The noninvasive echocardiographic evaluation of ventricular performance is an essential tool in the clinician’s assessment and management of children and adults with congenital heart disease. As noninvasive methods have continued to evolve, the importance of global and regional ventricular function has become better appreciated. Alterations in both ventricular geometry and loading conditions are the hallmarks of congenital heart disease and can often make the quantitative assessment of ventricular function challenging. This chapter will discuss traditional echocardiographic techniques in the evaluation of ventricular function in patients with congenital heart disease. Newer modalities for functional assessment, including three-dimensional echocardiography, strain and strain rate imaging, and cardiac magnetic resonance imaging, will be covered in greater detail in subsequent chapters in this text.
ECHOCARDIOGRAPHIC ASSESSMENT OF GLOBAL SYSTOLIC VENTRICULAR FUNCTION
Left Ventricular Shortening Fraction
One-dimensional wall motion analysis, or M-mode echocardiography, has traditionally been one of the most commonly used methods to measure the extent of LV shortening. Shortening fraction represents the change in LV short-axis diameter that occurs during systole:
where LVEDD represents LV end-diastolic dimension and LVESD represents LV end-systolic dimension (Fig. 3.1). Normal values for shortening fraction range between 28% and 44%. The short-axis view at the mid-papillary level is the echocardiographic view most frequently used to make these measurements. Similar to shortening fraction, fractional area change can also be measured in this orientation by determining the change in LV area that occurs during the cardiac cycle:
Normal values have been reported to be greater than 36% for fractional area change in adults. LV fractional shortening and fractional area change have been reported to be independent of changes in heart rate and age but are significantly affected by changes in ventricular preload and afterload.
Figure 3.1. Parasternal short-axis image at level of papillary muscles of left ventricle with M-mode measurement of left ventricular shortening.
M-mode–derived shortening fraction (FS%) of left ventricle:
Left ventricular ejection fraction (EF%) can be obtained as follows:
(From Oh JK, Seward JB, Tajik AJ. The echo manual. 3rd ed. [Figure 7-1, p. 110]. Philadelphia, Pa: Lippincott Williams & Wilkins, 2006.)
Left Ventricular Ejection Fraction
LV ejection fraction (LVEF) is the most commonly measured parameter of ventricular function. Global estimation LVEF is often determined in a qualitative fashion; however, using transthoracic or transesophageal echocardiography, two-dimensional echocardiography allows quantitative measurement of LVEF by assessing changes in ventricular volume during the cardiac cycle. The geometric model most commonly used to measure LVEF is the modified Simpson’s biplane method (Fig. 3.2). By using orthogonal apical four-chamber and two-chamber views of the left ventricle, this geometric model calculates LV end-diastolic (LVEDV) and LV end-systolic volume (LVESV) by summing equal sequential slices of LV area from each of these scan planes. LVEF can then be calculated as:
LVEF(%) = [LVEDV – LVESV]/LVEDV × 100
Normal values for LVEF range between 56% and 78%. Similar to shortening fraction, LVEF has been shown to be dependent on changes in ventricular loading conditions.
Accurate calculation of LV volume can occasionally be challenging due to foreshortening of the LV cavity. To circumvent this limitation, the area-length method to derive LVEF can also be used (Fig. 3.3). One of the more commonly used methods, termed the “bullet” method, uses the short-axis area of the left ventricle and the long-axis major LV length (from the apical four-chamber view):
Determination of ventricular volume and EF by this method has been shown to correlate well with invasively measured parameters of ventricular function.
Figure 3.2. Simpson’s biplane methodology to calculate left ventricular (LV) ejection fraction. A: Apical four-chamber and two-chamber views are used to calculate LV volume. LV ejection fraction is assessed from apical four-chamber (B and C) and two-chamber (D and E) views. (A, Adapted from Shiller NB, et al. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-dimensional Echocardiograms. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr. 1989;2:358–367. B–E, From Oh JK, Seward JB, Tajik AI. The echo manual. 3rd ed. [Figure 7-10, p. 115]. Philadelphia, Pa: Lippincott Williams & Wilkins, 2006.)
Figure 3.3. Left ventricular (LV) dimensions. A: Mea-surement of the major long-axis and minor short-axis dimension of the left ventricle from the apical four-chamber view. B: Similar measurements of the LV long-axis and short-axis dimensions can be obtained from the parasternal long-axis view. C: LV short axis measured in the parasternal short-axis view. (Adapted from Shiller NB, et al. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-dimensional Echocardiograms. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr. 1989;2:358–367.)
New echocardiographic technology and advancements in image processing have allowed improved acquisition of ventricular volume. Studies have validated the ability of three-dimensional echocardiography to obtain accurate and reproducible estimates of LV and right ventricular (RV) volumes and EF. While this imaging modality has historically been limited by the time-consuming reconstruction of acquired images, the introduction of real-time three-dimensional imaging has significantly enhanced the quantitative assessment of ventricular volume and function.
Automated border detection (ABD) is another imaging technology that uses acoustic quantification to differentiate the myocardium from the blood pool and thereby allows enhanced visualization of the endocardial border. End-diastolic and end-systolic LV area can be continuously displayed with this modality, enabling determination of ventricular volume, fractional area change, and even pressure-volume or pressure-area loops. Excellent correlation of ABD with other noninvasive and invasive measurements of ventricular function has been reported in some adult studies, but data are lacking in patients with congenital heart disease with altered ventricular geometry.
Left Ventricular Mass
LV mass can be calculated using several echocardiographic methodologies. The unifying principle behind these various measurements is to subtract the volume of the LV cavity from the volume encompassed by the LV epicardium—leaving a “shell” of myocardial muscle volume that can be converted to LV mass by factoring in the specific gravity of myocardium. Devereux and colleagues (1986) have described an M-mode formula to derive LV mass using the short-axis LV dimension as follows:
where 1.04 is the specific gravity of myocardium, LVID is the LV internal dimension, PWT is the posterior wall thickness, IVST is the interventricular septal wall thickness, and 0.8 is a correction factor. Two-dimensional echocardiographic and, more recently, three-dimensional echocardiographic methodologies have been shown to be superior to M-mode–derived measures of LV mass. The two most common two-dimensional approaches include the area-length and the truncated ellipsoid methods. Both of these methodologies use a short-axis view of the left ventricle at the papillary muscle level and an apical four-chamber or two-chamber view to measure the LV long-axis length. LV mass is calculated using LV dimensions and wall thicknesses (measured in centimeters) at end diastole (Fig. 3.4). Normal values for both pediatric and adult cohorts have been published using the area-length or truncated ellipsoid methods.
VELOCITY OF CIRCUMFERENTIAL FIBER SHORTENING AND THE STRESS-VELOCITY INDEX
The rate of LV fiber shortening can be noninvasively assessed by M-mode echocardiography. This measurement, termed the mean velocity of circumferential fiber shortening (Vcf), is normalized for LVEDD and can be obtained from the following equation:
where LVET represents LV ejection time. Reported normal values for mean Vcf are 1.5 ± 0.04 circumferences (circ)/s for neonates and 1.3 ± 0.03 circ/s for children between 2 and 10 years of age. This index assesses not only the degree of fractional shortening but also the rate at which this shortening occurs. To normalize Vcf for variation in heart rate, LVET is divided by the square root of the RR interval to derive a rate-corrected mean velocity of circumferential fiber shortening (Vcfc). Normal Vcfc has been reported to be 1.28 ± 0.22 and 1.08 ± 0.14 circ/s in neonates and children, respectively. Because Vcfcvalues are corrected for heart rate, a significant decrease in Vcfcbetween neonates and children has been attributed to increased systemic afterload with advancing age. Vcf is sensitive to changes in contractility and afterload but relatively insensitive to changes in preload. Similar to fractional shortening, this parameter relies on the elliptical shape of the left ventricle and is invalid with altered LV geometry.
Figure 3.4. Calculation of left ventricular (LV) mass. Calculation of LV mass by the area-length method and truncated ellipsoid method (see text). (Adapted from Shiller NB, et al. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-dimensional Echocardiograms. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr. 1989;2:358–367.)
Because the majority of ejection phase indices, including shortening fraction, EF, and Vcfc, are dependent on the underlying loading state of the left ventricle, measures of wall tension, namely circumferential and meridional end-systolic wall stress, have been proposed to assess myocardial performance in a relatively load-independent fashion. Colan and colleagues (1984) have previously described a stress-velocity index that is an inverse linear relationship between Vcfc and end-systolic wall stress (Fig. 3.5). This stress-velocity index is independent of preload, is normalized for heart rate, and incorporates afterload, resulting in a noninvasive measure of LV contractility that is independent of ventricular loading conditions. This index can therefore differentiate states of increased ventricular afterload from decreased myocardial contractility. While the stress-velocity index is appealing, the clinical application of this index has been limited by its cumbersome acquisition and its time-consuming off-line. This index is also limited in patients with altered ventricular geometry and wall thickness, features that are hallmarks of congenital heart disease.
Figure 3.5. Stress-velocity index for assessment of left ventricular (LV) systolic function. A: Parameters used to calculate the stress-velocity index. Note the simultaneous phonocardiogram (identifying the first (S1) and second (S2) heart sounds), ECG, carotid pulse tracing (arrow), and M-mode echocardiogram. Parameters measured include LV end-diastolic (EDD) and end-systolic (ESD) dimensions and LV ejection time (ET). B: Graphic representation of the relationship between the mean rate-corrected velocity of circumferential LV fiber shortening (Vcfc) and the LV end-systolic wall stress (œ es). To normalize Vcf for variation in heart rate, it is divided by the square root of the RR interval to derive a rate-corrected mean velocity of circumferential LV fiber shortening (Vcfc). Values above the upper limit of the mean relationship imply an increased inotropic state, whereas values below the mean imply depressed contractility. (From Colan SD, Borow KM, Neumann A. Left ventricular end-systolic wall stress-velocity of fiber shortening relation: a load independent index of myocardial contractility, J Am Coll Cardiol. 1984;4:715–724.)
Doppler Parameters of Left Ventricular Systolic Function
Echocardiographic evaluation of systolic dysfunction has primarily relied on one-dimensional measures of LV shortening or two-dimensional measures of LV volume change that are often difficult to assess in patients with distorted ventricular geometry. Doppler measures of global ventricular function have been reported to be a potentially more reproducible and sensitive measure of ventricular function.
Left Ventricular dP/dt
Doppler echocardiography can be used in the quantitative evaluation of LV systolic function. If mitral regurgitation (MR) is present, the peak and mean rate of change in LV systolic pressure (dP/dt) can be derived from the ascending portion of the continuous-wave MR Doppler signal. This rate of change of ventricular pressure is determined during the isovolumic phase of the cardiac cycle before opening of the aortic valve. Using the simplified Bernoulli equation, two velocity points along the MR Doppler envelope are selected from which a corresponding LV pressure change can be derived (Fig. 3.6). This change in LV pressure can then be divided by the change in time between the two Doppler velocities to derive the LV dP/dt. Normal values for mean dP/dt have been reported to be greater than 1200 mm Hg/s for the left ventricle. While more time-consuming to perform, peak dP/dt correlates more accurately with invasive cardiac catheterization measurements. To ascertain peak LV dP/dt noninvasively, the MR signal is digitized to obtain the first derivative of the pressure gradient curve from which peak positive and peak negative LV dP/dt as well as the time constant of relaxation (Tau) can be calculated. While reflective of myocardial contractility, LV dP/dt is significantly affected by changes in preload and afterload.
Myocardial Performance Index (Tei Index)
The myocardial performance index (MPI) is a Doppler-derived quantitative measure of global ventricular function that incorporates both systolic and diastolic time intervals. The MPI is defined as the sum of isovolumic contraction time (ICT) and isovolumic relaxation time (IRT) divided by ejection time (ET): MPI = (ICT + IRT)/ET (Fig. 3.7). The components of this index are measured from routine pulsed-wave Doppler signals at the atrioventricular (AV) valve and ventricular outflow tract of either the left or right ventricle. To derive the sum of ICT and IRT, the Doppler-derived ejection time for either ventricle is subtracted from the Doppler interval between cessation and onset of the respective AV valve inflow signal (from the end of the Doppler A wave to the beginning of the Doppier E wave of the next cardiac cycle).
Alternatively, tissue Doppler has been used to measure the MPI. While appealing because of the simultaneous measurement of these time intervals, care needs to be taken because published values for this tissue Doppler technique differ from the pulsed-wave Doppler-derived MPI. Increasing values of the MPI correlate with increasing degrees of global ventricular dysfunction.
Both adult and pediatric studies have established normal values for the MPI. In adults, normal LV and RV MPI values are 0.39 ± 0.05 and 0.28 ± 0.04, respectively. In children, similar values for the LV and RV are reported to be 0.35 ± 0.03 and 0.32 ± 0.03, respectively. The MPI has been shown to be a sensitive predictor of outcome in adult and pediatric patients with acquired and congenital heart disease. Because the MPI incorporates measures of both systolic and diastolic performance, this index may be a more sensitive early measure of ventricular dysfunction in the absence of other overt changes in isolated systolic or diastolic echocardiographic indices. In addition, because the MPI is a Doppler-derived index, it has been reported to be easily applied to the assessment of both LV and RV function as well as complex ventricular geometries found in patients with congenital heart disease. The MPI, however, does have significant limitations. It is significantly affected by changes in loading conditions and has a paradoxical change with high filling pressure or severe semilunar valve regurgitation (“pseudo-normalization”). In addition, the combined nature of this index fails to readily discriminate between abnormalities of systolic or diastolic performance.
ECHOCARDIOGRAPHIC ASSESSMENT OF REGIONAL SYSTOLIC VENTRICULAR FUNCTION
Both transthoracic and transesophageal echocardiography are ideally suited to evaluate regional wall motion abnormalities. These wall motion abnormalities are characterized by reduced systolic thickening and decreased inward endocardial excursion. Echocardiographic assessment of regional systolic function is best facilitated in the LV short-axis view at the level of the papillary muscles. In the American Society of Echocardiography’s 17-segment model, the left ventricle is divided into six myocardial segments at this level: anterior, anteroseptal, anterolateral, inferolateral, inferior, and inferoseptal (Fig. 3.8). Qualitative visual assessment of wall thickening is graded as normal, hypokinetic (reduced systolic thickening), akinetic (absent systolic thickening), or dyskinetic (paradoxical thinning). Additional views are needed to evaluate all myocardial segments.
Figure 3.6. Measurement of dP/dt (A) and calculation of left ventricular (LV) dP/dt from the mitral regurgitation jet (B). This still frame demonstrates the Doppler velocity curve of the mitral regurgitation jet obtained during transesophageal echocardiography in a child with dilated cardiomyopathy and severe LV dysfunction. Using the modified Bernoulli equation, the LV dP/dt is the change in LV pressure measured from 1.0 m/s to 3.0 m/s divided by the change in time between these two LV pressure points:
(A, Used with permission from Mayo Clinic.)
Figure 3.7. Myocardial performance index (MPI) for assessment of left ventricular (LV) global function. A: MPI represents the ratio of isovolumic contraction time (ICT) and isovolumic relaxation time (IRT) to ventricular ejection time (ET): MPI = (ICT + IRT)/ET. B: Pulsed-wave Doppler interrogation in the apical four-chamber view at the level of the mitral valve leaflets. The duration of ICT + IRT is measured from the cessation of mitral valve inflow to the onset of AV valve inflow of the next cardiac cycle (interval a). C: Pulsed-wave Doppler interrogation within the LV outflow tract in the apical five-chamber view. Ventricular ejection time is measured from the onset to cessation of LV ejection (interval b).
(A, From Eidem BW, et al. Nongeometric quantitative assessment of right and left ventricular function: myocardial performance index in normal children and patients with Ebstein anomaly. J Am Soc Echocardiogr. 1998;11:849–856.)
Tissue Doppler Imaging and Strain Rate Imaging
Quantitative assessment of regional systolic LV function, as detailed earlier, has centered on the evaluation of segmental endocardial excursion and LV wall thickening. These semiquantitative methods often fail to discriminate between active and passive myocardial motion. Newer echocardiographic modalities, including tissue Doppler imaging and strain rate imaging, offer a potentially more quantitative and accurate approach to the assessment of regional myocardial contraction and relaxation.
Tissue Doppler echocardiography is a more recent addition to the armamentarium of the echocardiographer. By incorporating a high pass filter, tissue Doppler allows the display and quantitation of the low-velocity high-amplitude Doppler shifts present within the myocardium as opposed to the higher-velocity lower-amplitude Doppler signals more commonly measured within the blood pool (Fig. 3.9). Tissue Doppler is less load-dependent than corresponding Doppler velocities from the blood pool and has systolic and diastolic components. These velocities are heterogenous depending on ventricular wall and position.
Measurement of myocardial wall velocities by TDI has been shown to be a promising modality for assessment of longitudinal systolic performance. Studies have demonstrated significant changes in mitral annular systolic TDI velocities in adult patients with LV dysfunction and elevated LV filling pressures.
Figure 3.8. Seventeen segment model for analysis of left ventricular wall motion proposed by the American Society of Echocardiography. A: Apical (four-, three-, and two-chamber) and parasternal short-axis views demonstrate the 16 myocardial segments + apical cap. B: Typical coronary artery distribution pattern to these myocardial segments. Note: Coronary arterial supply is variable and may differ from the distribution pattern demonstrated. (From Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18:1440–1463. Used with permission.)
Tissue Doppler velocities, however, cannot differentiate between active contraction and passive motion, which is a major limitation when assessing regional myocardial function. Regional strain rate corresponds to the rate of regional myocardial deformation and can be calculated from the spatial gradient in myocardial velocity between two neighboring points within the myocardium. Regional strain represents the amount of deformation (expressed as a percentage) or the fractional change in length caused by an applied force and is calculated by integrating the strain rate curve over time during the cardiac cycle. Strain measures the total amount of deformation in either the radial or longitudinal direction, while strain rate calculates the velocity of shortening (Fig. 3.10). These two measurements reflect different aspects of myocardial function and therefore provide complementary information. In contrast to tissue Doppler velocities, these newer indices of myocardial deformation are not influenced by global heart motion or tethering of adjacent segments and therefore are better indices of true regional myocardial function.
ECHOCARDIOGRAPHIC ASSESSMENT OF DIASTOLIC VENTRICULAR FUNCTION
Doppler echocardiography has historically been an essential noninvasive tool in the quantitative assessment of LV diastolic function. Abnormalities of ventricular compliance and relaxation can be demonstrated by characteristic changes in mitral inflow and pulmonary venous Doppler patterns. The addition of newer methodologies, including tissue Doppler echocardiography and flow propagation velocities, enhance the ability of echocardiography to define and quantitate these adverse changes in diastolic performance. Because diastolic dysfunction often precedes systolic dysfunction, careful assessment of diastolic function is mandatory in the noninvasive characterization and serial evaluation of patients with congenital heart disease.
Figure 3.9. A. Normal mitral annular (A), septal annular (B), and tricuspid annular (C) pulsed-wave longitudinal tissue Doppler velocities. Note the normal characteristic pattern of a larger early diastolic velocity (E wave) compared with late diastolic velocity (A= wave). The S wave is the systolic wave. B: Impact of increasing age on tissue Doppler velocities. C: Impact of increasing left ventricular end-diastolic dimension on tissue Doppler velocities. (From Eidem BW, et al. Clinical impact of altered left ventricular loading conditions on Doppler tissue imaging velocities: a study in congenital heart disease. J Am Soc Echocardiogr. 2005;18:830–838.)
Noninvasive evaluation of diastolic function in normal infants and children is influenced by a variety of factors, including age, heart rate, and the respiratory cycle. Reference values detailing both mitral and pulmonary venous Doppler velocities in a large cohort of normal children have been established (Table 3-1). Similar to many echocardiographic parameters, these Doppler velocities are also significantly affected by loading conditions, making determination of diastolic dysfunction by using these parameters alone very challenging in patients with congenital heart disease.
Figure 3.10. Schematic representation of longitudinal (A) and radial (B) strain and strain rate imaging. In the longitudinal direction, strain represents myocardial shortening (systole) and lengthening (diastole), whereas strain rate represents the rate at which shortening or lengthening occurs. Similarly, radial strain represents myocardial thickening (systole) and thinning (diastole), whereas strain rate represents the rate at which thickening or thinning occurs. AVC, aortic valve closure; MVO, mitral valve opening; sys, systolic; diast, diastolic. C: Normal Doppler-based strain acquired in an apical four-chamber orientation at the basal septum. D: Two-dimensional strain obtained in an apical four-chamber view in a normal child. Note the multiple colored curves that represent the various strain patterns in each myocardial segment. E: Two-dimensional strain in a patient with hypertrophic cardiomyopathy. Strain is determined from the apical four-, three-, and two-chamber views. Bull’s eye diagram (bottom right) demonstrates strain in each myocardial segment. Note the decreased strain in the anterior septal, inferior, and septal wall segments. (A and B, used with permission from Luc Mertens, MD.)
Evaluation of Diastolic Ventricular Function—Technical Considerations
A complete Doppler assessment of a ventricle’s diastolic performance must include analysis of the flow signals across the AV valve and within the proximal central venous system (either pulmonary veins for the left ventricle or systemic veins for the right ventricle). Inaccurate assessment will result from attempts to draw conclusions from only one or the other of these flow signals. It is also critically important to obtain these flow signals appropriately or all subsequent conclusions drawn from them will be erroneous. The ultrasound instrument should be set at the lowest frequency and with the smallest sample volume (for pulsed Doppler) possible. This will maximize axial and lateral flow velocity resolution. Low-velocity filtering is used to eliminate tissue motion artifacts. These filters need to be set lower (200 to 600 Hertz) for pulsed-wave interrogation than for continuous-wave Doppler studies (800 to 1200 Hertz). For all signals, the Doppler beam must be aligned as close to parallel as possible with the interrogated flow. Color flow Doppler is extremely useful in achieving optimal alignment.
For AV valve evaluation, the pulsed-wave sample volume is positioned between the tips of the open valve leaflets (Fig. 3.11). This will place the sample volume “below” the anatomic AV valve annulus, at a point within the proximal ventricular inflow tract. In many patients, the apical four-chamber view may not the best position to record AV valve signals. In fact, for the mitral valve, the best alignment is often achieved from the apical long-axis (“two-chamber”) view. This is because normal mitral flow is directed somewhat laterally and posteriorly to the cardiac apex. This flow direction becomes even more pronounced in the dilated heart. Tricuspid inflow signals are often best recorded from a parasternal transducer position. Medial rotation and inferior angulation from the long-axis image will produce a “tricuspid inflow” view that can be used to sample this valve.
Figure 3.11. Normal mitral inflow (A) and pulmonary venous inflow Doppler (B). E, early diastolic wave; A, atrial filling wave; S, systolic venous wave; D, diastolic venous wave; Ar, atrial reversal wave.
Recordings of central venous flow signals must be made within the vein, not at the junction of the vein and the receiving atrium or vena cava. In adults, it is generally recommended that the sample volume be at least 1 cm “upstream” from the venous orifice. In children, shorter distances must be accepted due to their smaller size, but the sample volume must be placed within the body of the vein to accurately record the flows, especially reversal flows.
The mitral valve inflow signal (Fig. 3.11) is divided into early (E wave) and atrial (A wave) components at the point where the mid-diastolic flow velocity curve changes from a negative to a positive slope (the E-at-A velocity). If no change in slope occurs or if the E-at-A velocity occurs at a velocity greater than one-half of the peak E velocity, then the signal should be considered fused. Deceleration time and total A wave duration should not be measured from fused signals. Mitral A wave duration includes the interval from the E-at-A velocity to cessation of forward flow.
Similarly, division of the pulmonary vein forward flow signal (Fig. 3.11) is made at the point where the flow velocity curve changes slope. Systolic flows occur before and diastolic flows occur after the slope change. Pulmonary vein atrial reversal (PVAR) duration is measured from the onset to cessation of reversed flow occurring after the P wave on the simultaneously recorded, single-lead surface electrocardiogram (ECG). These measurements can be made in the same manner for flow signals recorded at the tricuspid valve and in the systemic (usually hepatic) veins.
The intrathoracic pressure changes associated with normal respiration markedly alter the filling of the right ventricle. Therefore, it is generally recommended that evaluation of right heart flow patterns be made at end-expiration. Alternatively, multiple sequential cycles can be averaged to account for the respiratory variation. Respiration has less effect on LV filling, but it is still wise to average the values from at least three consecutive signals.
Mitral Inflow Doppler
Mitral inflow obtained by pulsed-wave Doppler echocardiography represents the diastolic pressure gradient between the left atrium and left ventricle (Fig. 3.11). The early diastolic filling wave, or E wave, is the dominant diastolic wave in children and young adults and represents the peak left atrium–to–LV pressure gradient at the onset of diastole. The deceleration time of the mitral E wave reflects the time period needed for equalization of left atrial (LA) and LV pressure. The late diastolic filling wave, or A wave, represents the peak pressure gradient between the left atrium and the left ventricle in late diastole at the onset of atrial contraction. Normal mitral inflow Doppler is characterized by a dominant E wave, a smaller A wave, and a ratio of E and A waves (E:A ratio) between 1.0 and 3.0. Normal duration of mitral deceleration time and isovolumic relaxation time varies with age and has been reported in both pediatric and adult populations. Mitral inflow Doppler velocities are affected not only by changes in LV diastolic function but also by a variety of additional hemodynamic factors, including age, altered loading conditions, heart rate, and changes in atrial and ventricular compliance. Interpretation of characteristic patterns of mitral inflow must be carefully evaluated, with particular attention paid to the potential impact of each of these hemodynamic factors on mitral inflow Doppler velocities.
Pulmonary Venous Doppler
Pulmonary venous Doppler, combined with mitral inflow Doppler, provides a more comprehensive assessment of LA and LV filling pressures. Pulmonary venous inflow consists of three distinct Doppler waves: a systolic wave (S wave), a diastolic wave (D wave), and a reversal wave with atrial contraction (Ar wave) (Fig. 3.11). In normal adolescents and adults, the characteristic pattern of pulmonary venous inflow consists of a dominant S wave, a smaller D wave, and a small Ar wave of low velocity and brief duration. In neonates and younger children, a dominant D wave is often present with a similar brief low-velocity, or even absent, Ar wave.
With worsening LV diastolic dysfunction, LA pressure increases, leading to diminished systolic forward flow into the left atrium from the pulmonary veins with relatively increased diastolic forward flow, resulting in a diastolic dominance of pulmonary venous inflow (Fig. 3.12). More important, both the velocity and duration of the pulmonary venous atrial reversal wave are increased. Pediatric and adult studies have demonstrated that an Ar wave duration greater than 30 ms longer than the corresponding mitral A wave duration or a ratio of pulmonary venous Ar wave to mitral A wave duration greater than 1.2 is predictive of elevated LV filling pressure (Fig. 3.13).
Patterns of Diastolic Dysfunction
Before attempting to analyze Doppler data regarding diastolic ventricular function, one must assess the general cardiac status of the patient. In the absence of abnormal anatomic/functional findings or clinical symptoms, Doppler data that exist slightly outside the 95% confidence limits may simply represent normal variation. However, in the presence of symptoms or clear cardiac abnormalities, these deviations are much more likely to represent clinically significant diastolic dysfunction.
In discussions of diastolic function, two distinctive abnormal patterns of ventricular filling are usually recognized: abnormal relaxation and restrictive filling. However, the Doppler manifestations of diastolic dysfunction are probably better thought of as a continuum of gradually changing filling patterns, beginning with normal and ending with irreversible restrictive filling (Fig. 3.12). It is possible for a patient to move toward either a more or less severe level over time. Successful therapy may lead the patient to display a lesser degree of dysfunction. Alternatively, disease progression may move the filling patterns toward the more severe end of the spectrum.
Figure 3.12. Inflow in children and adults. A: Spectrum of mitral and pulmonary venous inflow patterns in diastolic dysfunction in children (see text). B: Pulsed-wave mitral inflow Doppler in an adult demonstrating abnormal relaxation pattern with E:A ratio of less than 1. C: Pulsed-wave mitral inflow Doppler demonstrating restrictive filling pattern with increased E wave velocity, decreased A wave velocity, and E:A ratio greater than 3. D: Mitral inflow Doppler in adolescent with hypertrophic cardiomyopathy. Note the prominent mid-diastolic filling wave (“L wave”) consistent with severely impaired left ventricular relaxation. E: Pulsed-wave pulmonary venous inflow Doppler. Note prominent atrial reversal velocity and prolonged duration. AV, atrioventricular; E, early filling wave; A, atrial filling wave; S, systolic filling wave; D, diastolic filling wave; VAR, atrial reversal wave. (A, From Olivier M, O’Leary PW, Pankranz S, et al. Serial Doppler assessment of diastolic function before and after the Fontan operation. J Am Soc Echocardiogr. 2003;16:1136–1143.)
Using this concept of diastolic disease, one can identify four “grades” of diastolic dysfunction. Normal filling can be thought of as grade “0” dysfunction. Figure 3.12 displays representative normal mitral valve and pulmonary vein flow tracings. Exact values will depend on both age and heart rate at the time of the recording. These diagrams demonstrate the Doppler flow patterns observed at the AV valve and in the central veins for the various grades of diastolic dysfunction. Grade 0 is the normal flow pattern and is shown on the far left. As ventricular diastolic function deteriorates, flow patterns shown farther to the right of the figure become apparent. These filling patterns represent a continuum of ventricular compliance and function. A single patient can display a variety of patterns depending on loading conditions, their stage of disease, and the success of therapeutic maneuvers. Only grade 4 dysfunction (irreversible restrictive filling) implies a permanent change in ventricular function.
Figure 3.13. Pulmonary venous Doppler in the assessment of left ventricular (LV) diastolic function. A: Changes in pulmonary venous Doppler with diastolic dysfunction. Note the significant increase in atrial reversal velocity and duration with increasing degrees of diastolic dysfunction. Significant changes in systolic and diastolic filling also occur (see text). MVO, mitral valve opening; MVC, mitral valve closure. B: Diagram depicts mitral valve and pulmonary vein Doppler flow tracings. Diastolic dysfunction with increased LV filling pressure leads to increased duration and velocity of pulmonary venous atrial reversal wave. A, atrial filling wave; A-d, duration of atrial filling wave; D, pulmonary vein diastolic flow wave; DT, mitral deceleration time; dTVI, time-velocity integral of pulmonary vein diastolic flow wave; E, early filling wave; ECG, electrocardiogram; PVAR, pulmonary vein atrial reversal wave; PVAR-d, duration of pulmonary vein atrial reversal flow; S, pulmonary vein systolic flow wave; sTVI, time-velocity integral of pulmonary vein systolic flow wave. C: Measurement of pulmonary venous atrial reversal duration. D: Measurement of duration of mitral atrial filling wave. (From O’Leary PW, Durongpisitkul K, Cordes TM, et al. Diastolic ventricular function in children: a Doppler echocardiographic study establishing normal values and predictors of increased ventricular end-diastolic pressure. Mayo Clin Proc. 1998;73:616–628.)
Abnormal relaxation is considered to be grade 1 diastolic dysfunction. This is the initial abnormality seen in most forms of heart disease, and ventricular compliance is usually still normal. Abnormal relaxation is especially common in disorders producing myocardial hypertrophy. The AV valve early filling velocity is reduced and the atrial component of ventricular filling becomes dominant (E/A ratio <1.0). Diastolic ventricular relaxation is slowed, resulting in prolongation of the isovolumic relaxation time and the mitral deceleration time. Venous diastolic velocity decreases in parallel with the E wave. A slight increase in the systolic velocity can be observed. Venous atrial reversals are variable but usually remain within normal limits at this stage (Fig. 3.12).
As the patient transitions from the early/mild stage of abnormal relaxation to more advanced diastolic dysfunction, the AV valve E wave velocity will increase. This increase in early velocity is due primarily to increasing atrial pressure, caused by deterioration of diastolic function (reduced ventricular compliance). This increase in pressure “restores” the trans-AV valve flow gradient in early diastole and creates an AV valve inflow pattern with a normal E/A ratio, leading to the term “pseudo-normalization.” In our schema for grading diastolic disease, this is referred to as grade 2 diastolic dysfunction and can be distinguished from truly normal filling in one of two ways. A patient has grade 2 dysfunction when he demonstrates a “normal” AV valve filling pattern and has an atrial reversal in the central vein that is abnormally large and long (velocity greater than 95% confidence limit and reversal duration usually 20 ms longer than the AV valve A wave; Fig. 3.14). This is usually associated with moderate diastolic impairment, mildly to moderately elevated atrial mean pressure, and rising ventricular end-diastolic pressure. In patients where venous flow signals are poor or confusing, one can acutely reduce ventricular preload and then reassess the filling patterns. This is most conveniently done by having the patient perform a Valsalva maneuver. In the setting of grade 2 dysfunction, E wave velocity will decrease, the A wave will increase, and deceleration time will lengthen during Valsalva, unmasking the underlying relaxation abnormality by decreasing atrial filling (preload). A truly normal patient will display symmetrical reductions in E and A wave velocity, and deceleration time will not change significantly after a Valsalva maneuver.
The filling pattern associated with the most advanced stage of diastolic disease is restrictive filling. Flow signals in this group display a high-velocity, but abbreviated, AV valve E wave, shortened deceleration time, and little additional ventricular filling with atrial contraction (Fig. 3.13). Central venous flows are decreased in systole due to increased mean atrial pressure. Early diastolic flow velocities are increased due to elevated venous pressure “rushing” flow to cross the AV valve as it opens, but duration of diastolic flow is reduced, reflecting the abbreviated AV valve E wave and markedly reduced ventricular compliance. Atrial reversal is now quite prominent, assuming sinus rhythm and normal atrial contractility. Venous atrial reversal duration is now much longer than the AV valve A wave (greater than 30 ms).
Figure 3.14. Pseudo-normal (grade 2) diastolic filling abnormality. Top left: Two-dimensional image in adult with hypertrophic cardiomyopathy. Top right: Mitral inflow Doppler suggestive of normal early (E) and atrial (A) filling velocities with normal E:A ratio. Bottom right: Pulmonary venous Doppler with prominent atrial reversal velocity and duration. Bottom left: Tissue Doppler at the medial septal annulus with significantly decreased early annular and septal velocities.
Both grades 3 and 4 diastolic dysfunctions are characterized by restrictive filling patterns. The difference between these stages of diastolic dysfunction has to do with reversibility, bringing us back to the concept of a continuum. The patient who presents with restrictive filling and improves with treatment (later displays a filling pattern consistent with either grade 1 or 2 dysfunction) initially had grade 3 dysfunction. The patient who retains a restrictive filling pattern, despite all treatments, has the most severe form of diastolic dysfunction and is classified as grade 4 dysfunction (irreversible restrictive filling).
Clinical Utility of Diastology
Many common cardiac disorders can result in impaired diastolic ventricular function. In children and adults, diastolic dysfunction can even precede the onset of systolic dysfunction. As a result, serial examinations demonstrating increasing diastolic dysfunction provide a valuable marker of disease progression. For example, in patients with aortic regurgitation, diastolic filling patterns will remain normal or at a grade 1 level (abnormal relaxation) until ventricular compliance decreases. This decrease in compliance will be manifested by a change to a pseudo-normalized filling pattern (grade 2 dysfunction). This change in Doppler pattern indicates that the ventricle has exceeded the limits of its Starling curve and can be used by the clinician as a guide to timing for surgical intervention.
Qualitative versus Quantitative Diastology
The concepts described thus far have focused on outlining Doppler patterns that are associated with normal or abnormal ventricular diastolic performance. The grading continuum provides a “semiquantitative” approach to classifying the severity of the abnormal filling pattern observed. Researchers have also tried to develop formulae to quantitate diastolic cardiac pressures. However, clinicians are not yet able to truly perform quantitative assessments of diastolic function in most children.
There are two exceptions. First, it is possible to indirectly “measure” LA mean pressure in the patient with a restrictive atrial septal defect. This is done by recording the maximal LA–to–right atrial (RA) flow signal with continuous-wave Doppler. The signal is then traced to determine the mean “gradient” between the atria. It is best to trace multiple, consecutive cycles, to account for respiratory variation. The gradient across the atrial septum can then be added to the assumed (or measured) RA pressure to give the mean LA pressure. The most common clinical scenarios in which this can be applied are the neonate with hypoplastic left heart syndrome (HLHS) and a restrictive PFO and, less commonly, the patient with mitral stenosis and a small atrial septal defect. This concept can also be applied to the patient with a “fenestrated” Fontan circulation (Fig. 3.15). In this case, the gradient indicates by how much the mean “RA” pressure exceeds the neo-LA pressure. If the patient’s central venous pressure is known, the LA pressure can be determined by subtracting the mean “fenestration” gradient from the central venous pressure value. This can be helpful in the cardiac intensive care unit, allowing noninvasive assessment of both transpulmonary gradient and LV preload.
Figure 3.15. Fenestrated Fontan connection with continuous “right atrial (RA)”–to–neo–left atrial (LA) shunt. The Doppler flow pattern, assessed for mean gradient, is helpful to quantitate the pressure difference between the two “atrial” chambers. In this patient, the RA–to–LA mean pressure difference was 6 mm Hg. This is consistent with a low (normal) transpulmonary gradient. The patient’s central venous pressure was 14 mm Hg, which would predict a mean LA pressure of 8 mm Hg. LA, left atrium; RV, right ventricle; C, Fontan connection.
Second, a gross estimation of LV end-diastolic pressure can be made by examining the relative durations of the mitral A wave and the pulmonary vein atrial reversal (Fig. 3.13). It has been demonstrated that a pulmonary vein atrial reversal duration that exceeds the A wave duration by more than 29 ms provides a relatively reliable marker for elevated end-diastolic pressure (18 mm Hg or greater). It must be noted that the sensitivity and specificity for this value were 90% and 86%, respectively. This reemphasizes the need to interpret Doppler data in conjunction with the overall assessment of cardiac status. Clearly some normal children can have “abnormal” Doppler flow patterns. The presence of these flow patterns in a patient with cardiac disease will have much greater predictive value than when they are seen in an otherwise normal child.
Limitations and Pitfalls of Doppler Evaluation of Diastolic Ventricular Function
Although Doppler echocardiography can provide tremendous insights into diastolic ventricular function, there are limits to our current understanding. Almost all of the preceding discussion assumes that the patient is in a regular sinus rhythm at the time of the evaluation. Irregular rhythms are difficult to analyze and require that the cardiac cycle length be “matched” when comparing venous and AV valve flow variables. Junctional or ventricular rhythms make assessments invalid that depend on atrial contraction.
The most significant pitfall inherent to this type of diastolic evaluation is the fact that AV valve and venous flow patterns are significantly influenced by variations in ventricular preload. Conditions of reduced volume loading (prolonged fasting, diuretic use) can potentially make significant diastolic dysfunction appear less severe (analogous to the Valsalva maneuver when used to detect “pseudo-normal” filling). Markedly increased volume loads (regurgitation, left-to-right shunts) can produce flow patterns suggestive of severe diastolic dysfunction even when the ventricular compliance is nearly normal. The echocardiographer must take into account the loading conditions present at the time of the evaluation before making a final assessment of the ventricle. As a result, we can only state the diastolic function is normal or abnormal if loading conditions are normal. Conversely, if loading is abnormal (especially if there are increased volume loads present), then we are really able to evaluate diastolic filling pressures, not the underlying myocardial function, with these techniques.
Some congenital heart defects can make diastolic evaluation difficult. AV valve stenosis makes this method of assessment nearly meaningless. It is impossible to separate the disturbed AV valve and venous flows caused by the stenosis from those caused by the ventricle. One must then rely on other techniques (isovolumic relaxation time, tissue Doppler, or automated border detection) to assess diastolic function. Significant AV valve regurgitation can alter systolic flow in the central veins. In these cases, one must rely on AV valve flow patterns and venous atrial reversals more heavily. Tissue Doppler imaging can also be very helpful in these patients. Large atrial septal defects result in equilibration of atrial pressures and make it impossible to separate RV from LV diastolic activity. The flow patterns will reflect the function of the more compliant (“healthier”) ventricle in the presence of a large atrial septal defect. This is not a problem in the functionally univentricular heart because both atria are committed to the same ventricle. Also, in keeping with the concept of diastolic disorders presenting as a continuum, not all patients with diastolic abnormalities display flow patterns that are easily placed into one of the four broad categories of dysfunction. In these cases, one may not be able to specifically “grade” the degree of disease, but it is usually possible to identify the patient as abnormal.
Last, some patients may not have optimal signals available for analysis. In these cases, it is best to state that the examination was not adequate to comment on diastolic function. Attempts to use signals obtained from poor sample volume positions or of inadequate clarity will usually result in incorrect conclusions about the status of the ventricle.
NEWER ECHOCARDIOGRAPHIC TECHNIQUES TO EVALUATE DIASTOLIC VENTRICULAR FUNCTION
Tissue Doppler Imaging
Tissue Doppler imaging is particularly well suited to the quantitative evaluation of LV diastolic function. Both early (Ea) and late (Aa) annular diastolic velocities can be readily obtained with the use of tissue Doppler echocardiography (Fig. 3.9). Similar to systolic tissue Doppler velocities, differences in diastolic velocities exist between (a) the subendocardium and subepicardium, (b) from cardiac base to apex, and (c) between various myocardial wall segments. Previous studies have reported an excellent correlation between the early annular diastolic mitral velocity and simultaneous invasive measures of diastolic function at cardiac catheterization. Early annular diastolic velocities also appear to be less sensitive to changes in ventricular preload compared with the corresponding early transmitral Doppler inflow velocity. These diastolic tissue Doppler velocities, however, are affected by significant alterations in preload. The impact of afterload on tissue Doppler velocities is less controversial, with many studies documenting significant changes in systolic and diastolic annular velocities with changes in ventricular afterload. Therefore, the clinical use of tissue Doppler velocities in patients with valvar stenosis or other etiology of altered ventricular afterload needs to be interpreted carefully in light of this limitation.
Tissue Doppler velocities have been shown to be clinically helpful in the discrimination between normal and pseudo-normal transmitral Doppler filling patterns. In addition to changes incurred by loading conditions, alterations in LA pressure and LVEDP also affect the early transmitral diastolic velocity. However, the corresponding tissue Doppler velocity is characteristically decreased in patients with pseudo-normal filling, allowing differentiation of this abnormal filling pattern from one of normal transmitral Doppler inflow. Clinical reports have suggested a ratio of the early transmitral inflow Doppler signal to the lateral mitral annular early diastolic velocity (mitral E/Ea) as a noninvasive measure of LV filling pressure. Nagueh and colleagues (1997) demonstrated a significant correlation of mitral E/Ea with invasively measured mean pulmonary capillary wedge pressure, whereas subsequent studies have further validated this ratio and reported its applicability in a variety of hemodynamic settings. Additional novel indices of LV diastolic function using tissue Doppler echocardiography have recently been reported that may further expand the role of this modality in the clinical evaluation of LV filling pressures.
Tissue Doppler has also been shown to be of considerable clinical value in the differentiation of constrictive from restrictive LV filling. Evaluation of patients with constrictive pericarditis and restrictive cardiomyopathy with two-dimensional echocardiography and even invasive cardiac catheterization may fail to confidently differentiate these two disease states. Because the myocardium in patients with constrictive pericarditis is most commonly normal, the corresponding tissue Doppler velocities are also normal. However, patients with restrictive cardiomyopathy have been shown to have significantly decreased early diastolic as well as systolic tissue Doppler velocities, allowing separation of these two distinct clinical entities.
Tissue Doppler Studies in Normal Children
To date, a number of transthoracic echocardiographic studies have been performed in children to establish normal reference values of tissue Doppler velocities in this cohort (Table 3.2). Similar to previously published reports for adults, pediatric tissue Doppler velocities vary with age, heart rate, wall location, and myocardial layer. In addition, pulsed-wave tissue Doppler velocities are also highly correlated with parameters of cardiac growth, most notably LVEDD and LV mass, with the most significant changes in these velocities occurring during the first year of life (Fig. 3.9). In a published large series of infants and children, tissue Doppler velocities did not correlate significantly with other more commonly used measures of systolic and diastolic ventricular performance including LV shortening fraction, LV and RV myocardial performance indices, and transmitral inflow Doppler. This lack of correlation in part is likely due to pulsed-wave tissue Doppler assessing longitudinal ventricular function while other more traditional two-dimensional and Doppler methods assess radial and global measures of ventricular performance.
Similar to previously published adult normative data, normal values for the E/Ea ratio in children have also been reported. These values are also affected by age, heart rate, ventricular wall location, LV dimension, and LV mass. Values for E/Ea are highest in neonates and decrease with advancing age primarily due to an increased Ea velocity over this time period. Simultaneous echo:cath measurements correlating the E/Ea ratio in children with invasive measures of LV filling pressure are lacking to date. In a small cohort of children, invasive cardiac catheterization measures of LV function were compared with simultaneously obtained color M-mode and Doppler parameters of LV performance. The ratio of early diastolic mitral annular tissue Doppler velocity to flow propagation velocity (Ea/Vp) correlated closely with invasive LV end-diastolic pressure while the septal Ea velocity correlated with the time constant of relaxation (tau).
Color M-mode Flow Propagation Velocity
Flow propagation of early diastolic filling from the mitral annulus to the cardiac apex can be quantitated by color M-mode echocardiography (Fig. 3.16). As opposed to mitral inflow Doppler, this propagation velocity has been shown to be significantly less affected by changes in heart rate, LA pressure, and loading conditions and therefore may more accurately reflect changes in myocardial relaxation. Numerous studies have demonstrated a significant decrease in flow propagation velocity in patients with diastolic dysfunction of varying etiology. In addition, Ea/Vp has also been shown to be a significant predictor of congestive heart failure and outcome in patients after myocardial infarction. This ratio of flow propagation and Doppler tissue imaging velocity may also be helpful in distinguishing a normal mitral inflow pattern from one of pseudo-normalized mitral inflow. In a small cohort of children undergoing simultaneous cardiac catheterization and transthoracic echocardiography, Border and colleagues (2003) showed a significant correlation between invasively measured LVEDP and the ratio of peak early transmitral Doppler flow velocity to flow propagation velocity (E/Vp). Similar studies have been published for adult data.
Figure 3.16. Measurement of flow propagation velocity (Vp) from color M-mode Doppler in the assessment of left ventricular (LV) diastolic function. A: Diagram demonstrating sequential pulsed Doppler mitral inflow signals as they are propagated from the base to the apex. B: Vp is determined by the slope of the first clearly demarcated aliasing velocity (white line) during early LV filling. C: Paired examples of mitral inflow pulsed Doppler and color Doppler flow propagation. Note that as diastolic dysfunction worsens, the slope of Vp decreases. E, early filling wave; A, atrial filling wave; TD, time delay in ventricular filling. (A and C, From Garcia MJ, Thomas JD, Klein AL. New Doppler echocardiographic applications for the study of diastolic function. J Am Coll Cardiol. 1998;32:865–875.)
Left Atrial Volume
LA volume (LAV) has been identified as a marker of chronically increased LV filling pressure and has been increasingly appreciated as a clinical predictor of adverse cardiovascular outcomes in adults with cardiac disease. Studies evaluating LAV in normal infants and children and in young patients with hypertrophic cardiomyopathy have recently been published.
Several methods to measure LAV have been reported, including the biplane area-length method, the prolate ellipse method, the biplane Simpson method, and three-dimensional echocardiographically derived LAV. The biplane area-length method is demonstrated in Fig. 3.17. Maximal LA area is planimetered at end ventricular systole just before opening of the mitral valve in the orthogonal apical four-chamber and two-chamber views. Care is taken to exclude the confluence of the pulmonary veins and the LA appendage. The length of the left atrium is measured in each of these orthogonal planes using a perpendicular line from the midpoint of the plane of the mitral annulus to the superior aspect of the LA free wall. LAV is calculated as follows:
LAV is most commonly indexed to body surface area. The normal range for LAV in adults is 22 ± 6 mL/m2. Similar indexed values for LAV in normal children over 3 months of age have also been reported.
Figure 3.17. Left atrial volume (LAV). A: Calculation of LAV using the biplane area-length method. Left atrial length is measured in two orthogonal planes (apical four-chamber and two-chamber views) with the shorter length used to calculate LAV. LA area is traced in both views with care taken to exclude the LA appendage and entrance of the pulmonary veins. Example of LAV measured in the apical four-chamber (B) and two-chamber views (C). (From Oh JK, Seward JB, Tajik AJ. The echo manual. 3rd ed. [Figure 7–6, p. 112]. Philadelphia, Pa: Lippincott Williams & Wilkins, 2006.)
ECHOCARDIOGRAPHIC ASSESSMENT OF RIGHT VENTRICULAR FUNCTION
Echocardiographic assessment of RV function has been limited due to the geometric shape of the right ventricle. Doppler echocardiography has historically been useful in the noninvasive prediction of RV systolic and pulmonary artery pressures. However, quantification of RV systolic function by M-mode or two-dimensional echocardiography has relied on the visual assessment of relative RV wall motion or semiquantitative measurements of fractional area change in RV dimension or volume. Newer echocardiographic modalities that have shown promise in quantifying RV function include tricuspid annular plane systolic excursion (TAPSE), additional Doppler measures of RV performance (myocardial performance index, RV dP/dt, and Doppler tissue imaging), acoustic quantification, and three-dimensional echocardiography.
Tricuspid Annular Plane Systolic Excursion
Unlike the radially shortening left ventricle, the right ventricle primarily shortens in a longitudinal direction. TAPSE is an M-mode technique that quantitates the longitudinal motion of the lateral tricuspid annulus during the cardiac cycle (Fig. 3.18). Normal values for TAPSE have been published for both adult and pediatric populations. Similar to other quantitative parameters of ventricular functional assessment, TAPSE has been shown to be dependent upon age, cardiac size, and loading conditions.
Figure 3.18. Tricuspid annular plane systolic excursion (TAPSE). Apical four-chamber view with M-mode through lateral tricuspid annulus. TAPSE is measured as the maximal M-mode excursion during systole = 26 mm.
Right Ventricular Myocardial Performance Index
As described previously, the MPI is a Doppler-derived measure of global ventricular function that can be applied to any ventricular geometry (Fig. 3.7). Studies have validated the ability of the MPI to quantitatively assess RV function in adults and patients with congenital heart disease. In addition, the MPI has demonstrated prognostic power in discriminating outcome in patients with either RV or LV failure. Care, however, must be exercised in using this index in patients with congenital heart disease with altered RV preload or afterload. The RV MPI has been shown to be relatively independent of changes in chronic loading conditions, but the impact of acute changes in physiologic loading are significant and need further definition.
Right Ventricular dP/dt
Similar to the left ventricle, the rate of pressure change over time can also be used as a measure of RV systolic function in patients with tricuspid regurgitation. RV dP/dt has been shown to have correlation with invasive measures of RV performance. RV dP/dt has also been shown to be helpful in the serial assessment of RV function in children with HLHS. Similar to LV limitations with this parameter, RV dP/dt is affected by changes in loading conditions.
Right Ventricular Tissue Doppler Imaging
A relatively new addition to the quantitative evaluation of RV function is tissue Doppler imaging. Tricuspid annular motion has been shown to correlate with RV function in previous studies. TDI has been shown to be a reproducible noninvasive method of assessing systolic and diastolic annular motion and RV function (Fig. 3.10). While affected by both afterload and preload, studies in adults and children with TDI have demonstrated these velocities to be less influenced by altered preload than corresponding mitral or tricuspid inflow Doppler. In particular, isovolumic acceleration appears to be the least load dependent tissue Doppler parameter (Fig. 3.19) and has been shown to correlate with clinical outcome in various disease states as well as cardiac transplantation rejection.
Figure 3.19. Isovolumic acceleration (IVA) at the lateral tricuspid annulus. IVA is measured by the peak isovolumic contraction velocity divided by the time to peak acceleration. In this example, IVA = [0.1 m/s] / (0.033 s) = 3.03 m/s2.
Acoustic Quantification and Right Ventricular Function
Acoustic quantification uses ABD techniques to measure the absolute change and rate of change in RV volume. This modality has been shown to correlate with other invasive methods of RV functional assessment in adults with abnormalities of global RV function. Automated border methods have also shown good correlation with magnetic resonance imaging in assessing changes in RV volume and systolic function. Feasibility of acoustic quantification in the noninvasive transthoracic evaluation of RV function in normal children has also been reported. Ongoing investigation is needed to establish the potential of this technique for the identification and serial evaluation of RV dysfunction in children.
Three-Dimensional Echocardiography and Right Ventricular Function
Recent advances in three-dimensional echocardiography have enabled the noninvasive evaluation of RV volume and function. Because three-dimensional echocardiography can be used to evaluate RV geometry in multiple spatial planes, accurate assessment of changes in RV volume during the cardiac cycle is now possible. Application of this new modality to the evaluation of RV volume and systolic function in adults and children appears promising, and is discussed in detail later in this text.
Evaluation of Right Ventricular Diastolic Function
When RV compliance is significantly reduced (a “stiff” ventricle) and pulmonary pressures are low, it is possible for even atrial contraction to “open” the pulmonary valve and cause forward flow into the pulmonary artery. This can be seen on either continuous- or pulsed-wave Doppler signals obtained from the main pulmonary artery (Fig. 3.20). This phenomenon is most often observed in patients with chronic RV outflow obstruction. In the early postoperative period, this pattern can reflect reduced cardiac output in patients on mechanical positive pressure ventilation. The positive intrathoracic pressures generated by the ventilator impair the RA’s ability to contribute to forward flow. Paradoxically, in the late follow-up of patients after tetralogy of Fallot repair, this pattern (pulmonary arterial forward flow due to atrial contraction) has been associated with improved exercise performance. This is likely due to the fact that a poorly compliant right ventricle will “accept” less regurgitant flow, and thereby has more effective “forward” output, than a normally compliant ventricle. In either situation, the presence of this atrial forward flow in the pulmonary artery is a reliable sign of reduced RV compliance and represents significantly abnormal diastolic function (usually grade 2 or greater).
ECHOCARDIOGRAPHIC ASSESSMENT OF SINGLE VENTRICLE FUNCTION IN PATIENTS WITH COMPLEX CONGENITAL HEART DISEASE
Quantitative measurement of ventricular function in patients with functional single ventricles can be challenging. In most cases, a visual estimate of systolic function from two-dimensional images is used. Quantitative echocardiographic assessment is limited by complex ventricular geometry, often with associated abnormalities of wall motion.
Figure 3.20. Restrictive right ventricular (RV) filling in postoperative tetralogy of Fallot. Parasternal short-axis scan with pulsed-wave Doppler interrogation in the main pulmonary artery. Note the antegrade forward flow (arrow) into the pulmonary artery with atrial contraction. This Doppler pattern is consistent with decreased RV compliance.
Similar to novel techniques used to assess RV function, Doppler echocardiography holds promise in the potential evaluation of global single ventricle function. However, only limited studies to date have addressed either dP/dt or the MPI in patients with functional single ventricles. Data are lacking on the ability of these new Doppler indices to predict outcome in patients with complex single ventricle anatomy. Finally, three-dimensional echocardiography and cardiac magnetic resonance imaging hold promise in the nongeometric assessment of ventricular volume and function but have yet to be comprehensively evaluated in patients with congenital heart disease.
Anconina J, Danchin N, Selton-Suty C, et al. Noninvasive estimation of right ventricular dP/dt in patients with tricuspid valve regurgitation. Am J Cardiol. 1993;71:1495–1497.
Appleton CP, Galloway JM, Gonzalez MS, et al. Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease. J Am Coll Cardiol. 1993;22:1972–1982.
Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol. 1988;12:426–440.
Basnight MA, Gonzalez MS, Kershenovich SC, et al. Pulmonary venous flow velocity: relation to hemodynamics, mitral flow velocity and left atrial volume, and ejection fraction. J Am Soc Echocardiogr. 1991;4:547–548.
Border WL, Michelfelder EC, Glascock BJ, et al. Color M-mode and Doppler tissue evaluation of diastolic function in children: simultaneous correlation with invasive indices. J Am Soc Echocardiogr. 2003;16:988–994.
Chen C, Rodriguez L, Guerrero JL, et al. Noninvasive estimation of the instantaneous first derivative of left ventricular pressure using continuous-wave Doppler echocardiography. Circulation. 1991;83:2101–2110.
Chen C, Rodriquez L, Lethor RA, et al. Continuous wave Doppler echocardiography for noninvasive assessment of left ventricular dP/dt and relaxation time constant from mitral regurgitation spectra in patients. J Am Coll Cardiol. 1994;23:970–976.
Chung N, Nishimura RA, Holmes DR Jr, et al. Measurement of left ventricular dP/dt by simultaneous Doppler echocardiography and cardiac catheterization. J Am Soc Echocardiogr. 1992;5:147–152.
Colan SD, Borow KM, Neumann A. Left ventricular end systolic wall stress velocity of fiber shortening relation. A load independent index of myocardial contractility. J Am Coll Cardiol. 1984;4:715–724.
Denault AY, Gorcsan J III, Mandarino WA, et al. Left ventricular performance assessed by automated border detection and arterial pressure. Am J Physiol. 1997;272:H138–H147.
Devereaux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986;57:450–458.
D’hooge J, Heimdal A, Jamal F, et al. Regional strain and strain rate measurements by cardiac ultrasound: principles, implementation and limitations. Eur J Echocardiogr. 2000;1:154–170.
Donovan CL, Armstrong WF, Bach DS. Quantitative Doppler tissue imaging of the left ventricular myocardium: validation in normal subjects. Am Heart J. 1995;130:100–104.
Eidem BW, McMahon CJ, Ayres NA, et al. Impact of chronic left ventricular preload and afterload on Doppler tissue imaging velocities: a study in congenital heart disease. J Am Soc Echocardiogr. 2005;18:830–838.
Eidem BW, McMahon CJ, Cohen RR, et al. Impact of cardiac growth on Doppler tissue imaging velocities: a study in healthy children. J Am Soc Echocardiogr. 2004;17:212–221.
Eidem BW, O’Leary PW, Tei C, et al. Usefulness of the myocardial performance index for assessing right ventricular function in congenital heart disease. Am J Cardiol. 2000;86:654–658.
Eidem BW, Tei C, O’Leary PW, et al. Nongeometric quantitative assessment of right and left ventricular function: myocardial performance index in normal children and patients with Ebstein anomaly. J Am Soc Echocardiogr. 1998;11:849–856.
Franklin RC, Wyse RK, Graham TP, et al. Normal values for noninvasive estimation of left ventricular contractile state and afterload in children. Am J Cardiol. 1990;65:505–510.
Frommelt PC, Ballweg JA, Whitstone BN, et al. Usefulness of Doppler tissue imaging analysis of tricuspid annular motion for determination of right ventricular function in normal infants and children. Am J Cardiol. 2002;89:610–613.
Frommelt PC, Snider AR, Meliones JN, et al. Doppler assessment of pulmonary artery flow patterns and ventricular function after the Fontan operation. Am J Cardiol. 1991;68:1211–1215.
Garcia MJ, Ares MA, Asher C, et al. Color M-mode flow velocity propagation: an index of early left ventricular filling that combined with pulse Doppler peak E velocity may predict capillary wedge pressure. J Am Coll Cardiol. 1997;29:448–454.
Garcia MJ, Rodriguez L, Ares M, et al. Myocardial wall velocity assessment by pulsed Doppler tissue imaging: characteristic findings in normal subjects. Am Heart J. 1996;132:648–656.
Garcia MJ, Smedira NG, Greenberg NL, et al. Color M-mode Doppler flow propagation is a preload insensitive index of left ventricular relaxation: animal and human validation. J Am Coll Cardiol. 2000;35:201–208.
Geva T, Powell AJ, Crawford EC, et al. Evaluation of regional differences in right ventricular systolic function by acoustic quantification echocardiography and cine magnetic resonance imaging. Circulation. 1998;98:339–345.
Gorcsan J III, Romand JA, Mandarino WA, et al. Assessment of left ventricular performance by on-line pressure area relations using echocardiographic automated border detection. J Am Coll Cardiol. 1994;23:242–252.
Gulati VK, Katz WE, Follansbee WP, et al. Mitral annular descent velocity by tissue Doppler echocardiography as an index of global left ventricular function. Am J Cardiol. 1996;77:979–984.
Gutgesell HP, Paquet M, Duff DF, et al. Evaluation of left ventricular size and function by echocardiography. Results in normal children. Circulation. 1977;56:457–462.
Ha JW, Ommen SR, Tajik AJ, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy using mitral annular velocity by tissue Doppler echocardiography. Am J Cardiol. 2004;94:316–319.
Hagler DJ, Seward JB, Tajik AJ, et al. Functional assessment of the Fontan operation: combined two-dimensional and Doppler echocardiographic studies. J Am Coll Cardiol. 1984;4:745–764.
Harada K, Suzuki T, Tamura M, et al. Role of age on transmitral flow velocity patterns in assessing left ventricular diastolic function in normal infants and children. Am J Cardiol. 1995;76:530–532.
Harada K, Suzuki T, Tamura M, et al. Effect of aging from infancy to childhood on flow velocity patterns of pulmonary vein by Doppler echocardiography. Am J Cardiol. 1996;77:221–224.
Heimdal A, Stoylen A, Torp H, et al. Real-time strain rate imaging of the left ventricle by ultrasound. J Am Soc Echocardiogr. 1998;11:1013–1019.
Helle-Valle T, Crosby J, Edvardsen T, et al. New noninvasive method for assessment of left ventricular rotation: speckle tracking echocardiography. Circulation. 2005;112(20):3149–3156.
Henry WL, Gardin JM, Ware JH. Echocardiographic measurements in normal subjects from infancy to old age. Circulation. 1980;62:1054–1061.
Henry WL, Ware J, Gardin JM, et al. Echocardiographic measurements in normal subjects. Growth-related changes that occur between infancy and early adulthood. Circulation. 1978;57:278–285.
Isaaz K, Munoz del Romeral L, Lee E, et al. Quantitation of the motion of the cardiac base in normal subjects by Doppler echocardiography. J Am Soc Echocardiogr. 1993;6:166–476.
Kanzaki H, Nakatani S, Kawada T, et al. Right ventricular dP/dt (max), not dP/dt (max), noninvasively derived from tricuspid regurgitation velocity is a useful index of right ventricular contractility. J Am Soc Echocardiogr. 2002;15:136–142.
Kapusta L, Thijssen JM, Cuypers MH, et al. Assessment of myocardial velocities in healthy children using tissue Doppler imaging. Ultrasound Med Biol. 2000;26:229–237.
Kaul S, Tei C, Hopkins JM, et al. Assessment of right ventricular function using two-dimensional echocardiography. Am Heart J. 1984;107:526–531.
Klein AL, Tajik AJ. Doppler assessment of pulmonary venous flow in healthy subjects in patients with heart disease. J Am Soc Echocardiogr. 1991;4:379–392.
Koestenberger M, Ravekes W, Everett AD, et al. Right ventricular function in infants, children, and adolescents: reference values of the tricuspid annular plane systolic excursion (TAPSE) in 640 healthy patients and calculation of z score values. J Am Soc Echocardiogr 2009; 22: 715-9.
Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005; 18:1440–1463.
Langeland S, D’hooge J, Wouters PF, et al. Experimental validation of a new ultrasound method for the simultaneous assessment of radial and longitudinal myocardial deformation independent of insonation angle. Circulation. 2005;112:2157–2162.
Lopez L, Colan S, Frommelt PC, et al. Recommendations for quantitation methods during the performance of a pediatric echocardiogram: a report from the Pediatric Measurements Writing Group of the American Society of Echocardiography Pediatric and Congenital Heart Disease Council. J Am Soc Echocardiogr. 2010; 23: 465–95.
Mahle WT, Coon PD, Wernovsky G, et al. Quantitative echocardiographic assessment of the performance of functionally single right ventricle after the Fontan operation. Cardiol Young. 2001;11:399–406.
McDicken WM, Sutherland GR, Moran CM, et al. Colour Doppler velocity imaging of the myocardium. Ultrasound Med Biol. 1992;18:651–654.
McMahon CJ, Nagueh SF, Eapen RS, et al. Echocardiographic predictors of adverse clinical events in children with dilated cardiomyopathy: a prospective clinical study. Heart. 2004;90:908–915.
McMahon CJ, Nagueh SF, Pignatelli RH, et al. Characterization of left ventricular diastolic function by tissue Doppler imaging and clinical status in children with hypertrophic cardiomyopathy. Circulation. 2004;109:1756–1762.
Michelfelder EC, Vermillion RP, Ludomirsky A, et al. Comparison of simultaneous Doppler- and catheter-derived right ventricular dP/dt in hypoplastic left heart syndrome. Am J Cardiol. 1996;77:212–214.
Mulvagh S, Quinones M, Kleiman N, et al. Estimation of left ventricular end-diastolic pressure from Doppler transmitral flow velocity in cardiac patients independent of systolic performance. J Am Coll Cardiol. 1992;20(1):112–119.
Nagueh SF, Middleton KJ, Kopelen HA, et al. Doppler tissue imaging. A noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol. 1997;30:1527–1533.
Nishimura RA, Abel MB, Hatle LK, et al. Assessment of diastolic function of the heart: background and current applications of Doppler echocardiography. Part II. Clinical studies. Mayo Clin Proc. 1989;64:181–204.
Nishimura RA, Abel MD, Hatle LK, et al. Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocardiography: effect of different loading conditions. Circulation. 1990;81:1488–1497.
Nishimura RA, Abel MD, Housman, PR, et al. Mitral flow velocity curves as a function of different loading conditions: evaluation by intraoperative transesophageal Doppler echocardiography. J Am Soc Echocardiogr. 1989;2:79–87.
Oh JK, Appleton CP, Hatle LK, et al. The noninvasive assessment of left ventricular diastolic function with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 1997;10(3):246–270.
O’Leary PW, Durongpisitkul K, Cordes TM, et al. Diastolic ventricular function in children: a Doppler echocardiographic study establishing normal values and predictors of increased ventricular end-diastolic pressure. Mayo Clin Proc. 1998;73:616–628.
Olivier M, O’Leary PW, Pankranz S, et al. Serial Doppler assessment of diastolic function before and after the Fontan operation. J Am Soc Echocardiogr. 2003;16:1136–1143.
Pai RG, Yoganathan AP. Toomes C, et al. Mitral E wave propagation as an index of left ventricular diastolic function. I: its hydrodynamic basis. J Heart Valve Dis. 1998;7: 438–444.
Penny DJ, Rigby ML, Redington AN. Abnormal patterns of interventricular flow and diastolic filling after the Fontan operation: evidence for incoordinate ventricular wall motion. Br Heart J. 1991;66:375–378.
Quinones MA, Gaasch WH, Alexander JK. Influence of acute changes in preload, afterload, contractile state and heart rate on ejection and isovolumic indices of myocardial contractility in man. Circulation. 1976;53:293–302.
Quinones MA, Gaasch WH, Cole JS, et al. Echocardiographic determination of left ventricular stress-velocity relations. Circulation. 1975;51:689–700.
Quinones MA, Waggoner AD, Reduto LA, et al. A new, simplified and accurate method of determining ejection fraction with two-dimensional echocardiography. Circulation. 1981;64: 744–753.
Reeder GS, Currie PJ, Hagler DJ, et al. Use of Doppler techniques (continuous-wave, pulsed-wave, and color flow imaging) in the noninvasive hemodynamic assessment of congenital heart disease. Mayo Clin Proc. 1986;61:725–744.
Rowland DG, Gutgesell HP. Noninvasive assessment of myocardial contractility, preload, and afterload in healthy newborn infants. Am J Cardiol. 1995;75:818–821.
Rychik J, Tian ZY. Quantitative assessment of myocardial tissue velocities in normal children with tissue Doppler imaging. Am J Cardiol. 1996;77:1254–1257.
Silverman NH, Ports TA, Snider AR, et al. Determination of left ventricular volume in children: echocardiographic and angiographic comparisons. Circulation. 1980;62(3):548–557.
Sluysmans T, Sanders SP, van der Velde M, et al. Natural history and patterns of recovery of contractile function in single left ventricle after Fontan operation. Circulation. 1992;86: 1753–1761.
Sutherland GR, Stewart MJ, Groundstroem WE, et al. Color Doppler myocardial imaging: a new technique for the assessment of myocardial function. J Am Soc Echocardiogr. 1994;7:441–458.
Taggart NW, Cetta F, O’Leary PW, Seward JB, Eidem BW. Left atrial volume in children without heart disease and in those with ventricular septal defect or patent ductus arteriosus or hypertrophic cardiomyopathy. Am J Cardiol 2010;106:1500–4.
Tei C, Dujardin KS, Hodge DO, et al. Doppler echocardiographic index for assessment of global right ventricular function. J Am Soc Echocardiogr. 1996;9:838–847.
Tei C, Ling LH, Hodge DO, et al. New index of combined systolic and diastolic cardiac performance index: correlation with simultaneous measurements of cardiac catheterization measurements. J Am Soc Echocardiogr. 1995;26:357–366.
Tei C. New noninvasive index for combined systolic and diastolic ventricular function. J Cardiol. 1995;26:135–136.
Weidemann F, Eyskens B, Jamal F, et al. Quantification of regional left and right ventricular radial and longitudinal function in healthy children using ultrasound-based strain and strain imaging. J Am Soc Echocardiogr. 2002;15:20–28.
Weidemann F, Jamal F, Sutherland GR, et al. Myocardial function defined by strain rate and strain during alterations in inotropic states and heart rate. Am J Physiol Heart Circ Physiol. 2002;283:H792–H799.
Williams RV, Ritter S, Tani LY, et al. Quantitative assessment of ventricular function in children with single ventricles using the Doppler myocardial performance index. Am J Cardiol. 2000;86:1106–1110.
Zoghbi WA, Habib JB, Quinones MA. Doppler assessment of right ventricular filling in a normal population: comparison with left ventricular filling dynamics. Circulation. 1990;82:1316–1324.
1.Which of the following is CORRECT regarding left ventricular ejection fraction?
A.Is best measured in the parasternal long-axis and short-axis imaging planes.
B.Is load dependent.
C.Normal range is between 46 – 70%.
D.Is best measured by M-mode.
E.Is calculated by the following formula: [LVEDD – LVESD] / LV EDD × 100.
2.Which of the following is MOST suggestive of left-ventricular diastolic dysfunction?
A.Mitral inflow Doppler E:A ratio of 2.0
B.Mitral E/Ea ratio of 6.0
C.LA volume index of 22 ml/m2
D.Ratio of pulmonary venous atrial reversal duration to mitral A wave duration of 1.5
E.Mitral inflow Doppler E-wave deceleration time of 180 msec
3.The normal value for LV dP/dt is which of the following?
A.250 mmHg / sec
B.400 mmHg / sec
C.800 mmHg / sec
D.1000 mmHg / sec
E.>1200 mmHg / sec
4.Color M-mode flow propagation velocity is a measure of which of the following?
A.Left ventricular systolic function
B.Left ventricular diastolic function
C.Combined left-ventricular systolic and diastolic function
D.Left atrial filling pressure
E.Right-ventricular systolic function
5.Which of the following is the most load-independent measure of left-ventricular systolic function?
A.Myocardial performance index
B.Left-ventricular ejection fraction
E.Stress – velocity index
6.The myocardial performance index is calculated by which of the following formulae?
A.[ICT + IRT] / ET
B.[LVEDD – LVESD] / [(LVEDD) × LVET]
C.0.85 × [(LA four-chamber area) × (LA 2-chamber area)] / LA length
D.[LVEDD – LVESD] / LVEDD x 100
E.1.04 [(LVID + PWT + IVST)3 – LVID3] × 0.8 × 0.6g
7.Which of the following is CORRECT regarding the velocity of circumferential fiber shortening?
A.Values are highest in infants and neonates.
B.Is not impacted changes in preload or afterload.
C.Is not dependent upon ventricular geometry.
D.Best measured by 2-dimensional echocardiography.
E.Changes in this parameter during childhood attributed to increasing in ventricular preload with aging.
8.The following data are most suggestive of what status of LV diastolic function?
Mitral E wave velocity = 1.2 m/sec
Mitral A wave velocity = 0.3 m/sec
Lateral mitral E/Ea = 18.0
LA volume index = 59 cc/m2
Pulmonary vein Ar duration = 140 msec
Mitral A wave duration = 70 msec
A.Normal diastolic filling
E.Indeterminant filling pattern
9.Which of the following parameters is BEST suited to assess right ventricular diastolic function?
B.RV myocardial performance index (MPI)
C.RV fractional area change (FAC)
D.RV tissue Doppler velocities
E.Tricuspid annular plane systolic excursion (TAPSE)
10.Which of the following is most consistent with right-ventricular diastolic dysfunction?
A.RV MPI = 0.30
B.TAPSE = 20 mm
C.RV FAC = 50%
D.RV dP/dt = 300 mmHg
E.Antegrade flow into main pulmonary artery with atrial contraction
1.Answer: B. LV EF is a load-dependent measure of LV systolic function. Normal reported values are between 56 – 78%. LV EF is typically measured from orthogonal apical four-chamber and two-chamber images utilizing the modified Simpson’s biplane method. The formula to calculate this measurement is: LV EF% = [LVEDV – LVESV]/LVEDV × 100.
2.Answer: D. A ratio of pulmonary venous atrial reversal duration to mitral A wave duration greater than 1.2 is consistent with significantly elevated LV filling pressure. Other parameters that would suggest diastolic dysfunction would be a mitral Doppler E:A ratio > 3.0, Mitral E/Ea ratio > 15, LA volume index > 29 ml / m2, and a mitral inflow E wave deceleration time < 100 msec.
3.Answer: E. The normal LV dP/dt is greater than 1200 mmHg / sec.
4.Answer: B. Color M-mode flow propagation velocity is a measure of the diastolic suction force of the left ventricle and represents the propagation of mitral inflow Doppler from the base to the cardiac apex.
5.Answer: E. The stress – velocity index is a measurement that includes both the velocity of circumferential fiber shortening and end-systolic wall stress. This index is independent of preload, normalized for heart rate, and incorporates afterload resulting in a noninvasive measure of LV contractility that is independent of ventricular loading conditions.
6.Answer: A. The MPI sums the isovolumic time periods (ICT and IRT) and is then divided by the ventricular ejection time. Answer B is the formula for LV shortening fraction, Answer C for LA volume, Answer D for LV ejection fraction, and Answer E for LV mass.
7.Answer: A. The velocity of circumferential fiber shortening is an M-mode measurement that relies on the elliptical shape of the left ventricle. It is highest in neonates and infants. It is relatively independent of preload, but significantly impacted by changes in afterload. Values decrease during childhood due to increases in afterload with aging.
8.Answer: D. Restrictive filling is characterized by a mitral Doppler E:A ratio > 3.0, lateral mitral E/Ea > 15, and a ratio of pulmonary venous atrial reversal duration to mitral A-wave duration > 1.2. This patient also has severe LA dilatation with a severely increased LA volume index.
9.Answer: D. Tissue Doppler velocities can assess the longitudinal motion and velocity of the right ventricle in both early (Ea) and late (Aa) diastole. RV dP/dt, FAC, and TAPSE are all systolic measures of RV function, while RV MPI is a quantitative measure of combined systolic and diastolic function.
10.Answer: E. Antegrade flow across the pulmonary valve during diastole is consistent with a stiff right ventricle with significantly decreased compliance. The listed RV FAC and TAPSE values represent normal RV systolic function. The RV MPI is also normal and is consistent with normal combined RV systolic and diastolic function. The RV dP/dt value is decreased and indicates decreased RV systolic function.