SHERIF F. NAGUEH, MD WILLIAM A. ZOGHBI, MD
14 Evaluation of Right Ventricular Diastolic Function INTRODUCTION PATHOPHYSIOLOGY Right Atrial and Ventricular Dimensions Inferior Vena Cava Diameter and Respiratory Collapse Tricuspid and Pulmonary Regurgitation Signals by Continuous Wave Doppler Tricuspid Inflow Hepatic Venous Flow Tissue Doppler Imaging FUTURE RESEARCH
INTRODUCTION Assessment of right ventricular (RV) function is an important component of the comprehensive evaluation of cardiac function in patients with known or suspected heart disease. RV function may be normal when left ventricular (LV) function is depressed, and conversely, RV dysfunction may occur in the presence of normal LV function. Therefore, a careful evaluation of RV function is essential irrespective of LV functional status. In this chapter, we will discuss the assessment of RV diastolic function with echocardiographic and Doppler techniques.
PATHOPHYSIOLOGY RV diastolic function is determined by a number of factors at the cellular, myocardial, and cardiac chamber levels. Therefore, RV
filling patterns and RV filling pressures reflect the net balance of many variables. Active relaxation is among the important determinants of RV diastolic function and is dependent on calcium uptake by the sarcoplasmic reticulum, intrinsic contractility, uniformity of relaxation, and the load-dependent properties of relaxation. Ventricular suction and active myocardial relaxation in health lead to a small positive pressure gradient between the right atrium and the right ventricle, hence the predominant RV filling in early diastole. In addition, recent animal studies with threedimensional real-time echocardiography have drawn attention to the presence of vortical motion during early diastolic RV filling, which is reduced with chamber dilatation.1 This vortical motion can facilitate RV filling by shunting kinetic energy that could otherwise lead to increased convective deceleration and therefore a reduced right atrial (RA) to RV pressure gradient. With impaired RV relaxation, an increase in RA pressure is needed to maintain adequate RV filling and stroke volume. Myocardial stiffness, RV chamber geometry (dimensions and wall thickness), and RA systolic function determine RV filling later in diastole. In particular, RA systolic function appears to play an important compensatory role in preventing heart failure in the presence of pulmonary hypertension.2 In addition, factors extrinsic to the right ventricle determine RV filling, including pericardial properties, LV filling, and extrinsic compression by mediastinal masses or large pleural effusions. In turn, RV filling can affect LV diastolic volume and pressure.3 It is possible to assess RV relaxation invasively by using highfidelity pressure catheters to measure peak negative pressure/time change (dP/dt) and the time constant of pressure decay during isovolumic relaxation (τ). Both measurements, however, are load dependent,4,5 with an inverse linear relation to systolic load. There is a paucity of data with respect to human measurements that 171
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Chapter 14 • Evaluation of Right Ventricular Diastolic Function include small numbers of patients with coronary artery disease,6 pulmonary hypertension,5 and hypertrophic cardiomyopathy.7 RV chamber stiffness can also be quantified using the combination of RV diastolic pressures and volumes.4,8 In comparison with invasive measurements, echocardiography has the advantages of safety, versatility, and portability, and therefore is the modality that is most frequently utilized to gain insight into RV diastolic function and filling pressures (Table 14-1).
Right Atrial and Ventricular Dimensions The assessment of RV diastolic function should begin with the evaluation of RV dimensions and systolic function, as patients with reduced RV systolic performance have diastolic dysfunction. RV systolic function is usually assessed in a qualitative manner by paying attention to RV dimensions and fractional area change. This is done utilizing two-dimensional echocardiography, with images acquired from the parasternal, apical, and subcostal views. Likewise, the presence of RV hypertrophy is associated with diastolic dysfunction. RA volume is another useful parameter obtained with twodimensional echocardiography. It is usually increased in patients with RV diastolic dysfunction. RA volumes should be considered when drawing conclusions about RA pressure in patients with
TABLE 14-1 ECHO DOPPLER INDICES FOR ASSESSMENT OF RIGHT VENTRICULAR DIASTOLIC FUNCTION 1. Right atrial volumes (maximum, minimum, and emptying fraction) 2. Inferior vena cava diameter and collapse index 3. Downslope of tricuspid regurgitation jet by continuous wave (CW) Doppler 4. Deceleration rate of pulmonary regurgitation jet by CW Doppler 5. Tricuspid inflow velocities (E, A, E/A ratio, and deceleration time of E velocity) 6. Hepatic venous flow (systolic, diastolic, and atrial reversal velocities) 7. Tricuspid annulus early (Ea) and late (Aa) diastolic velocities by tissue Doppler (TD) 8. Isovolumic relaxation time by TD: time between end of systolic velocity and onset of Ea 9. Early (SRe) and late (Sra) diastolic strain rate
NORMAL RA VOLUME
RA
equivocal findings in Doppler parameters. Although RA volumes can be measured at any time during the cardiac cycle, maximal RA volumes (Fig. 14-1) are most frequently measured before tricuspid valve opening at end systole; RA minimum volume is measured after tricuspid valve closure at end diastole. RA emptying fraction can be computed as the difference between RA maximum and minimum volumes/RA maximum volume. In patients with increased mean RA pressure, RA maximum and minimum volumes are increased, whereas RA emptying fraction is decreased.9 The correlation of RA volumes with RA pressure, however, is weak and is heavily modified by RA stiffness and contractility. In addition, RA volumes may be increased for reasons other than diastolic dysfunction, such as atrial fibrillation and tricuspid valve disorders.
Inferior Vena Cava Diameter and Respiratory Collapse Inferior vena cava (IVC) diameter and its change during inspiration are useful indicators of RA pressure. Previous studies have noted that the segment within 2 cm of the RA-IVC junction is the region most responsive to changes in respiratory effort.10,11 In particular, IVC expiratory and inspiratory diameters as well as percent collapse were reported to have significant relations with RA pressure in patients with spontaneous respiration.9–11 Clinically, IVC imaging is acquired in the subcostal view at rest and with inspiratory effort, or a “sniff test.” The presence of at least 50% collapse is usually seen with an RA pressure less than 10 mmHg, whereas patients with RA pressure greater than 10 mmHg typically exhibit less than 50% IVC collapse.11 Figure 14-2 is from a patient with an increased RA mean pressure (>20 mmHg) who exhibits a dilated IVC and minimal change in IVC diameter with inspiration. The limitations of this method occur in patients with dyspnea and those on mechanical ventilation. In patients on mechanical ventilation, IVC percent collapse relates poorly (Fig. 14-3) to mean RA pressure,9,12 whereas IVC diameter at expiration has a somewhat better correlation (r = .58). An IVC diameter no greater than 12 mm appears highly accurate in identifying patients with an RA pressure less than 10 mmHg, whereas a diameter greater than 12 mm has no predictive value in this population.12 In addition, it is possible to image the left hepatic vein from the same window. In one study, the transverse diameter of this vein at expiration and inspiration, as well as end expiratory apnea, was shown to relate significantly to mean RA pressure in a group
MARKEDLY ENLARGED RA
RA
Figure 14-1 Right atrial (RA) end systolic volume from two patients: one with normal RA volume at 26 ml (left) and the other with pulmonary hypertension, a dilated and hypertrophied right ventricle, and a markedly enlarged right atrium, with a maximum volume of 156 ml.
Chapter 14 • Evaluation of Right Ventricular Diastolic Function Expiration
Inspiration
Normal RAP
Figure 14-2 Examples of inferior vena cava (IVC) diameter changes with inspiration (between arrows) from a patient with normal right atrial pressure (RAP) (upper panel) and another with increased RAP (lower panel). In the upper panel, there is complete collapse of the IVC with inspiration, whereas in the lower panel, the IVC is dilated with minimal change in its diameter with inspiration. The latter observation is consistent with an RAP >20 mmHg.
Mean right atrial pressure by catheter (mmHg)
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r = –0.63, y = 16.6 – 0.16x n = 35, SEE = 4.4 mmHg
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IVC collapse index (%) Figure 14-3 Relation between mean right atrial pressure and inferior vena cava (IVC) percent collapse. Patients on mechanical ventilation are shown as blue circles, whereas those with spontaneous breathing are shown as red circles. A significant inverse correlation was present only in the group with spontaneous breathing. (From Nagueh SF et al: Relation of mean right atrial pressure to echocardiographic and Doppler parameters of right atrial and right ventricular function. Circulation 1996;93:1160–1169.)
of 32 patients presenting with acute myocardial infarction.13 Assessment of the left hepatic vein diameter could be helpful in patients where the IVC is not well visualized. However, there is a paucity of data on the clinical application of this approach in patients on mechanical ventilation.
Tricuspid and Pulmonary Regurgitation Signals by Continuous Wave Doppler The rate of rise and fall in tricuspid regurgitation (TR) jet velocity by continuous wave (CW) Doppler parallels the corresponding events in RV pressure, assuming minimal fluctuations of RA pressure throughout the cardiac cycle. Therefore, it is possible to calculate RV peak positive and peak negative dP/dt by using the TR jet and applying the modified Bernoulli equation to convert the TR velocity to RV pressure. In one study,14 a strong correlation was observed between the invasive measurement and the noninvasive estimate of peak negative dP/dt. The limitations of this approach include the need for a complete TR signal and the underestimation of peak negative dP/dt in patients with an RA “v” wave pressure of at least 10 mmHg. For clinical application, one depends more on the shape of the signal (slow decay of the peak velocity to baseline) than the actual measurement, as shown in Figure 14-4. A pulmonary regurgitation (PR) signal by CW Doppler can be recorded in many patients, particularly in the presence of pulmonary hypertension. In addition, it is possible to enhance the signal by using intravenous contrast.15 Once an adequate signal is recorded, its peak velocity can be used to estimate mean pulmonary artery pressure, whereas its end diastolic velocity in conjunction with mean RA pressure can be used to estimate pulmonary artery diastolic pressure.16 Discrepancies may occur if RV end diastolic pressure is significantly different than mean RA pressure. In addition, in the absence of significant PR, the deceleration slope and the pressure half-time of the PR jet by CW Doppler can provide unique insight into RV diastolic function. Patients with increased RV stiffness and rapidly rising RV diastolic pressure have a rapid equalization of the pressure gradient between the pulmonary artery and the right ventricle and therefore a short pressure half-time (Fig. 14-5). In one study, which used right heart catheterization, a pressure half-time of no greater than
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Chapter 14 • Evaluation of Right Ventricular Diastolic Function NORMAL RV FUNCTION
DEPRESSED RV FUNCTION
Figure 14-4 Example of tricuspid regurgitation jets by CW Doppler from two patients: one with normal right ventricular (RV) function (left) and the other with depressed RV function (right). Notice the slow decay of the peak velocity to the baseline from the patient with depressed RV systolic function compared with the normal, as indicated by the slope of the yellow arrows.
Figure 14-5 Example of pulmonary regurgitation jets by CW Doppler from two patients: one with normal right ventricular (RV) diastolic pressure (left) and the other with highly increased RV diastolic pressures (right). Notice the very steep deceleration of pulmonary regurgitation from the patient in the right panel as indicated by slope of the yellow arrows.
150 ms was the best predictor of RV involvement in patients presenting with acute inferior wall myocardial infarction.17 The same investigators reported that this parameter was the only predictor of overall in-hospital clinical events in the same patient population.18
Tricuspid Inflow Pulsed-wave (PW) Doppler recording of tricuspid inflow is essential for the assessment of RV filling. Care should be exercised to obtain the best alignment with the direction of blood flow, which typically requires a medial movement of the transducer from the conventional apical position.19 The recording is obtained by placing a 1–2 mm sample volume at the valve annulus and tips with filter and gain adjustments to obtain a clear signal. Respiratory variability is an additional factor that needs to be considered with measurements taken at end expiratory apnea or as the average of five to seven consecutive cardiac cycles. The latter approach has been shown to yield identical results to those obtained at end expiratory apnea.20
Similar to mitral inflow, tricuspid inflow (Fig. 14-6) is analyzed for peak early (E) and late (A) diastolic velocity, deceleration time (DT) of E velocity, duration of A velocity, and the fraction of RA contribution to RV filling (the atrial filling fraction [AFF]). All measurements except for the A duration are obtained from the Doppler recordings at the level of the valve tips. The A duration is measured from the recording at the level of the tricuspid annulus. Because the tricuspid and pulmonary valves are in different planes, isovolumic relaxation time (IVRT) is measured by Doppler using two time intervals, as the difference between the duration from the QRS complex to onset of tricuspid inflow and the interval from the QRS complex to end of pulmonic flow. Alternatively, IVRT can be calculated by subtracting the time between the QRS complex and the end of pulmonic ejection from the duration of the TR jet. Early diastolic RV filling is reduced with normal aging,20,21 which should be considered when drawing conclusions about RV diastolic function using tricuspid inflow velocities. In general, patients with impaired RV relaxation have a reduced E/A ratio, a prolonged IVRT and DT, and an increased AFF. As RA pres-
Chapter 14 • Evaluation of Right Ventricular Diastolic Function
Hepatic Venous Flow The flow in the hepatic veins is largely determined by RA pressure during the cardiac cycle. In normal subjects, antegrade flow from the hepatic veins to the RA occurs in systole (S) and diastole (D). With RA contraction, as well as in late ventricular systole (Vr), brief retrograde flow (Ar) occurs into the hepatic veins.23 It is feasible to record high-quality signals by transthoracic imaging from the subcostal window. It is also possible to record them by transesophageal echocardiography (TEE) in the course of a transesophageal examination.24 The sample volume (3–4 mm) is placed 1–2 cm in the hepatic veins, close to their entrance into the IVC. Similar to tricuspid inflow velocities, flow should be recorded for five to seven consecutive cardiac cycles or at end expiratory apnea. E VAR
VVR A
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30 r = 0.66 n = 35 y = –1 + 9.6x SEE = 3.8 mmHg
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Figure 14-6 Schematic diagram of tricuspid inflow (left) and hepatic venous flow (right). E, peak early diastolic velocity; A, peak late diastolic velocity; AT, acceleration time of E velocity; DT, deceleration time of E velocity; VS, peak systolic velocity; VD, peak diastolic velocity; VVR, midsystolic reversal velocity; VAR, peak atrial reversal velocity; AR dur, duration of atrial reversal velocity. (From Nagueh M et al: Relation of mean right atrial pressure to echocardiographic and Doppler parameters of right atrial and right ventricular function. Circulation 1996;93:1160–1169.)
Figure 14-7 Examples of normal tricuspid inflow (left), impaired relaxation (middle), and restrictive filling (right). E, early velocity; A, velocity with atrial contraction.
Quantitative measurements include the peak velocity, the duration, and the time-velocity integral (TVI) of velocity at each of the phases (see Fig. 14-6), as well as the proportion of forward flow during systole and diastole, using either peak velocity or TVI measurements. Such parameters can be used to assess mean RA pressure in patients who are in sinus rhythm.9 This is based on the following premise: Systolic forward flow from the hepatic veins to the RA depends on RA relaxation, RV systolic function, and RA pressure. In the presence of a normal RA pressure, predominant flow occurs in systole (Fig. 14-9). As the RA pressure increases, the pressure gradient between the hepatic veins and the right atrium decreases, and correspondingly forward systolic flow decreases.9,25 This abnormal pattern of flow is most exaggerated in patients with restrictive physiology with large atrial and venous reversals.22 Systolic forward flow parameters, particularly systolic filling fraction (systolic flow/total antegrade flow), derived from either TVIs or maximal velocities, have been successfully applied to estimate RA pressure noninvasively in patients with a variety of diseases, including those on mechanical ventilation (Fig. 14-10). Ar duration is also of value, as it has been shown to
Mean right atrial pressure by catheter (mmHg)
sure increases, E/A ratio increases and DT shortens (Fig. 14-7). However, the individual response is highly variable and dependent on the interplay between many hemodynamic parameters, such that the E/A ratio has a significant positive relation with mean RA pressure but with a wide scatter (Fig. 14-8). Nevertheless, in patients with RV systolic dysfunction, a short DT is usually associated with increased filling pressures.9 In addition, diastolic TR, when present and in the absence of atrioventricular (AV) block, indicates the presence of increased RV stiffness and highly increased RV filling pressures.22
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Tricuspid E/A ratio Figure 14-8 Relation between tricuspid E/A ratio and mean right atrial pressure. (From Nagueh SF et al: Relation of mean right atrial pressure to echocardiographic and Doppler parameters of right atrial and right ventricular function. Circulation 1996;93:1160–1169.)
Chapter 14 • Evaluation of Right Ventricular Diastolic Function
Figure 14-9 Examples of hepatic venous flow. In the example shown on the left, forward flow occurs predominantly in systole, which corresponds to a mean right atrial (RA) pressure ≤5 mmHg. In the example on the right, the peak systolic and diastolic velocities are similar, corresponding to mean RA pressure of 5–10 mmHg.
SYSTOLIC FILLING FRACTION 30 r = –0.86 n = 35 y = 21.6 – 24x SEE = 2.5 mmHg
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Figure 14-10 Correlation between mean right atrial pressure and right atrial systolic filling fraction calculated using the time-velocity integral (left) and peak systolic velocity (right). (From Nagueh SF et al: Relation of mean right atrial pressure to echocardiographic and Doppler parameters of right atrial and right ventricular function. Circulation 1996;93:1160–1169.)
relate to RA pressure9,26 and late diastolic RV pressures (Fig. 14-11). These principles are not applicable to patients in nonsinus rhythms or with cardiac transplants, tricuspid valve disease (significant stenosis or regurgitation and prosthetic valves), or pericardial compression syndromes (tamponade or constriction). However, hepatic venous flow may still be helpful in these conditions. For example, patients with severe TR usually exhibit systolic flow reversal (Fig. 14-12) into the hepatic veins.27 Likewise, hepatic venous flow can help differentiate pericardial constriction from restrictive cardiomyopathy. In patients with constrictive physiology, a predominant systolic or biphasic flow pattern is frequently recorded. In addition, respiratory flow variation presents unique insight into RV and LV filling, where RA and RV filling increase with inspiration and the Vr and Ar velocities become more prominent with expiration.28 The latter observation is
dependent upon increased LV filling with expiration in the presence of a taut pericardium, which leads to reduced RV filling with RA contraction. Accordingly, RA contraction results in increased flow into the hepatic veins during expiration. Table 14-2 shows a practical summary for estimating mean RA pressure using an IVC collapse index and hepatic venous flow.
Tissue Doppler Imaging Tissue Doppler imaging (TDI) allows the recording of myocardial velocity during the cardiac cycle, including velocities at the tricuspid annulus. In addition, using TDI or recently developed speckle tracking technology, one can measure local rates of systolic compression and early and late diastolic expansion of the myocardium (systolic and diastolic strain rates, respectively). For assessment of RV global diastolic function, tricuspid annulus velocities
Chapter 14 • Evaluation of Right Ventricular Diastolic Function
Figure 14-11 Hepatic venous flow from a patient with pulmonary hypertension and increased late diastolic right ventricular pressures and stiffness. Notice the prominent AR (atrial reversal) velocity.
Figure 14-13 Example of tissue Doppler recording of myocardial velocities from the right ventricular free wall in a normal subject. The inset shows the location of the sample volume at the right side of the tricuspid annulus. Notice the presence of an Sa peak velocity of 15 cm/s, a peak Ea velocity of 18 cm/s, and an Ea/Aa ratio >1. IVRT, isovolumic relaxation time between end of Sa and onset of Ea; Sa, systolic ejection velocity; Ea, early diastolic velocity; Aa, late diastolic velocity.
examination of function of multiple segments simultaneously, in the same beat; however, an estimate of mean myocardial velocities is provided. The velocity measured by color TDI is therefore lower than the maximal velocity measured by PW Doppler, which should always be considered when normal values and results are compared among different studies. The following indices of diastolic function are measured by TDI at the tricuspid annulus: ❒ ❒ ❒ ❒ ❒ ❒ Figure 14-12 Hepatic venous flow from a patient with severe tricuspid regurgitation. Notice the presence of flow reversal during systole.
TABLE 14-2 SUMMARY OF RIGHT ATRIAL PRESSURE (RAP) ESTIMATION USING INFERIOR VENA CAVA (IVC) COLLAPSE INDEX AND HEPATIC VENOUS FLOW MEAN RAP (mmHg)
IVC % COLLAPSE
HEPATIC VEINS
0–5 5–10 10–15 ≥20
≥50 ≥50 <50 <50
VS > VD VS = VD VS < VD Flow only with VD
VS = systolic velocity; VD = diastolic velocity.
are recorded by placing the PW Doppler sample volume (4– 5 mm) at the right border of the annulus. It is also possible to use color Doppler two-dimensional images to obtain a display of myocardial and annular velocities. The advantages of the PW approach include online beat-to-beat evaluation and the spectral display of velocities. On the other hand, color TDI allows the
Early diastolic velocity (Ea) Late diastolic velocity (Aa) Ea/Aa ratio RV regional IVRT (Fig. 14-13) Early diastolic strain rate Late diastolic strain rate
A number of studies have evaluated the utility of Ea, Aa, and the Ea/Aa ratio to assess RV diastolic function. Patients with RV diastolic dysfunction usually have reduced Ea velocity and a reduced Ea/Aa ratio. Aa velocity may be increased in the early course of diastolic dysfunction, whereas with increased RV late diastolic pressures, it may decrease. Using these simple and reproducible velocity measurements, a number of investigators have reported on RV diastolic function in several cardiac disorders. These included patients with coronary artery disease,29 inferior wall myocardial infarction and RV involvement,30 dilated cardiomyopathy,31 hypertrophic cardiomyopathy,32 obesity,33,34 congenital heart disease,35 and systemic36 and pulmonary hypertension.37 While the observations in this chapter support an important clinical role for TDI-derived velocities, there have been no direct validation studies in animals or humans against invasive measurements of negative dP/dt or τ. Similar to early diastolic velocity at the mitral annulus, tricuspid Ea is load dependent in normal ventricles.38 On the other hand, the tricuspid Ea/Aa ratio appears unchanged with preload reduction.38 Notwithstanding, existing studies support the conclusion that tricuspid annulus Ea velocity is not positively affected by preload in patients with RV dysfunction, given the presence of an inverse correlation between Ea and mean RA pressure in cardiac patients.39 Accordingly, the ratio of
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Chapter 14 • Evaluation of Right Ventricular Diastolic Function tricuspid E velocity to annular Ea velocity has been applied to predict RV filling pressures (Figs. 14-14 and 14-15), in an analogous manner to the use of mitral velocities, in both animal40 and human studies.39,41 In the human studies, different groups of patients were evaluated, and overall an E/Ea ratio greater than 6 had a sensitivity of 79% and a specificity of 73% for mean RA pressure of at least 10 mmHg.39 The good correlation of tricuspid E/Ea ratio to mean RA pressure was noted in patients with and without RV systolic dysfunction, as well as in those on mechanical ventilation.39
TRICUSPID INFLOW
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In cardiac transplant recipients, the ratio of E to Ea is also useful (Fig. 14-16), where a ratio greater than 8 had a sensitivity of 78% and a specificity of 85% for RA pressure of at least 10 mmHg.41 Furthermore, Ea of the tricuspid annulus had no significant relation to RA pressure and was not altered by pressure changes. Accordingly, the E/Ea ratio readily detected changes in mean RA pressure of at least 5 mmHg (Fig. 14-17) with a sensitivity of 70% and a specificity of 75%.41 These observations are in contrast to the limited role of hepatic venous flow in the transplant population as a result of mechanical dissociation between the donor and recipient atria, which alters the systolic and diastolic components of hepatic venous flow and renders their interpretation more challenging. A recent study reported on the clinical application of another TDI-derived measurement, namely the time interval between the end of tricuspid annular systolic velocity and the onset of annular Ea. The latter time interval had a significant inverse correlation with mean RA pressure. In a study of 21 patients, a time interval of less than 59 ms had a sensitivity of 80% and a specificity of 88% in identifying patients with RA pressure greater than 8 mmHg.42 There are advantages to determining mean RA pressure by using TDI. In the case of RV regional IVRT, this is a single measurement that is not affected by angulation. In addition, the tricuspid E/Ea ratio and the above time interval are particularly helpful in patients without subcostal windows where there is concomitant inability to image the IVC and acquire hepatic venous flow. However, these methods may not be accurate in the presence of nonsinus rhythms and tricuspid valve disease.
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FUTURE RESEARCH
Ea
Aa
–20 Figure 14-14 Upper panel shows early (E) and late (A) diastolic tricuspid inflow velocities. Lower panel shows the annular velocities during systolic ejection (Sa) and early (Ea) and late (Aa) diastole. The E/Ea ratio is 6.75, predicting a mean right atrial pressure of 12 mmHg (catheter pressure 11 mmHg). (From Nageh MF et al: Estimation of mean right atrial pressure using tissue Doppler imaging. Am J Cardiol 1999;84:1448–1451.)
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Evaluation of RV diastolic function is important clinically. Echocardiography and Doppler provide several complementary methods for evaluation of RV diastolic function and prediction of mean RA pressure. These include the evaluation of cardiac structure and function; RV, RA, and IVC size; myocardial velocities; strain rate with tissue Doppler and speckle tracking technology; and hepatic venous flow patterns. These parameters allow a
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Figure 14-15 Upper panel: regression plot between mean right atrial pressure (RAP) and tricuspid E/Ea ratio in 62 patients with simultaneous invasive and echocardiographic measurements. Lower panel: Bland-Altman plot of Doppler-derived RAP versus catheter RAP. Mean difference between Doppler and catheter pressures was 0.3 ± 3.7 mmHg. Upper and lower lines represent mean + and mean −2 SDs, respectively. (From Nageh MF et al: Estimation of mean right atrial pressure using tissue Doppler imaging. Am J Cardiol 1999;84:1448–1451.)
Chapter 14 • Evaluation of Right Ventricular Diastolic Function 25
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Figure 14-16 Left, relation between mean right atrial pressure (RAP) and tricuspid E/Ea ratio in patients who have undergone cardiac transplantation. Right, Bland-Altman plot of Doppler-derived RAP versus catheter RAP. (From Sundereswaran L et al: Estimation of left and right ventricular filling pressures after heart transplantation by tissue Doppler imaging. Am J Cardiol 1998;82:352–357.)
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Figure 14-17 Left: relation between changes in mean right atrial pressure (RAP) and those predicted by Doppler in patients who have undergone cardiac transplantation. Right: Bland-Altman plot of changes in RAP by Doppler and changes in mean RAP by right heart catheterization. (From Sundereswaran L et al: Estimation of left and right ventricular filling pressures after heart transplantation by tissue Doppler imaging. Am J Cardiol 1998;82:352–357.)
comprehensive approach to the evaluation of RV diastolic function and its effect on filling pressures. The availability of threedimensional technology will undoubtedly improve quantification of RV volumes and systolic function. Whether three-dimensional technology will further improve the evaluation of RV diastolic function remains to be determined. In addition, the presence of sensitive indices of RV diastolic function such as early diastolic strain rate may help in the earlier diagnosis of RV dysfunction in cardiomyopathic disorders, as in patients with arrhythmogenic RV dysplasia, where conventional echocardiography may not be diagnostic of RV disease. Furthermore, there is a need to study the presence of systolic and diastolic RV intraventricular dyssynchrony, its impact on global RV diastolic function, and the effect of different RV pacing sites on RV performance. Finally, these different methods to assess RV function can be used to track functional changes in response to medical/surgical therapy for
several cardiovascular disorders that affect the right ventricle, including congenital heart disease and pulmonary hypertension. REFERENCES 1. Pasipoularides A, Shu M, Shah A, et al: Diastolic right ventricular filling vortex in normal and volume overload states. Am J Physiol Heart Circ Physiol 2003;284:H1064–H1072. 2. Gaynor SL, Maniar HS, Bloch JB, et al: Right atrial and ventricular adaptation to chronic right ventricular pressure overload. Circulation 2005;112: I212–I218. 3. Moore TD, Frenneaux MP, Sas R, et al: Ventricular interaction and external constraint account for decreased stroke work during volume loading in CHF. Am J Physiol Heart Circ Physiol 2001;281:H2385–H2391. 4. Leeuwenburgh BP, Steendijk P, Helbing WA, Baan J: Indexes of diastolic RV function: Load dependence and changes after chronic RV pressure overload in lambs. Am J Physiol Heart Circ Physiol 2002;282: H1350–H1358.
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