of the regurgitant jet and the surface area of the left atrium. Keep in mind that only the mosaic area of the regurgitation jet should be included when determining jet area. For grading of mitral regurgitation using jet area, see Table 7–1.

In the case of eccentric jets, the greatest surface area may fall outside the tomographic plain imaged and may result in underestimation of the severity of mitral regurgitation. Eccentric wall-hugging jets (Coanda effect) also lead to underestimation of the severity of mitral regurgitation. On the other hand, conditions that cause excessive pressures in the left ventricle such as severe systemic hypertension and aortic stenosis can lead to overestimation of mitral regurgitation due to a very high-velocity jet extending far into the left atrium. For these reasons, it is recommended that jet area not be used as the sole method for quantification of mitral regurgitation.19

Vena Contracta20

Visualize the mitral valve in the ME LAX view and zoom in to optimize image size. With the aliasing velocity (Nyquist limit) set to between 50 and 60 cm/s and color gain settings adjusted to reduce background noise, position the color Doppler sector over the mitral valve and visualize the regurgitant jet. When the tomographic plane is aligned with the regurgitant orifice, color Doppler should display an area of systolic flow convergence proximal to the valve, a color jet into the left atrium, and a narrow neck of color as the jet passes through the regurgitant orifice. This narrowest part as it emerges from the coaptation site of the leaflets is referred to as vena contracta, and its width, measured perpendicular to the direction of regurgitation, correlates well with mitral regurgitation severity determined by means of regurgitant volume and effective regurgitant orifice area. The maximal diameter during any portion of systole is recorded (Figure 7–15). Once again, the color Doppler sector should be kept as small as possible to obtain maximal temporal resolution. Measurement of the vena contracta should be made perpendicular to the coaptation line formed by the anterior and posterior leaflets in order to avoid a false increase in vena contracta from a tangential imaging plane. Thus, the midesophageal long-axis view, which transects the mitral valve perpendicular to the line of coaptation, is the optimal view to measure vena contracta. Repeating the measurement over several cardiac cycles will also increase the accuracy of this method. Vena contracta was proposed to be a load-independent measure of mitral regurgitation, but subsequent data have proven that alterations in afterload can affect the apparent severity in an unpredictable fashion.21 It is therefore recommended that hemodynamic parameters be adjusted during measurement to approximate awake conditions.

Regurgitant Volume, Regurgitant Fraction, and Effective Regurgitant Orifice area

Flow across an incompetent valve is always greater than the effective forward stroke volume. In mitral regurgitation, the difference between forward stroke volume and flow across the mitral valve is equal to regurgitant volume. The effective forward stroke volume can be measured in the left ventricular outflow tract or across the pulmonic valve in the absence of significant regurgitation of the aortic or pulmonic valves.

RVolMitral = SVMV − SVLVOT

SVMV = MV Annulus Area × VTIMV (at the level of the MV annulus)

and

MV Annulus Area = πr2

or, more practically,

(Mitral Annulus Diameter)2 × 0.785

Another method used to calculate the MV annulus area is based on the fact that the mitral valve annulus is elliptical in shape rather than circular. Determination of the area requires that 2 measurements of the mitral annulus are made in perpendicular planes in mid-diastole:

MV Annulus Area = π/4 × AB

A = annular diameter in one plane (cm)

B = annular diameter in a plane perpendicular to plane A (cm)

SVLVOT = LVOT Area × VTILVOT

and

LVOT Area = πr2

or, more practically,

Where SV = Stroke volume

MV = Mitral valve

LVOT = Left ventricular outflow tract

VTI = Velocity-time integral

RF = Regurgitant fraction

RVol = Regurgitant volume

EROA = Effective regurgitant orifice area

MR = Mitral regurgitation

The result must be carefully interpreted because a small operator error in measurement will have a major impact on the squared calculation. For quantitative parameters of mitral regurgitation as determined through the above formulae, refer to Table 7–1.

Proximal Isovelocity Surface Area (Pisa)22

In mitral regurgitation, flow accelerates when approaching the regurgitant orifice. This results in concentric hemispheric shells of increasing velocity as the valve is approached. The area of one such hemisphere is referred to as proximal isovelocity surface area (Figure 7–16). By applying color Doppler to the mitral valve in the midesophageal views, the regurgitant jet can be displayed. As determined by convention, flow towards the mitral valve in the ME LAX view will be displayed as differing intensities of red. When the Nyquist limit is reached, as invariably happens with high velocities achieved in mitral regurgitation, the direction of flow apparently reverses, a phenomenon referred to as aliasing. This apparent reversal is not a true reversal, but rather an inability to measure high velocities. By adjusting the baseline of the color Doppler scale upwards (in the direction of regurgitant flow), the velocity at which aliasing will occur can be adjusted in order to alter the radius of the aliasing hemisphere. It is recommended that the color Doppler baseline be adjusted in order to achieve an aliasing contour with a radius of 11 to 15 mm. Smaller radii result in flattening of the aliasing hemisphere and larger radii result in a cone-shaped aliasing contour.23 The radius of the hemisphere should be measured from the narrowest part of the jet to the contour where aliasing occurs first, and the velocity of blood at the aliasing contour is obtained from the top of the color Doppler scale (see Figure 7–16). The area of the hemisphere is then calculated with the following formula:

Surface Area of Hemisphere (cm2) = 2πr2

where π = 3.14 and r is the radius of the aliasing contour, measured from the narrowest part of the color jet.

The flow at the surface area where aliasing occurs can then be calculated using the following formula:

2πr2 × Va

where Va is aliasing velocity from the top of the color legend.

The maximal isovelocity surface area should occur at the instant of maximal velocity through the regurgitant orifice. This can be measured by applying continuous-wave Doppler to the regurgitant jet and measuring the peak velocity (Figure 7–17). The principle of conservation of mass states that flow in a closed system should be equal at all points; therefore, flow rate at the effective regurgitant orifice area (EROA) should equal the flow rate at any given isovelocity surface area. Thus, the effective regurgitant orifice area can be calculated by the following equation:

where r is the radius of the first contour of aliasing, Va is the aliasing velocity, EROA is the effective regurgitant orifice area, and Vmax is the maximal regurgitant velocity obtained with continuous-wave (CW) Doppler.

Once the effective regurgitant orifice area has been determined, regurgitant volume can also be calculated by using the velocity-time integral of the mitral valve regurgitant jet.

RVol = EROA × VTIMitral Regurgitant Jet

where RVol is the regurgitant volume and VTIMitral Regurgitant Jet is the velocity-time integral of the mitral regurgitant jet as measured with CW Doppler trace.

The examiner should keep in mind that the proximal isovelocity surface area method assumes a flat surface area proximal to the regurgitant orifice. In the case of an angled ventricular surface area of the mitral valve, a correction factor should be used to improve the accuracy of this method. The effective regurgitant orifice area should be multiplied by α/180, where α is the angle of the proximal converging surfaces (Figure 7–18).

In spite of relatively low frame rates, 3D color Doppler imaging allows for a more accurate determination of the proximal isovelocity surface area (Figure 7–19).24 For instance, in functional mitral regurgitation the proximal isovelocity surface area is not hemispherical but a hemiellipsoid. Three-dimensional color Doppler may avoid underestimation of severity of mitral disease using the proximal isovelocity surface area method.

Pulmonary Venous Flow Patterns

Pulsed-wave (PW) Doppler can be used to assess pulmonary venous flow patterns in order to quantify mitral valve regurgitation. In order to visualize the left upper pulmonary vein, the probe is pulled back and turned to the left from the midesophageal four-chamber view until the left atrial appendage is observed. The left upper pulmonary vein will be superior and posterior to the left atrial appendage, and parallel alignment for Doppler analysis could be optimized by rotating the multiplane angle forward to between 20° and 60°. The right upper pulmonary vein can be visualized by obtaining the bicaval view and then rotating the probe towards the right, beyond the aortic root. Slight withdrawal of the probe will allow visualization of the right upper pulmonary vein. Placement of the color Doppler cursor over the pulmonary veins showing flow predominantly towards the probe will help to correctly identify these vessels. Pulmonary venous flow patterns are obtained by placing the cursor of the pulsed-wave Doppler approximately 1 cm into the pulmonary vein under interrogation.

A normal pulmonary venous flow pattern has a large forward systolic component (S-wave), a slightly smaller forward diastolic component (D-wave), and a small reversed component (A-wave) caused by atrial contraction. Should reversal of the systolic component occur, severe mitral regurgitation can be diagnosed with a specificity of 100% and sensitivity of 90% (Figure 7–20).25 However, systolic blunting of flow (S < D), as seen with atrial fibrillation or diastolic dysfunction, is diagnostic only of an elevation in left atrial pressure.26 In the case of severe eccentric mitral regurgitation, the wall-hugging jet may cause systolic flow reversal in only some of the pulmonary veins. It is therefore important to assess pulmonary venous flow in both left- and right-sided pulmonary veins.

Other Doppler Measures for Determining MR Severity

Pulsed-wave Doppler assessment of transmitral inflow patterns can also aid in the grading of mitral regurgitation. In the midesophageal four-chamber view, the pulsed-wave Doppler cursor should be positioned at the level of the leaflet tips during ventricular filling. A spectral Doppler trace of the transmitral inflow pattern should then be recorded. Large regurgitant volumes such as in severe mitral regurgitation result in increased left atrial pressures at the end of systole. The subsequent high diastolic gradient between left atrium and left ventricle results in an E-wave dominant inflow pattern, with the E-wave velocity typically exceeding 1.2 m/s.27,28 In the case of the transmitral inflow pattern being dominated by the A-wave, severe mitral regurgitation can be excluded.28

Continuous-wave (CW) Doppler interrogation of the mitral regurgitant jet also contributes to the grading of mitral regurgitation. The normal spectral Doppler trace of lesser degrees of mitral regurgitation is parabolic in shape and follows the pressure gradient between the left ventricle and left atrium during systole. Large regurgitant volumes result in a rise in the left atrial pressure during systole and also results in an inability of the left ventricle to achieve normal peak systolic pressures. The resultant decrease in pressure gradient between the left ventricle and atrium causes an early peaking, truncated spectral Doppler trace seen in severe mitral regurgitation (Figure 7–21). The quality of spectral Doppler trace is also helpful. In mild mitral regurgitation the jet is faint, but in severe mitral regurgitation a very dense spectral Doppler trace can be obtained. A faint trace results from small numbers of red blood cells passing through the regurgitant orifice, but large regurgitant volumes cause a dense representation of the jet.27

When grading mitral regurgitation with TEE under general anesthesia, one should consider the effect of altered loading conditions on the circulation and the effect it will have on the indices used to grade mitral regurgitation. Reduction in ventricular filling, systemic vascular resistance, and blood pressure typically occurs in anesthetized patients and can decrease the apparent degree of mitral regurgitation compared to preoperative assessments. In order to gain more reliable information it may be necessary to simulate awake loading conditions by maintaining preload or increasing afterload through the administration of a vasopressor.29 Cancellation of mitral valve surgery based on intraoperative findings after preoperative assessment indicated a need for surgery should therefore be made with great caution.

The normal mitral valve area is 4 to 5 cm2. Reduction of the mitral valve area to less than 2.5 cm2 requires an increase in the atrioventricular pressure gradient to maintain an adequate cardiac output and often marks the onset of symptoms during exercise.30 An increase in left atrial pressure results in atrial enlargement and eventually the onset of atrial dysrhythmias, uaually atrial fibrillation.31 New-onset atrial fibrillation typically leads to an acute worsening of symptoms as a result of loss of atrial contribution to left ventricular filling and the rapid ventricular rates. Elevated left atrial pressures also result in pulmonary hypertension and eventually alterations in right ventricular function and tricuspid regurgitation.32 As mitral stenosis progresses further, the presence of low cardiac output and atrial fibrillation is a common cause of left atrial thrombi and embolic events (Figure 7–22). Echocardiographic evaluation of patients with mitral stenosis should therefore aim to exclude the presence of intracardiac thrombi, especially when there is a history of embolic events.33 In rheumatic mitral stenosis, left ventricular function can be reduced secondary to scarring of the basal inferolateral wall of the ventricle and by impaired diastolic function in patients with pulmonary hypertension as a consequence of septal displacement.34 Acute attacks of rheumatic heart disease can result in a pancarditis with subsequent ventricular dysfunction.

The most common cause of mitral stenosis is rheumatic heart disease.35 Progressive inflammatory reaction in valve tissue results in thickening of the leaflet tips and fusion of anterior and posterior leaflets in the commissural areas, with subsequent reduction in valve opening. In long-standing rheumatic heart disease or after recurrent episodes, varying degrees of thickening and calcification of the leaflet bodies and bases can also occur. Chordae tendineae are typically thickened and shortened, leading to reduced movement of the mitral leaflets. Mitral regurgitation commonly occurs with rheumatic mitral stenosis.

Degenerative calcification of the mitral annulus is a rare cause of mitral stenosis and mostly occurs in the presence of other diseases that accelerate calcification. These diseases include certain connective tissue abnormalities, hyperparathyroidism, systemic lupus erythematosis, rheumatoid arthritis, systemic carcinoid disease, amyloid deposition, mediastinal radiation therapy, systemic hypertension, and aortic stenosis.

Congenital mitral stenosis presents in childhood and is rarely seen. One rare congenital anomaly responsible for mitral stenosis is a parachute mitral valve. In this condition, all the chordae originate from a single papillary muscle, and mitral stenosis is the result of impaired leaflet motion during diastole.36 Other developmental anomalies, such as cor triatriatum or a supravalvular membrane, can also simulate mitral stenosis even though the mitral valve apparatus is usually normal.

Atrial myxoma, an intracardiac tumor, typically causes left ventricular inflow obstruction, and the patient may present with intermittent signs of mitral stenosis.

Two-Dimensional Imaging

In early rheumatic mitral stenosis, thickening of the leaflet tips is commonly seen while the bases of the leaflets are still pliable. This results in bowing of the leaflets during diastole, which gives a typical hockey stick appearance to the anterior mitral leaflet (see Figure 7–10). As the disease process progresses, calcification of the leaflets and annulus becomes apparent and involvement of the subvalvular apparatus can be seen in the transgastric two-chamber view. The chordae tendineae may be thickened, calcified, and shortened. These pathological changes of the mitral valve apparatus pose important limitations on the suitability of certain interventions to address mitral stenosis. As a consequence, various scoring systems have been proposed to grade severity and aid selection of the most appropriate intervention. Among others, the Wilkins and Cormier scores are commonly used to predict the potential success of closed mitral commissurotomy.37,38

In the transgastric mitral valve short-axis view, mitral valve area can be determined by means of planimetry. This method shows good correlation with the actual mitral valve area as measured on excised valves when used in transthoracic echocardiography.39 However, the fact that the mitral valve is cone shaped during diastole could lead to inaccuracies in measurement of mitral valve area by means of planimetry. The tomographic plane should therefore be carefully aligned with the mitral valve orifice, and mitral valve area planimetry should be performed at the level of the leaflet tips. The lowest gain settings to allow visualization of the whole mitral valve area should be selected to avoid underestimation. For grading of mitral stenosis severity based on mitral valve area, refer to Table 7–2.

Left atrial enlargement occurs as a consequence of the increased left atrial pressure in mitral stenosis. With transesophageal echocardiography, left atrial size can be assessed in the midesophageal long-axis or four-chamber views; however, left atrial measurements have been validated only in the parasternal long-axis view on transthoracic echocardiography.40 In the presence of left atrial enlargement and especially atrial fibrillation, echocardiographic evaluation of patients with mitral stenosis should aim to exclude the presence of intracardiac thrombi (Figure 7–23). The presence of spontaneous echo contrast should also be noted, as this indicates sluggish flow with a very high risk for the development of thrombi.41 Finally, in the midesophageal four-chamber view, bowing of the interatrial septum towards the right is an indication of elevated left atrial pressures.

Significant long-standing mitral stenosis initially results in pulmonary venous hypertension and subsequently pulmonary arterial hypertension. This is followed by right ventricular hypertrophy and right ventricular and atrial enlargement. In the presence of functional tricuspid regurgitation, continuous-wave Doppler of the tricuspid regurgitant jet can be used to calculate systolic right ventricular and pulmonary artery pressures. Acute right ventricular pressure overload with an under-filled left ventricle can cause the interventricular septum to move towards the left, resulting in a D-shaped appearance of the left ventricle in the transgastric midpapillary short-axis view (Figure 7–24). The presence of pulmonary hypertension is an important consideration in the management of mitral stenosis. The degree of pulmonary hypertension, however, helps little in the determination of mitral valve area, as a wide range of pulmonary pressures can be found for the same degree of mitral stenosis.42

Rheumatic heart disease seldom affects the mitral valve only. The aortic and tricuspid valves can also be affected, and careful examination of these valves is indicated.43 Furthermore, structurally abnormal valves are predisposed to infective endocarditis. Affected valves should therefore be carefully examined for the presence of vegetations and signs of infection.44

Doppler Measurements

Pressure Gradient

Left atrial pressure increases as mitral stenosis progresses. The result is an increase in transvalvular pressure gradient with a subsequent increase in flow velocity across the mitral valve. This velocity can be used to calculate the pressure drop from left atrium to left ventricle by applying the simplified Bernoulli equation.

ΔP = 4v2

where ΔP is the pressure gradient and v is the velocity.

In significant mitral stenosis, velocities resulting from the pressure gradient are often higher than what can be recorded with pulsed-wave Doppler, and therefore continuous-wave Doppler is used to ensure that the accurate maximum velocity is measured. In the midesophageal long-axis view that allows best alignment with direction of transmitral inflow, the continuous-wave Doppler cursor is applied across the mitral valve and a spectral Doppler trace is recorded with sweep speed set to 75 cm/s or more. Increasing sweep speed improves visual discrimination between 2 points and thus, improves accuracy of measurements. In severely deformed valves, the use of color Doppler imaging will help to identify the position and direction of mitral valve inflow. A single spectral Doppler profile is selected, and the trace function used to follow the outline from the beginning of the E-wave to the end of the A-wave. Automated software available on most ultrasound systems will calculate maximum velocity, velocity-time integral, and mean and peak gradients (Figure 7–25). For grading of mitral stenosis according to pressure gradients, refer to Table 7–2. In a patient with atrial fibrillation, the spectral Doppler profile should be traced in five cardiac cycles where the heart rate is close to being regular to obtain an average transvalvular gradient.45

Situations that result in alterations of cardiac output will affect flow across the valve and hence the measured pressure gradient. Increases in cardiac output will result in an increased flow across the valve and an increase in calculated gradient, whereas decrease in cardiac output will result in the opposite. Other factors that influence measured gradients include heart rate and the presence of severe mitral regurgitation.46

Mitral Valve Area by Pressure Half Time Method47

Diastole causes the left ventricular pressure to drop below left atrial pressure. This pressure gradient opens the mitral valve and causes rapid early left ventricular filling, resulting in a relative quick decline in flow as the left atrial pressure becomes equal to left ventricular pressure. This mid-diastolic cessation of flow is referred to as diastases. In the presence of mitral stenosis, left ventricular filling occurs slower due to obstruction caused by the stenotic valve, and the pressure gradient between left atrium and left ventricle persists during diastole. The more severe the stenosis, the longer it takes for transmitral pressure gradient and flow velocities to decline.

To assess the time required for transmitral gradient to decline, a spectral Doppler trace of the transmitral inflow velocities should be obtained. In this instance, the caliper function is selected and the first cursor is placed on the peak velocity measured by spectral Doppler trace. The second cursor is positioned on the slope of the early velocity, immediately before the onset of the A-wave, resulting in a line connecting the two cursors, which represents the deceleration slope (see Figure 7–25). This deceleration slope may in some cases appear as two slopes, with the initial decline being more rapid than the decline during the latter part of diastole. In these cases it is recommended that the pressure decline slope during the latter part of diastole be used.48 The ultrasound system will automatically calculate the time it takes for the pressure gradient to decline to half of what it was at the beginning of diastole, a variable known as the pressure half time (P1/2t) that is inversely related to mitral valve area. Mitral valve area (MVA) can be calculated from the P1/2t with the following equation:

MVA (cm2) = 220/P1/2t

The accuracy of the P1/2t method for determining mitral valve area also depends on the compliance of the left atrium and the left ventricle. Conditions that result in altered compliance of either chamber, such as left ventricular diastolic dysfunction, will make the mitral valve area calculated from the P1/2t inaccurate.45 The presence of aortic regurgitation may have an influence on the calculated mitral valve area by this method as well. If an aortic regurgitation jet is directed onto the ventricular surface of the anterior mitral valve leaflet, the opening of the mitral valve may be limited, with subsequent overestimation of mitral stenosis severity. On the other hand, significant aortic regurgitation will result in a more rapid rise in left ventricular pressure than can solely be attributed to filling through the mitral valve. The decline in pressure gradient between left ventricle and left atrium will be more rapid, and hence result in underestimation of the severity of mitral stenosis.49,50

An irregular heart rate as in atrial fibrillation may result in significant differences in P1/2t mitral valve area determinations when different beats are traced. Therefore, similar to when transvalvular pressure gradients are obtained, it is recommended that P1/2t be measured in a number of cardiac cycles and averaged.51 Rapid heart rates result in fusion of the A- and E-waves, making it hard to accurately confirm the deceleration slope with the caliper function.

Using the P1/2t method for determining mitral valve area has only been validated in natural valves. In the case of degenerate or malfunctioning bioprosthetic or mechanical valves, use of this method results in inaccurate grading of inflow obstruction.52

Mitral Valve Area by Deceleration Time53

Similar to the P1/2t method described above, the time that it would take for the gradient across a stenotic mitral valve to decline to zero can also be used to determine mitral valve area. This measurement is referred to as deceleration time. By using the caliper function in the same fashion as described for the P1/2t method, software integrated into the ultrasound systems will calculate the deceleration time. This measurement, however, requires the second cursor to be placed on the baseline in such a way that the line connecting the two cursors runs along the slope of the early velocity before the A-wave. An inverse ratio between mitral valve area and deceleration time exists, and mitral valve area can be calculated by the following equation:

MVA (cm2) = 759/DT(ms)

The limitations to using this measurement are the same as described above for P1/2t.

Mitral Valve Area by Continuity Equation54

In a closed system, flow (cm3/s) will be equal in all parts at any given time. For this to be valid, velocity of flow has to increase in areas where the cross-sectional area of the system is reduced. This principle is referred to as the conservation of flow and is mathematically represented by the continuity equation (Figure 7–26).

In mitral stenosis, the continuity equation can be used in two ways to calculate mitral valve area. The first method requires transmitral flow to be equal to left ventricular stroke volume; in other words, there can be no aortic or mitral regurgitation.54 As a second method, the proximal isovelocity surface area can be used. This method is unaffected by the presence of valvular regurgitation.

With competent left-sided valves and mitral stenosis, the continuity equation is applied as follows:

1. According to the conservation of flow principle, forward stroke volume (SV) in the left ventricular outflow tract (LVOT) will be equal to the forward stroke volume across the mitral valve.

2. Forward stroke volume in the left ventricular outflow tract is calculated as follows: In deep transgastric long-axis or transgastric long-axis views, pulsed-wave Doppler is applied to obtain a spectral Doppler trace of left ventricular outflow tract flow velocity. By using the trace function, a single spectral Doppler envelope is outlined and velocity-time integral (VTI; in cm) is obtained. In the midesophageal aortic valve long-axis view, left ventricular outflow tract diameter is measured during ejection, ie, with open aortic valve. This measurement should be made in systole within 1 cm from the coaptation point of aortic valve leaflets. Accuracy is improved by using zoom to enlarge the image as much as possible, and by performing more than one measurement and using the largest obtained. Stroke volume can then be calculated as follows:

   

   Where π = 3.14

   LVOT = Left ventricular outflow tract

   VTI = Velocity-time integral of the LVOT in centimeters

   d = Diameter of the LVOT, and the assumption is made that the LVOT cross-sectional area is circular

3. Next, in the midesophageal four-chamber view, continuous-wave Doppler is placed through the mitral valve opening with the sweep speed set to 75mm/s or more. A spectral Doppler trace of transmitral inflow is recorded. Again the trace function is used to obtain the velocity-time integral of transmitral inflow, and measurement of several cardiac cycles is averaged to improve accuracy. The continuity equation is then used to calculate mitral valve area:

   SVLVOT = SVTransmitral

   where

   0.785 × D2LVOT × VTILVOT = MVA × VTIMV

   Thus,

   

   Where DLVOT = Left ventricular outflow tract diameter

   MVA = Mitral valve area

   VTI = Velocity-time integral

   SV = Stroke volume

   MV = Mitral valve

To use this method accurately, one should consider beat-to-beat variation in stroke volume with ventilation. Various measurements made during different cardiac cycles may result in inaccurate calculations. To reduce error, a number of measurements should be averaged, and if possible, ventilation stopped when spectral Doppler tracings are recorded. Arrhythmias such as atrial fibrillation can result in significant differences in stroke volume from beat to beat, and will have a significant impact on the mitral valve area determined by this method. Furthermore, forward flow is always greater across incompetent valves than forward flow across competent valves. This discrepancy makes the above-described method inappropriate in mixed mitral valve disease or in aortic regurgitation.45

The second application of continuity equation uses the proximal isovelocity surface area method55 in a similar way as that described for determination of effective regurgitant orifice area in mitral regurgitation (Figure 7–27A). The mitral valve is visualized in midesophageal four-chamber view, and color Doppler sector is applied over the mitral valve. The transducer and color Doppler sector are oriented to display maximum transmitral flow velocity. The baseline on the color scale is adjusted downward towards the direction of flow. A Nyquist limit of 21 cm/s is recommended as mitral valve area is progressively underestimated with higher aliasing velocities.56 Flow away from the transducer appears blue by convention, but as the accelerating color hemispheres reach aliasing velocity, the color will alias and change to yellow. The hemisphere radius is measured from the aliasing (blue to yellow) contour to the narrowest part of mitral valve inflow. Using the color-suppress mode will help to accurately determine the narrowest part of mitral valve opening. Once again, it is important to accurately determine the hemispheric radius as this value is squared during calculation, resulting in exaggeration of any errors. Where temporal resolution (frame rate) is low, the biggest radius over a number of cardiac cycles should be measured. Continuous-wave Doppler is then applied across the valve to obtain a spectral Doppler trace of the transmitral inflow and the maximum velocity is measured. Mitral valve area can be calculated as follows:

Where PISA = Proximal isovelocity surface area

r = Radius of proximal isovelocity contour

Va = Aliasing velocity obtained from the bottom of the color Doppler scale

Vmax = Maximum velocity measured across mitral valve during diastole

Since the maximum PISA radius occurs at the same time as maximum transmitral inflow velocity, and since measurements are commonly not taken during the same cardiac cycle, they should be repeated over several cardiac cycles to increase accuracy. In the presence of atrial fibrillation where stroke volume varies between cardiac cycles, determination of mitral valve area with the proximal isovelocity surface area method is inaccurate. Furthermore, true hemispheric shells require a flat surface area, and since the mitral valve surface area is often not flat, an angle correction factor should be used to improve accuracy (Figure 7–27B). In such cases, the mitral valve area should be multiplied by α/180, where α is the angle subtended by the mitral leaflets.55

Mitral Valve Resistance

Most indices used to quantify the severity of mitral stenosis are influenced by flow across the valve at time of measurement. Therefore, significant variations in measurements can occur in the same patient subsequent to changes in cardiac output. This has led to the use of valve resistance as a flow-independent index of the hemodynamic burden of stenosed valves, as both pressure gradient and flow are incorporated in its calculation.

Where

VR = Valve resistance in dyne.s.cm−5

TMGmean = Mean transmitral pressure gradient

Q = Transmitral flow rate in cm3/s calculated as stroke volume/diastolic filling period

1333 = Conversion factor to metric units

Mitral valve resistance was found to be the best predictor of resting and stressed pulmonary artery pressures in patients with mitral stenosis, when compared with mitral valve area and mean transmitral pressure gradient. This is considered important, as a stressed pulmonary artery pressure is the only independent predictor of exercise capacity.57 It has, however, become apparent that valve resistance does increase as flow increases, and its unpredictability makes the use of this index contentious.58

Three-Dimensional Echocardiographic Assessment of Mitral Stenosis

The introduction of real-time 3D echocardiography (RT3D) adds to the evaluation of mitral stenosis (Figure 7–28). Mitral valve pathology, and especially affected subvalvular apparatus, can be clearly visualized from any desired orientation. Three-dimensional imaging allows for accurate planimetry of the mitral valve area. Good correlation was found between mitral valve area measured by planimetry in 3D imaging and mitral valve area calculated by means of pressure half time and proximal isovelocity surface area.59 There is better inter-observer agreement with RT3D than 2D for the assessment of pre-valvuloplasty Wilkins score. After balloon valvuloplasty, the pressure half time method for calculating mitral valve area becomes inaccurate,60 and RT3D has been shown to be superior in quantifying mitral valve area in the immediate post-valvuloplasty period. During this time there is good correlation between mitral valve area measured with planimetry in 3D and the Gorlin method as applied during cardiac catheterization.61 The large number of recent publications on RT3D imaging reflects the rapidly growing body of knowledge on this exciting new development and the enthusiasm for it (see Chapter 24).