Chapter 6. Assessment of Left Ventricular Systolic Function

The assessment of ventricular systolic performance is one of the most important roles of perioperative echocardiography. Ventricular function is a key determinant of cardiac output, and global or regional dysfunction may be present before surgery or develop de novo perioperatively. Patients with coronary disease are particularly at risk. The ability of the echocardiographer to recognize such abnormalities is critical to optimal patient care.

In most clinical settings, the assessment of ventricular systolic function is performed qualitatively and relies heavily on the scanning ability and trained interpretive eye of the echocardiographer.1,2 The ability to accurately assess global and regional ventricular systolic function is one of the most difficult transesophageal echocardiographic (TEE) skills to acquire, and there is no shortcut to supervised training, ideally with access to an independent gold standard. Paradoxically, whereas quantitative methods may require more time for image acquisition and processing, interpretation of the results of such approaches may be relatively straightforward.

All the methods presented in this chapter were first described using transthoracic imaging methods and have been extrapolated to the transesophageal approach. However, it is worth noting that, in some situations, studies directly validating TEE-based applications have not been performed. Since right ventricular (RV) performance is arguably equally important, methods of assessing RV function are discussed in Chapter 13.

A basic understanding of ventricular physiology, in particular pressure-volume relations, is essential to appropriate utilization of available methods of assessing left ventricular (LV) systolic performance.

The cardiac cycle includes three basic phases: ventricular contraction, relaxation, and filling. LV contraction is initiated when, as a result of rising cytosol calcium levels, the actin and myosin filaments increase the degree to which they overlap, resulting in sarcomere shortening. As more and more cardiomyocytes are activated, the left ventricle begins to contract and LV pressure rises. The LV pressure continues to rise until it overcomes the left atrial pressure, at which point the mitral valve closes. During isovolumic contraction, the period between mitral closure and aortic opening, the LV pressure continues to rise. When it exceeds the aortic pressure, the aortic valve opens and blood is ejected. As ejection continues, LV pressure peaks and begins to decrease. When it decreases below the aortic pressure, the aortic valve closes and ejected blood continues to be propagated through the systemic circulation. On a cellular level, calcium is taken up by the sarcoplasmic reticulum, and the myofilaments enter a state of relaxation. Because the mitral and aortic valves are in a closed position, ventricular volume remains constant. This period is known as isovolumic relaxation. With continued relaxation, LV pressure decreases further and the mitral valve opens. LV filling occurs in response to the gradient between the left atrium and the ventricle. This first period of filling is known as the early diastolic filling period. A second, later component occurs after atrial contraction. One method of displaying the phases of the cardiac cycle is by plotting pressure versus volume, thus creating pressure-volume loops (Figure 6–1).

It might appear that indices of systolic performance should focus exclusively on isovolumic contraction and ejection. However, the diastolic filling portion of the pressure-volume loops is also relevant because it addresses the concept of preload, which, as described below, is an important determinant of many of the most commonly used indices of systolic function. A discussion of diastolic function itself may be found in Chapter 12.

Load Dependence

Overall cardiac performance is perhaps best measured by cardiac output or stroke volume (cardiac output/heart rate). These reflect not only ventricular systolic and diastolic function, but also function of the cardiac valves and pericardium. Ventricular systolic performance in turn is a function of intrinsic myocardial contractility and loading conditions. Thus, in discussing measures of ventricular systolic function, it is important to recognize that many of these are load dependent and that only a few are pure indices of myocardial contractility.

Preload is defined as the wall stress at end-diastole or the load the ventricle experiences before contraction is initiated. It is a function of venous return. Afterload is the wall stress during ventricular contraction or the load against which the ventricle ejects. In the absence of mechanical obstruction to ventricular emptying, such as aortic stenosis, it is a function of the systolic blood pressure.

An appreciation of the effect of loading conditions is particularly important in the intraoperative setting, where dynamic changes in loading typically occur. Preoperatively, preload may be reduced due to the patient's fasting status or, perhaps, from aggressive diuresis as treatment for the patient's underlying heart disease. In the noncardiac setting, an acute event associated with blood loss or fluid shifts may have led to hypovolemia. Induction of anesthesia typically is associated with vasodilation that may further reduce preload. In cardiac surgical patients, preload may be reduced after cardiopulmonary bypass if underlying shunts or regurgitant valve lesions have been corrected. This is compounded by the significant vasodilation that is typical of the period immediately after cardiopulmonary bypass.

Abrupt shifts in afterload also typically occur in the perioperative period. Anesthetic agents may reduce afterload, and surgical correction of outflow tract obstruction, such as aortic valve replacement for aortic stenosis, also may have a major effect. These changes do not invalidate the use of load-dependent indices of systolic function, but their effect must be understood if one is to use these measures appropriately.

In simple terms, load dependence refers to the fact that, for the same degree of intrinsic ventricular contractility, the index of systolic function will vary with the degree to which the ventricle is filled and/or the pressure against which it ejects. For example, in the presence of severe mitral regurgitation, a ventricle with normal contractility will have an LV ejection fraction (LVEF; a load-dependent index) that would be considered elevated in a normally loaded heart. Conversely, in the same setting, an LVEF that would be considered normal for a normally loaded heart would, in fact, indicate depressed function. Table 6–1 lists indices of ventricular systolic performance that can be derived with echocardiography.

Chamber Dimensions

The normal shape of the LV is symmetric with two relatively equal short axes and with the long axis running from the base through the mitral annulus to the apex. In the long-axis views, the apex is rounded, so the apical half of the ventricle resembles a hemiellipse. The basal half, however, is more cylindrical.

Initial evaluation of global systolic performance includes measurement of the linear dimensions of the LV cavity. Chamber dilation or hypertrophy often provides the first diagnostic clues of the underlying pathophysiology. The major long-axis measurement of ventricular dimension is made from the apical endocardium to the plane of the mitral valve by using a midesophageal four-chamber view (see Chapter 4). The minor short axis is measured perpendicular to a point one-third of the length of the long axis, moving from the base to the apex. Short-axis dimensions are often easier to obtain accurately with TEE and involve measurement of the end-diastolic anterior-posterior or medial-lateral diameter at the midpapillary level. A diameter larger than 5.4 cm is considered enlarged, but care must be taken to ensure that the papillary muscles are excluded from the line of measurement.

LV wall thickness is best determined from a transgastric long-axis or midpapillary short-axis view using M-mode or two-dimensional (2D) imaging. An end-diastolic wall thickness greater than 1.1 cm is considered increased. Although increased wall thickness is often viewed as being synonymous with left ventricular hypertrophy, this is incorrect, as left ventricular hypertrophy refers to increased left ventricular mass and LV mass may increase without an increase in thickness. LV mass is the total weight of the myocardium and is equal to the product of the volume of the myocardium and the specific density of cardiac muscle. LV mass can be derived from the transgastric midpapillary short-axis view by using a simple geometric cube formula:

LV Mass = {1.04 × [(LVID + PWT + IVST)3 − LVID3]} × 0.8 + 0.6 g

where LVID is the end-diastolic internal dimension (diameter), PWT is the inferolateral (posterior) wall thickness, IVST is the interventricular septal thickness, 1.04 is the specific density of the myocardium, and 0.8 and 0.6 are correction factors. Calculation of LV mass by TEE is comparable with transthoracic echocardiography (TTE); however, TEE measurements are higher by an average of 6 gm/m2 (see Table 4–2).3

Cardiac Output

Cardiac output is the product of stroke volume and heart rate. Whereas right heart catheterization using Swan-Ganz catheters is common in the perioperative period and provides the most widely used method for deriving cardiac output, the thermodilution method may be invalid in the setting of tricuspid regurgitation. Further, the devices are expensive, and placement may be risky in some patients, such as those with right-side cardiac masses. Echocardiographic methods are not used routinely for cardiac output determinations, in large part for logistic reasons. However, they are well validated and may provide an alternative or adjunct to thermodilution methods.

Echocardiographic measures of cardiac output are based on the continuity equation, which states that in the absence of valve dysfunction or shunting, blood flow is constant throughout the heart. Thus, cardiac output is equal to the forward flow across each of the cardiac valves. For a given valve, this assumption will be invalid if there is significant regurgitation or if valve flow reflects the augmented flow of a shunt lesion. Because of the circular and relatively fixed geometry of the ventricular outflow tracts and semilunar valves, and the relative ease of echocardiographic imaging of these sites, stroke volume calculations typically are derived by measuring forward flow across the LV outflow tract,4,5 aortic valve,6,7 or, less commonly, RV outflow tract.8 Although several methods have been proposed for measuring transmitral and transtricuspid flows, the complex dynamic geometry of the orifices of these valves makes them less desirable.

The measurement of the stroke volume starts with the velocity time integral, the integrated area under the curve of a pulsed Doppler spectrum. This represents the length of a column of blood moving through the targeted point in the heart per beat and has units of distance. Multiplying the velocity time integral by the cross-sectional area of the sampling site yields stroke volume. Cross-sectional area is calculated by using the formula for the area of a circle (πr2), where r is the cross-sectional diameter divided by 2. The product of stroke volume and heart rate is cardiac output. Although these methods were originally validated with transthoracic imaging, they have been successfully transposed to the transesophageal approach.

The most widely used method is shown in Figure 6–2. The velocity-time integral is recorded from a deep transgastric view of the LV outflow tract, and the LV outflow tract diameter is measured by using a midesophageal long-axis view.4,5 Ideally, the diameter should be measured at the same location as the velocity-time integral. Measurement of the LV outflow tract diameter from a transgastric view is less desirable because it relies on the lateral resolution of the image rather than on the superior axial resolution used when the measurement is taken from a midesophageal window. Once the stroke volume is calculated (cross-sectional area × velocity-time integral), multiplication by the heart rate yields cardiac output.

Commercially available echocardiographic systems have software packages designed to facilitate these calculations, typically included in the more extended analysis needed for Qp/Qs shunt calculations. However, it must be understood that, although shunts or valve regurgitation do not invalidate this calculation as a measure of flow at the site being interrogated, these flows may no longer simply reflect forward systemic cardiac output. For example, in the presence of aortic regurgitation, LV outflow tract flow will include the forward flow (cardiac output) and the regurgitant flow. Another caveat relates to the presence of valvular stenosis, where prestenotic accelerated flow signals and signals at or distal to the stenosis must be avoided.

A potential alternative to the Doppler imaging approach is to determine LV volumes at end-systole and end-diastole. The difference between the two measurements is the stroke volume (equal to LV end-diastolic volume minus LV end-systolic volume), which, when multiplied by heart rate, yields cardiac output. Echocardiographic methods for determining LV volume are described at greater length in subsequent sections dealing with LVEF.

Ejection Phase Indices

Echocardiographic images provide a series of methods for measuring the reduction in chamber dimension that occurs with systole, typically expressed as:

These ejection phase indices of systolic function include fractional shortening, fractional area change, and ejection fraction.

Fractional Shortening and Velocity of Circumferential Fiber Shortening

The simplest ejection phase index is fractional shortening, defined as:

This method dates back to the M-mode era of transthoracic echocardiography. Although theoretically of value in the symmetrically contracting heart, its ability to provide a sense of global ventricular function is limited when there is regional dysfunction. Thus, its use is waning. For reference, the lower limit of normal when using a transthoracic approach is 25% in men and 27% in women.3 Normal values using transesophageal views are reportedly similar but were derived from a smaller series of anesthetized patients.9

A variant of fractional shortening is the velocity of circumferential fiber shortening, defined as:

Fractional Shortening × Ejection Time

Ejection time can be measured on M-mode or LV outflow tract spectral Doppler. The lower limit of normal is 1.1 circumferences/second. Although it has been suggested that this is less preload dependent than ejection fraction,10 it is rarely used in the clinical setting.

Fractional area Change (area Ejection Fraction)

The tomographic slices of the left ventricle provided by 2D echocardiography provide another easily derived ejection phase index: fractional area change or area ejection fraction. This is defined as:

Originally described using transthoracic short-axis or apical views of the left ventricle, this index can be derived with transesophageal echocardiography by using transgastric short-axis views. Due to the apical foreshortening that is inherent in the TEE midesophageal four-chamber view, this parameter is not generally derived through this window. Although ventricular areas typically are outlined and measured by manual planimetry, systems with automatic boundary detection can automate the process and provide real-time displays of area and calculated fractional area change. Fractional area change derived from TEE and manual planimetry has been shown to correlate with ejection fraction when using nuclear methods in a variety of clinical settings,11–13 as has TEE-derived fractional area change assisted with automated boundary detection.14 Acceptable inter- and intra-observer variabilities also have been demonstrated,14 although Bailey and associates, in a study of pediatric patients with congenital heart disease, suggested an error of approximately 10% under optimal conditions.15 In symmetrically contracting ventricles, values were shown to be similar at multiple short-axis levels (60 ± 6%, mean ± standard deviation).16

It must be emphasized that although such approaches may be valid in patients with symmetric ventricular contraction, they have limited value in patients with regional wall motion abnormalities. Further, the presence of an excellent correlation between fractional area change and LVEF does not mean that the two values are identical. Thus, although it may be conceded that determinations of fractional area change are the most widely used means of quantitating ventricular function with TEE, the reader is encouraged to use the terms fractional area change or area ejection fraction rather than simply ejection fraction when referring to these calculations. The term ejection fraction should be reserved for calculations based on ventricular volumes (see below).

Volume Measurement and Ejection Fraction

The universal language for assessing LV systolic performance is ejection fraction (LVEF). Indeed, LVEF is measured routinely in invasive angiographic studies and with noninvasive echocardiographic, nuclear cardiologic, computed tomographic, and magnetic resonance methods. Although there are several quantitative echocardiographic approaches for calculating LVEF, a semiquantitative visual assessment is most widely applied in clinical transthoracic and transesophageal echocardiographic studies. This requires a trained eye. Although less desirable for research applications, this approach works well in the clinical setting in the hands of an operator with good scanning and interpretive skills.17

Quantitative Approaches

Quantitative approaches mandate excellent images with good endocardial definition and no apex-base foreshortening. Although the former is rarely a problem with TEE, the latter is common. Apex-base displays are typically optimized by using a midesophageal window with the transducer held in a retroflexed position, but it may be impossible to obtain an image that is not foreshortened. This may account, in part, for the fact that TEE-derived volumes generally underestimate those derived with other approaches. In using the midesophageal window, it may be necessary to move the imaging focus toward the apex and/or reduce the transducer frequency in order to optimally define the apical endocardium.

While this section will focus on 2D approaches, it is followed by an overview of newer three-dimensional (3D) approaches.

Modified Simpson's Rule Method (2D)

The Simpson's rule method is generally conceded to be the best method for deriving ventricular volumes, particularly in irregularly shaped ventricles.13 It is based on modeling the left ventricle as a series of stacked cylindrical disks capped by an elliptical disk apex. The volume for each cylindrical disk is quantified by using the equation:

where D1 and D2 are orthogonal diameters of the cylinder, and H is the height of the cylinder.

The elliptical disk calculation uses a different equation:

where A is the area of the ellipsoid segment, h is the height of the ellipsoid segment, and a and b are radii of the total ellipsoid.

The disks are summed for systole and diastole to yield diastolic and systolic volumes. The difference in volumes is then divided by the end-diastolic volume to calculate ejection fraction:

Fortunately, the operator can rely on ultrasound system software to make these calculations; otherwise, these calculations would be a laborious process (Figure 6–3). These methods have been validated in vivo using TEE,13,18 and the major advantage of this approach is that it makes no assumptions concerning LV geometry.

Area-Length Method (2D)

There are several echocardiographic methods for calculating LV volume based on modeling the left ventricle as one or more geometric figures.19 One of the most common, the area-length approach, models the left ventricle as a cylinder–hemiellipsoid. It is traditionally obtained on transthoracic images from the apical four-chamber and parasternal short-axis (papillary muscle) views. With TEE, a midesophageal view at 0° (four chamber) is used to determine the major axis length, and the area is planimetered by using a short-axis view at the level of the mitral valve.

Volume = (5 × Area × Length)/6

The area-length method has been validated extensively with the transthoracic approach and, to a lesser degree, TEE.13,18

A similar approach, the diameter-length method, models the left ventricle as a prolate ellipsoid:

where D1 and D2 are orthogonal short-axis diameters.18 In both approaches, it is important to avoid oblique short-axis images.

Quantitative Determination of Ejection Fraction

Each of the previously cited methods for deriving ventricular volume can be extrapolated to yield quantitative assessments of ejection fraction. The equation is as follows:

Isovolumetric Indices (dP/dt)

A more load-independent index of LV systolic performance is peak dP/dt, or the maximum rate of rise of LV pressure during systole. The echocardiographic method for deriving this parameter is based on the continuous-wave Doppler recording of the mitral regurgitant spectrum. This method is illustrated in Figure 6–4. As originally reported by Chen and colleagues,20 the time for velocity to rise from 1 m/s to 3 m/s is measured, and dP/dt is calculated with the following equation:

dP/dt = 32 × 1000/dt

Normal values for this parameter are 1610 ± 290 mm Hg/s.21 This calculation, which is automated in the analysis packages of many commercial ultrasound systems, is easy to perform but requires the presence of well-defined mitral regurgitant spectra. Although relatively afterload dependent, dP/dt is preload dependent.

Wall Stress

The common measures of LV systolic function discussed above do not differentiate between abnormalities of contractility and alterations in afterload or preload. LV wall stress, defined as the load opposing ejection, is therefore sometimes used to describe systolic function. Wall stress is dependent on cavity dimensions, wall thickness, and pressure, and can be described as meridional (longitudinal), circumferential, or radial (not used clinically). Meridional stress is calculated from an end-systolic midpapillary short-axis view as:

where P represents LV peak pressure, Ac is LV cavity area, and Am represents LV myocardial area (area of the muscle in the short-axis view). Normal values for meridional stress are 86 ± 16 × 103 dyne/cm2.

Circumferential stress is calculated from a midesophageal four-chamber view as:

where the additional variable L represents the LV long-axis length. Normal values for end-systolic circumferential stress are 213 ± 29 × 103 dyne/cm2

Load-Independent Methods of Assessing LV Contractility

LV contractility is an intrinsic property of the cardiomyocytes and an important determinant of overall ventricular systolic function. As initially reported by Suga and Sagawa,22 the best and most load-independent index of left contractility is end-systolic elastance, which is calculated from pressure-volume loops.

As shown in Figure 6–5, elastance is determined by plotting pressure-volume loops under variable loading conditions. In the invasive or intraoperative setting, such families of curves typically are created by abruptly reducing preload through caval occlusion. A similar but less dramatic decrease in preload can be achieved with the intravenous administration of nitroglycerin. End-systolic elastance is defined by the slope of the line joining the end-systolic points.

An extension of this approach is the determination of preload-recruitable stroke work. Stroke work is the integrated area within a pressure-volume loop. It is possible to calculate stroke work for the variably loaded loops and to plot this as a function of end-diastolic volume. The slope of this linear relation is preload-recruitable stroke work, another relatively load-independent index of contractility.

Values for end-systolic elastance and preload-recruitable work can be approximated with echocardiographic short-axis images and automatic boundary-tracking algorithms. In these approaches,23,24 area becomes a surrogate for volume. Pressure must be recorded invasively, typically by transmitral placement of a high-fidelity catheter. Specialized computer analysis capabilities are needed to plot the pressure-area loops and calculate elastance or preload-recruitable work. Values for end-systolic elastance and preload-recruitable stroke work are dependent on the size of the left ventricle, so it is impossible to precisely define a normal range.

To study the effect of volatile anesthetic agents on myocardial contractility, Declerck and coworkers24 evaluated 23 patients undergoing bypass surgery with TEE by using several indices of cardiac performance derived by automatic boundary-tracking technology. These included fractional area change, velocity of circumferential shortening, end-systolic elastance, and preload-recruitable stroke work. They reported that fractional area change and velocity of circumferential fiber shortening had poor sensitivity in detecting changes in contractility when compared with end-systolic elastance and preload-recruitable stroke work. Similar observations were made by Gorcsan and associates.25

Another variant of these methods is the measurement of preload-adjusted maximal power (stroke work/ end-diastolic volume2) validated by Mandarino and colleagues.26 Stroke work is the area within the pressure- volume loop. When echocardiographically derived pressure-area loops are substituted, the formula becomes:

To date, none of these pressure-area approaches have been used clinically. However, they provide essential research tools in studies of dynamically changing contractility. This is particularly true in settings where changing loading conditions invalidate load-dependent indices, as is typically the case perioperatively.

Because coronary revascularization is one of the primary indications for cardiac surgery and coronary disease is frequently present in patients undergoing noncardiac procedures, an understanding of the coronary vascular bed and the recognition of regional wall motion abnormalities is an important element of perioperative echocardiography. Regional dysfunction may be present preoperatively, develop de novo during surgery, or resolve intraoperatively after revascularization.27,28 Worsening wall motion after coronary artery bypass graft (CABG) surgery should be considered a prognostic indicator of adverse cardiovascular outcome. Swaminathan et al29 demonstrated in 1412 CABG surgery patients that subjects with worse regional wall motion immediately after surgical coronary revascularization had a twofold increased risk of death, myocardial infarction, or need for additional revascularization within the subsequent 2 years after surgery.

The echocardiographic manifestation of myocardial ischemia is impaired regional contraction, typically measured in terms of reduced wall thickening and/ or abnormal endocardial excursion. The latter typically is assessed visually and described in semiquantitative terms: hypokinesis (mild, moderate, or severe), akinesis, or dyskinesis. Hypokinesis is defined as reduced endocardial excursion, akinesis as the absence of endocardial excursion, and dyskinesis as outward systolic endocardial motion. The term aneurysm is used to describe segments in which there is diastolic deformity and dyskinesis, a frequent association.

Normally, the myocardium thickens by at least 30% ((end-systolic thickness − end-diastolic thickness)/end-diastolic thickness) × 100. Thickening of 10% to 30% is considered mildly reduced, and less than 10% thickening is considered severely impaired.

Recognition of regional dysfunction is facilitated by the presence of at least one normally contracting and thickening segment, which serves as a reference; however, because diffuse coronary disease may create the situation in which there is regionally variable dysfunction with no truly normal segment (ie, all segments are abnormal but to different degrees) identification of abnormal contraction patterns based solely on a comparison to adjacent ventricular segments can be misleading.

A complete assessment of LV regional performance requires multiple views that incorporate midesophageal and transgastric views (see Chapter 5). A complete echocardiographic evaluation of regional function is intrinsically redundant in the sense that each segment and each vascular bed is seen in more than one view. The apparent presence of a wall motion abnormality in a single view should prompt a careful reevaluation of the images to ensure that there has not been an interpretive error due to translation of the heart or suboptimal views (off-axis or apically foreshortened). Measurements of systolic wall thickening may be useful supplements to the visual assessment of endocardial excursion.

With TEE, the most difficult area to image is the LV apex. This is best seen with midesophageal views, typically with the probe in a retroflexed position and focus moved to the far field. Transgastric short- and long-axis views also may be used, with an emphasis on avoiding oblique imaging planes and ensuring that the imaging planes reach the apex rather than simply the base of the papillary muscles.

Assessment of the septum and inferior wall may be difficult when septal contour is distorted by primarily right-sided disease. Septal flattening that occurs exclusively in diastole occurs with RV volume overload, whereas systolic septal flattening is a manifestation of RV pressure overload. RV hypertension is generally associated with tricuspid regurgitation and RV dilation, so pure RV pressure overload is uncommon in the adult heart; a pattern of septal flattening throughout the cardiac cycle is more common. This may falsely create the appearance of septal and adjacent inferior wall hypokinesis.

Another secondary abnormality of the septum is the dyssynchrony that occurs in the setting of left bundle branch block, whether intrinsic or secondary to RV pacing. This creates a contraction pattern in which the septum appears to writhe, thus making it difficult to determine whether its excursion is normal. In these settings, the assessment of wall thickening may provide a better method of excluding an abnormality of regional contraction.

Seventeen-Segment Model

To standardize the nomenclature for LV segmentation across imaging modalities, the American Society of Echocardiography, with other subspecialty imaging societies, has adapted a 17-segment model.30 This replaces the 16-segment model previously used by echocardiographers, the differences being the addition of an apical cap as the 17th segment and renaming the posterior, lateral, and septal segments. This scheme is provided for reference in Figure 6–6, and Figure 6–7 provides a schematic assignment of each segment to a coronary vascular bed.

A semiquantitative approach to segmental function is the wall motion score in which each segment is assigned a score of 1 to 4 (1 = normal, 2 = hypokinetic, 3 = akinetic, and 4 = dyskinetic). These may be averaged to give a wall motion score index. Accounting for the severity of hypokinesis transforms this scoring system to: 1 = normal, 2 = mildly hypokinetic, 3 = severely hypokinetic, 4 = akinetic, and 5 = dyskinetic.

Although the methods discussed in this section currently are not available with all TEE systems and are used primarily with transthoracic imaging, they are included both to provide a framework for interpreting information from transthoracic echocardiograms and in anticipation of their more widespread incorporation into transesophageal studies (see Chapter 24).

Doppler Tissue Imaging

Doppler tissue imaging (DTI) is a form of pulsed Doppler that focuses on the low-frequency, high-amplitude signals that return from tissue. Because the temporal resolution of DTI is better than that of standard two-dimensional echocardiography, DTI has been reported to be better able to identify subtle differences in regional wall motion than two-dimensional echocardiography alone.31

DTI information may be displayed by color-coding the Doppler information and superimposing it over an M-mode or two-dimensional real-time scan (Figure 6–8) or as a velocity-versus-time spectral display of information originating from a specific sample volume within the heart. These display options are analogous to those for pulsed Doppler data originating from red blood cells.

The major limitation of these methods is the fact that they are influenced by translation of the heart. Thus, Doppler tissue imaging is unable to distinguish active motion of the heart based on myocardial contraction from passive motion due to translation. A second limitation derives from the angle dependence of tissue Doppler. Thus, as for blood-cell-derived Doppler data, tissue velocities are underestimated when the direction of motion is not parallel to the line of interrogation.

When the annulus rather than any particular myocardial segment is sampled in a four-chamber view, the technique provides indices of global LV performance. Although these methods have the potential to provide useful information concerning systolic and diastolic performances, their routine clinical use currently is limited largely to the assessment of diastolic function.

Nonetheless, the application of DTI intraoperatively has been reported,32 and it has been suggested that the technique may be useful in tracking systolic function in this setting. However, overlap between values for normal and abnormal segments make it impossible for this to be used as the only method of assessing ventricular function. Importantly, DTI provides one approach to sophisticated analyses of systolic function along with strain and strain rate determinations and assessment of myocardial twist/torsion.

Speckle Tracking Imaging

The behavior of ultrasound in myocardium (scattering, reflection, and interference) results in 2D images where the myocardium is characterized by speckles. These speckles can be tracked from frame to frame throughout the cardiac cycle, and when their motion is analyzed, it can provide an angle- and translation-independent tool for measuring strain and strain rate as well as measures of ventricular twist/torsion (Figure 6–9).

Strain and Strain Rate Imaging

Strain is a dimensionless quantity defined as the fractional change in length produced by the application of stress:

where length0 is the initial length.

The capability of deriving strain and strain rate echocardiographically from Doppler tissue imaging is available in most ultrasound systems (Figure 6–8).33 DTI-derived strain rate is approximated by the ratio of the difference in velocities recorded at two targets over the distance between the two targets:

Because strain and strain rate assess the relative length and motion of adjacent targets within the heart, they theoretically should be exempt from the influence of translation.34 Strain rate has been reported to provide a load-independent assessment of myocardial contractility that correlates well with end-systolic elastance,35 and peak systolic strain may provide an index of regional LV function.36,37 However, when derived from DTI, the measurements are angle dependent, as demonstrated by Urheim and colleagues,33 For this reason, and because it provides a means of deriving circumferential and radial strain, methods based on speckle tracking have gained popularity. Regardless of the approach (DTI or speckle tracking), strain rate determinations are limited by noise.38 Nonetheless, this evolving technology appears to be a valuable tool in the assessment of ventricular function both preoperatively and perioperatively.

Color Kinesis

Color kinesis, an echocardiographic technique based on automated border detection, compares tissue backscatter values between successive acoustic frames, detects pixel transitions between blood and myocardium, and color encodes these transitions in real time. Segmental analysis of color kinesis images thus provides an objective method for quantifying the spatio-temporal aspects of regional and global LV endocardial motion (Figure 6–10). It may be interpreted semiquantitatively by visual estimation or quantitatively with specially developed off-line analysis systems.39

In a study of patients undergoing minimally invasive coronary artery bypass grafting, Kotoh and colleagues40 suggested that color kinesis is a more sensitive marker of intraoperative ischemia than concurrent electrocardiographic monitoring. Further, Podgoreanu and coworkers41 demonstrated that quantitative color kinesis analysis of intraoperative LV function agrees more closely with expert analysis than interpretation of gray-scale images by less experienced readers. They concluded that quantitative color kinesis may be a useful adjunct to visual assessment, especially with less experienced reviewers. Despite its apparent merits, color kinesis is not widely available and is infrequently used.

Torsion/Twist

Recently there has been renewed interest in the apex-to-base rotational (twisting/untwisting) characteristics of left ventricular contraction and relaxation. These become particularly important in understanding the response to isolated abnormalities of afterload and preload as occur with valve disease, as well as more common ischemic heart disease. It is notable that the capability exists for performing these analyses with TEE using speckle tracking (Figure 6–11) or more cumbersome DTI-based approaches.

Contrast Echocardiography

Echocardiographic contrast agents capable of left heart opacification after an intravenous injection are valuable tools in transthoracic echocardiography because of their ability to improve endocardial definition. In general, transesophageal images provide excellent images that render contrast enhancement unnecessary. However, in patients in whom TEE images are suboptimal, particularly those who are obese or in whom there is interference by subdiaphragmatic air, contrast may facilitate endocardial border delineation. In addition, contrast may help delineate masses, enhance Doppler spectra, and define myocardial perfusion. It has been shown that contrast administration has no effect on intraoperative hemodynamics.42 If contrast is used, it is important that machine settings optimized for contrast be employed. These include harmonic imaging (available on newer TEE systems) and low mechanical index (power). Ideally, a preset for contrast imaging should be created for the system.

Recently, three-dimensional (3D) and real-time three-dimensional (4D or RT3D) echocardiography has become available on TEE probes. Arguably this has revolutionized the TEE assessment of mitral pathology and has become increasingly important in providing guidance for interventional cardiology procedures such as device repair of congenital defects. These techniques may also be used to assist in the qualitative assessment of ventricular systolic function, since multiple 2D images can be derived by post-acquisition cropping and rotation of single full-volume acquisitions and 3D slices of the ventricle can be obtained using conventional 2D windows (Figure 6–12). For the time being, however, full ventricular volumes are too large to be captured in truly real-time display using a transesophageal approach, and only semigated methods that create a full volume by electronically “stitching” together partial volumes exist. Similarly, while current off-line analysis tools can create detailed quantitative assessments of global and regional volumes and function using transthoracic 3D data, these methods have not yet been validated with TEE. However such tools should soon be available with the caveat that the difficulty of imaging the LV apex with TEE may ultimately limit the accuracy of volume and LVEF determinations.