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Doppler Flow Patterns in the Evaluation of Pulmonary Hypertension CARMEN GINGHINĂ, DENISA MURARU, AURORA VLĂDAIA, RUXANDRA JURCUŢ, B.A. POPESCU, ANDREEA CĂLIN, S. GIUŞCĂ “Prof. Dr. C.C. Iliescu” Institute of Cardiovascular Diseases, Bucharest, Romania Pulmonary arterial hypertension is defined as a group of diseases characterised by a progressive increase in pulmonary vascular load, leading to marked increase in pulmonary artery pressure, right ventricular failure and premature death. Given the nonspecific nature of its early symptoms and signs, pulmonary arterial hypertension (PAH) is often diagnosed in its advanced stages. Although clinical assessment is essential when initially evaluating patients with suspected PAH, echocardiography is a key screening tool in the diagnostic algorithm, because, in comparison with invasive measurements, it has the advantages of being safe, portable, and repeatable. Therefore, Doppler echo is the modality most frequently used in pulmonary hypertension patients. Several echocardiographic techniques centered on the Doppler principle (both conventional Doppler parameters and tissue Doppler imaging) used in the assessment of PAH magnitude and its cardiac effects are presented in this paper. They provide important data on the severity, possible causes and consequences of pulmonary hypertension, both initially and during follow-up, therefore having the ability to estimate disease progression, prognosis, or to monitor therapeutic response. Doppler echocardiography allows to noninvasively estimate systolic pulmonary arterial pressure (SPAP), mean and end-diastolic pulmonary arterial pressure, as well as the quantification of right ventricular (RV) function and the evaluation of pulmonary vascular resistance (PVR). Key words: pulmonary arterial hypertension, right arterial pressure, tissue Doppler imaging. Pulmonary arterial hypertension is defined as a group of diseases characterised by a progressive increase in pulmonary vascular load, leading to marked increase in pulmonary artery pressure, right ventricular failure and premature death [1]. The evaluation of pulmonary artery pressure is a routine part of an echocardiography examination. Although certain two-dimensional (2D) echocardiographic features can suggest pulmonary hypertension, Doppler echocardiography is the primary method for determining actual pulmonary pressures [2]. However, in certain cases it can be challenging or even impossible to make a definite diagnosis based solely on Doppler findings, because there is no single parameter to discriminate the presence of pulmonary hypertension or a specific cutoff value to work in any conditions. There are rather frequent false positive/false negative results and the influence of age, rhythm, preload or the technical pitfalls which render Doppler parameters more or less reproducible must be taken into account. To increase the accuracy of diagnosis, it is highly recommended to do a comprehensive evaluation by a multiple parameter approach, to avoid the most frequent pitfalls and to finally integrate the findings in clinical context. ROM. J. INTERN. MED., 2009, 47, 2, 109–121 A thorough Doppler assessment in pulmonary hypertension must cover 3 main objectives: estimation of pulmonary arterial pressure, evaluation of pulmonary vascular resistance and right ventricular function. DOPPLER ECHOCARDIOGRAPHY FOR ESTIMATION OF PULMONARY ARTERIAL PRESSURE Doppler echocardiography allows to noninvasively estimate systolic pulmonary arterial pressure (SPAP), as well as mean and enddiastolic pulmonary arterial pressure. SPAP is equivalent to right ventricular (RV) systolic pressure assuming there is no gradient in systole between the RV and pulmonary artery (PA) (such as infundibular or valvular pulmonary stenosis). The most common approach is to measure the peak velocity of a tricuspid regurgitant jet (TRVmax) and apply the modified Bernoulli equation (4TRVmax2 + estimated RAP). This method has a good correlation with invasive pressure measurements. However, the assessment of tricuspid regurgitation (TR) is thought to be problematic in 20% of healthy 110 Carmen Ginghină et al. subjects and up to 70% of patients suffering from chronic obstructive pulmonary disease (COPD). Contrast agents can be used to enhance the TR signal, but require venous catheterization [3]. Tricuspid regurgitation can be evaluated from multiple echocardiographic windows, including the parasternal inflow tract view, short-axis view at the base of the heart, and apical four-chamber view. From the apical position, the transducer needs to be angled more medially and inferiorly from the mitral valve signal. It should be emphasized that in the normal disease-free state, the tricuspid valve, because of its complex closure pattern, often exhibits mild degrees of valvular regurgitation, which may be confined to early systole. The 2 prevalence of regurgitation increases with patient age. The normal tricuspid regurgitation velocity is 1.7 to 2.3 m/s at rest. A higher velocity indicates pulmonary hypertension, right ventricular outflow tract (RVOT) obstruction, or pulmonic stenosis. When noted, the normal physiologic degrees of regurgitation are typically associated with relatively low tricuspid regurgitation velocities, implying right ventricular systolic pressures in the normal range. When the continuous wave Doppler spectrum of the tricuspid regurgitation jet is suboptimal, injection of agitated saline solution into an arm vein enhances the tricuspid regurgitation velocity signal (Fig. 1A,B). A B Fig. 1. – Transthoracic echocardiography, apical four-chamber view,continuous wave Doppler recording of tricuspid regurgitation velocity: A) suboptimal spectrum; B) enhanced signal after injection of agitated saline solution. Probably the most common cause of tricuspid regurgitation is functional valvular regurgitation secondary to annular dilation, altered RV geometry with apical displacement of tricuspid leaflets [4], which in turn may be the result of pulmonary hypertension of any cause. The severity of functional tricuspid regurgitation can range from mild to severe. The examiner should make sure that the maximum TR jet envelope is obtained, as any underestimation of the TR jet velocity will result in an underestimation of the pressure by a “squared” factor. The best approach is to position the transducer over the RV apex, medial to the 4-chamber view apical position. The subcostal approach may confer additional diagnostic power in patients with hyperexpanded lungs. Use of color flow Doppler helps in optimal alignment of the cursor with the regurgitant jet (Fig. 2A,B). Moreover, the velocity may be also underestimated if not measured at end expiration (Fig. 3A,B). An intense continuous wave Doppler signal usually indicates at least moderate TR. A duration of longer than 100 ms is usually considered significant. Marked TR is associated with an increased forward tricuspid flow velocity (but usually <1 m/s) and a rapid tricuspid inflow deceleration time. An early peaking TR jet by CW with a TR “cut-off” sign (similar to that seen with acute severe MR) is consistent with severe TR and is associated with early equalization of RA and RV pressures (Fig. 4). As stated before, for assessing the SPAP the best validated method is the modified Bernoulli equation. The tricuspid regurgitation jet can be used to determine right ventricular systolic pressure, by calculating the right ventricle to right atrial pressure gradient and then adding estimated right atrial pressure. 3 Doppler flow patterns and pulmonary hypertension 111 A B Fig. 2. – Transthoracic echocardiography, CW Doppler recording of TR from: A) apical 4-chamber view which would signify that PAP is normal (25mmHg) in the presence of mean RAP of 5 mmHg; B) subcostal approach, which allows better alignment with a more accurate estimation of increased PAP of approximately 46 mmHg. B A Fig. 3. – Transthoracic echocardiography CW Doppler recording of TR from apical 4-chamber view: A) a marked respiratory variation with a decreased TR velocity with inspiration; B) the optimal recording in held expiration with no variability of peak TR velocity. Fig. 4. – Transthoracic echocardiography CW Doppler recording of TR from apical 4-chamber view: note the features of severe tricuspid regurgitation (see text). A major variable in determining the right ventricular systolic pressure is the method by which a right atrial pressure (RAP) is either assumed or calculated. Multiple algorithms have been proposed, each of which has provided a relatively good correlation over a broad range of pulmonary artery pressures. Many laboratories use a floating constant of 5, 10, or 15 mm Hg, based on 112 Carmen Ginghină et al. the size of the right atrium and the severity of tricuspid regurgitation. Using this qualitative approach, when tricuspid regurgitation is mild and the right atrial size is normal, an assumed right atrial pressure of 5 mm Hg is used. For moderate degrees of tricuspid regurgitation with mild or no right atrial enlargement, an assumed constant of 10 mm Hg can be used. If tricuspid regurgitation is severe and noted in the presence of a dilated right atrium, an assumed constant of 15 mm Hg can be used. Instead, for a more precise estimation, several parameters have been proposed, such as: caval respiratory variability, flow recordings in hepatic or superior vena cava veins, tricuspid inflow or tissue Doppler recordings of RV free wall. The accuracy of RAP estimation is of key importance especially for intermediate TR jet 4 velocities, because it may discriminate between normal and abnormal PAP. A highly compliant vessel, the inferior vena cava changes shape and dimensions with changes in central venous pressure and the respiratory cycle. The size and respiratory variation of the inferior vena cava have been used to predict right atrial pressure. Dilation of the inferior vena cava suggests increased central venous pressure and may accompany volume overload states. The diameter of the inferior vena cava normally decreases more than 50% during inspiration. A blunted or absent inspiratory decrease in the inferior vena cava diameter suggests increased right atrial pressure. The most common estimation of RAP is based on caval respiratory index: if less than 50% then RAP is at least 10 mmHg (Fig. 5A,B). A B Fig. 5. – Transthoracic echocardiography subcostal view: A) two-dimensional image of a moderate dilated inferior vena cava; B) in the same patient, M-mode cursor placed at the inferior vena cava to assess the caval respiratory index. However, the significance of inferior vena cava (IVC) diameter and collapse with inspiration is limited in several categories: athletes, mechanically ventilated or dyspneic patients [5]. From the subcostal transducer location, alignment of the Doppler beam with inferior vena caval flow is difficult, and it has become customary to substitute hepatic vein flow for this purpose. Because hepatic vein flow and inferior vena caval flow are similar and because it is generally easier to align the Doppler signal with a hepatic vein, this is both useful and practical. Antegrade flow (toward the right atrium) has two main components: a larger systolic wave and a slightly smaller diastolic wave. Between these two antegrade flow patterns, at end-systole, a small retrograde flow pattern may be recorded. Likewise, during atrial systole, some retrograde flow is also present. Hepatic vein flow is respiratory cycle dependent with increased flow velocity during inspiration and decreased flow velocity (and a greater degree of retrograde flow) during expiration. Several disease states result in characteristic abnormalities of hepatic vein flow. As a surrogate for inferior vena caval flow, any condition that affects either right atrial pressure or filling will alter hepatic vein flow velocity. The evaluation of hepatic venous flow constitutes the cornerstone of Doppler assessment of RAP. As RAP increases, the pressure gradient between the hepatic veins and the RA decreases, thus lowering the forward systolic flow (Fig. 6A,B). The hepatic venous systolic filling fraction (calculated as the ratio between the time-velocity integral [TVI] of the systolic forward flow (PVS-wave), PVS and 5 Doppler flow patterns and pulmonary hypertension A 113 B Fig. 6. – Transthoracic echocardiography subcostal view hepatic venous Doppler flow in: A) healthy patient-normal hepatic vein inflow consists of flow reversal with atrial systole (A), systolic forward flow (S), forward flow nadir or reversal at end systole (atrial V wave), and diastolic forward flow (D). Note that systolic filling fraction is greater than 55% (68%) and that S velocity is higher than A velocity, both of which predict normal mean right atrial pressure. TVI, Time-velocity integral; B) PAH patient: systolic filling fraction is less than 55% (33%) and A wave is larger compared to systolic S wave. sum of PVS and diastolic forward flow pulse (PVD) TVIs) has been shown to be a predictor of RAP with dichotomous separation of RAP greater than 8 mm Hg by a hepatic vein systolic filling fraction of less than 55% with a sensitivity of 86% and a specificity of 90% [6]. Moreover, a larger A wave after atrial contraction compared to forward systolic S wave also predicts increased RAP [7][8]. The superior vena cava can be visualized from the suprasternal notch as a vertical structure just to the right of the aortic arch but it is more readily evaluated using transesophageal echocardiography. Both long- and short-axis views of the vessel are possible. Occlusion or external compression of the superior vena cava is a common clinical problem that can be assessed using echocardiography. Doppler interrogation of flow velocities into the superior vena cava is easy to obtain in all patients with congestive heart failure and makes it possible to estimate the severity of the impairment of the right circulatory function using simple categoric classes. The venous flow velocity pattern was considered normal when the systolic/diastolic ratio was ≥1 and ≤2, the flow pattern was categorized as “predominant systolic wave” when the ratio was >2, and as “predominant diastolic wave” when the ratio was <1 (Fig. 7A,B). The differentiation among normal, “predominant systolic wave,” and “predominant diastolic wave” central venous flow velocity patterns not only distinguished patients with normal from congestive heart failure patients with high right atrial pressure, but also differentiated patients with normal right heart hemodynamics from those in whom a normal right atrial pressure was associated with an impaired right ventricular function [9]. An advantage of tissue Doppler imaging (TDI) in assessing RAP is that it does not require subcostal imaging and allows 1-step method for assessment. It provides information independent of RV function and is still useful in mechanically ventilated patients. Two TDI techniques have been described for estimation of mean RAP. Both methods allow for dichotomous differentiation of mean RAP. To apply the technique, pulse wave TDI is performed at the lateral tricuspid annulus in the apical 4-chamber view. Tricuspid E/E’ ratio allows dichotomous differentiation of the mean RAP. An early tricuspid inflow velocity/early tricuspid annular motion (E/E’) ratio greater than 6 predicts a mean RAP greater than 10 mm Hg with a sensitivity of 79% and a specificity of 73% (Fig. 8A,B). The ratio of tricuspid peak early inflow velocity (E) obtained by Doppler to the tricuspid annular early diastolic velocity (E’) obtained by TDI was also studied and showed to have a weak correlation with RAP, but requires two Doppler measurements [6]. 114 Carmen Ginghină et al. A 6 B Fig. 7. – Superior vena cava Doppler flow with systolic wave (S) and diastolic wave (D): A) normal flow with S wave> D wave; B) abnormal flow S<D. A B Fig. 8. – Transthoracic echocardiography PW Doppler in apical 4-chamber view: A) tricuspid E/A ratio (1.1) measured with traditional PW Doppler; B) tissue Doppler imaging performed at the lateral tricuspid annulus E/E’ ratio (6) measured in a patient with elevated RAP and severe PH. Another method involves measuring the time interval between the end of the systolic annular motion to the onset of the E’ wave (RV regional isovolumic relaxation time [rIVRT]). RV rIVRT exhibits an inverse relation with mean RAP independent of the effect of RV end-diastolic or PA pressure (Fig. 9A,B). A RV rIVRT less than 59 milliseconds has a sensitivity of 80% and a specificity of 87.7% to determine mean RAP greater than 8 mm Hg. RV rIVRT inversely correlates with mean RAP with a correlation coefficient of 0.92 (95% confidence interval 0.82-0.97, P <0.001) [10]. The RV IVRT exhibits an inverse relationship to heart rate, and increases proportionately with PA systolic pressure when RAP is normal. However, when the RA fails or is volume overloaded, RAP is increased with an earlier tricuspid valve opening, so that RV IVRT shortens. Consequently, RV IVRT was found useful in the stable pediatric congenital heart disease population to predict PA systolic pressure, where compensatory RA hypertrophy would keep mean RA pressure normal, as compared to patients who are older or acutely ill, who tend to have more RV failure and higher RAP [10]. RAP reflects both left- and right-sided cardiac 7 Doppler flow patterns and pulmonary hypertension 115 A B Fig. 9. – Tissue Doppler imaging performed at the lateral tricuspid annulus in the apical 4-chamber view for measuring the RV rIVRT: A) in a patient with normal RAP; B) in a patient with elevated RAP. function and chamber volumes, and thus carries diagnostic, therapeutic, and prognostic values for patients with cardiac and/or pulmonary diseases. In addition to guiding the management of the fluid status in patients with heart failure, elevated mean RAP is a marker for increased mortality in patients with primary pulmonary hypertension, likely because it reflects decompensation of atrial systolic function after a long period of compensatory hypertrophy. The advantage of measuring RV rIVRT using TDI lies in the fact that it identifies mean RAP for patients with suboptimal subcostal views and thus may assist in treatment of these patients when their fluid status is in question. A practical way to assess SPAP in patients with cardiac shunts with optimal recording and alignment with Doppler flow (e.g. patients with patent ductus arteriosus or ventricular septal defects), may be the calculation of PASP using the difference between systolic blood pressure and peak systolic shunt gradient (Fig. 10A,B). A B Fig. 10. – Transthoracic echocardiography CW Doppler in a patient with patent ductus arteriosus: A) recording of tricuspid regurgitation velocity in apical 4-chamber view; B) recording peak systolic Ao-PA gradient (based on a simultaneously measured systolic systemic blood pressure of 125 mmHg, SPAP can be derived as SPAP=125–100=25 mmHg). 116 Carmen Ginghină et al. As we said before, Doppler echocardiography allows to noninvasively estimate systolic PAP, as well as mean and end-diastolic PAP. Doppler imaging is very useful to assess right ventricular pressure overload. Both pulmonary valve flow and tricuspid regurgitation velocity should be evaluated. In normal individuals, pulmonary artery flow has a symmetric contour with a peak velocity occurring in midsystole. As pulmonary pressure increases, peak velocity occurs earlier in systole and late systolic notching is often present. With increased pulmonary pressure, the right ventricular ejection pattern approximates more a leftsided ejection pattern. The acceleration time (time from onset to peak flow velocity) (AcT) can be measured and provides a rough estimate of the degree of increase in pulmonary artery pressure. In normal individuals, AcT exceeds 140 milliseconds and progressively shortens with increasing degrees of pulmonary hypertension. The shorter the acceleration time, the higher the pulmonary artery pressure. Most studies have suggested that at an AcT of less than 70 to 90 milliseconds, pulmonary artery systolic pressures will exceed 70 mm Hg. This assessment has been largely replaced by the more direct Doppler assessment of right ventricular systolic pressure from the tricuspid regurgitation signal. On occasion, in a patient without a measurable tricuspid regurgitation velocity, shortening of the pulmonary acceleration time may be the only evidence of pulmonary hypertension. The pulmonary artery acceleration time is easily measured in most patients, including those with chronic lung disease. Reliability of the method is less than when using the tricuspid regurgitant jet velocity, however. Mahan’s equation is simplest and preferred for estimating MPAP: MPAP = 79– 0.45 × (AcT). It should be noted that AcT is dependent on cardiac output and heart rate. With increased output through the cardiac chambers on the right side (as in atrial septal defect), AcT may be normal even when pulmonary artery pressure is increased. If the heart rate is slower than 60 beats per minute or more than 100 beats per minute, AcT needs to be corrected for heart rate. This method is rarely used in our practice. There is heavy dependence on the position of the Doppler sample volume because acceleration and velocities are higher along the inner edge of curvature of the pulmonary artery. Because the curvature is three-dimensional, positioning of the sample volume in the middle of the vessel in the imaged plane may 8 not avoid overestimation of velocity by sampling adjacent to the vessel wall in the orthogonal nonimaged plane. Furthermore, the short absolute time interval of AcT lends itself to high measurement error and lower reproducibility. Right ventricular ejection time shortens with increasing pulmonary hypertension. In contrast, the right ventricular pre-ejection time lengthens with increasing pulmonary arterial pressure. Although neither time is useful alone, the ratio of pulmonary acceleration time to total right ventricular ejection time or pre-ejection time can be used to estimate mean pulmonary artery pressure with correlation to mean pulmonary pressure similar or better than acceleration time alone. Again, the short values of these time intervals render them impractical for general clinical use. With severe pulmonary hypertension, a midsystolic notch may be present in the deceleration slope of the pulmonary artery Doppler flow profile (Fig. 11A,B). This notch is analogous to the midsystolic notch seen in M-mode examination of the pulmonary valve. The notch may be secondary to transient elevation of pulmonary artery pressure above right ventricular pressure due to a decrease in pulmonary artery compliance and an increase in main pulmonary artery size, impedance, and transmission time of the velocity wave. The presence of a mid-systolic notch in the pulmonary outflow Doppler profile is highly specific for pulmonary hypertension [11]. Data in the literature show that the pulmonary flow systolic notch (mid-systolic deceleration in pulmonary flow, as assessed using Doppler echocardiography) may distinguish proximally located obstructions in the pulmonary arterial vasculature from distal obstructions. This notch occurs significantly later in systole in patients with IPAH than in those with proximal pulmonary embolism. A novel and easily applicable echocardiographic sign with prognostic significance has been described, estimating the timing of pulmonary flow systolic notch as the ratio t1/t2: the time interval from the onset of pulmonary artery systolic flow to the maximal systolic flow deceleration (t1) is divided by the time interval from the maximal systolic flow deceleration to the end of pulmonary artery systolic flow (t2). This parameter seems to distinguish proximally located obstructions in the pulmonary arterial vasculature from distal obstructions in PPH; 9 Doppler flow patterns and pulmonary hypertension A 117 B Fig. 11. – Right ventricular outflow tract flow velocity recordings by pulsed wave Doppler echocardiography. The sample volume is placed in the region of the pulmonary valve annulus: A) normal flow pattern; B) flow velocity in pulmonary hypertension (note midsystolic cessation of flow – notching [arrow]). in the latter this notching appears significantly later than in patients with proximal pulmonary embolism. Thus, patients with pulmonary embolism with a t1/t2 ratio more than 1.0 may have an increased inhospital mortality risk and a limited haemodynamic improvement after pulmonary endarterectomy, because of distally located obstruction [12–14]. The position of the dicrotic notch on the PA pressure waveform approximates the mean PA pressure. Peak diastolic pressure gradient between the PA and the RV approximates mean PA pressure and, therefore, application of the modified Bernoulli equation to the peak. The pulmonary regurgitant (PR) flow velocity patterns in patients with pulmonary hypertension display significantly higher velocities than in patients with normal pulmonary pressures. The higher detection rate of PR flow in PH makes easier to estimate mean PAP and end-diastolic PAP using Bernoulli equation. Mean PA pressure can be calculated with the following formula: MPAP = 4 (PR peak velocity)² [15] (Fig. 12). Fig. 12. – Continuous wave Doppler interrogation of pulmonary regurgitation from the left parasternal window; note the peak diastolic pulmonary regurgitation velocity RV (1) and enddiastolic pulmonary regurgitation velocity (2). The continuous wave Doppler profile of pulmonary regurgitation velocity in a patient with normal pulmonary artery pressure may display a dip after atrial contraction, because the pressure difference between the pulmonary artery and right ventricle is small during diastole (Fig. 13). Conversely, when pulmonary pressure is high, right atrial contraction usually does not make a notable change in the pressure gradient, with no dip in the signal of pulmonary regurgitation [2]. Normally, the pulmonary regurgitation end-diastolic pressure gradient is less than 5 mmHg. An increase in this pressure gradient (> 5mmHg) has been found to correlate with systolic dysfunction, diastolic dysfunction, increased brain natriuretic peptide, and decreased functional status [16]. PA end-diastolic pressure is frequently used as an estimate of pulmonary capillary wedge pressure. 118 Carmen Ginghină et al. The presence of pulmonary regurgitation (PR) can be exploited to estimate PA end-diastolic pressure. The application of the modified Bernoulli equation to the end-diastolic PR velocity, adding to this an estimate 10 of RAP, provides an estimation of PA diastolic pressure (Fig. 12). The diastolic PA pressure can be estimated using the following formula: Diastolic PA pressure = 4(end PR V)² + estimated RAP [17]. Fig. 13. – Continuous wave Doppler spectrum of pulmonary regurgitation velocity in a patient with normal pulmonary artery pressure (note the dip in pulmonary velocity – red arrows). DOPPLER ECHOCARDIOGRAPHY FOR DETERMINATION OF PULMONARY VASCULAR RESISTANCE Doppler echocardiography has significantly impacted clinical medicine by its ability to determine intracardiac hemodynamics noninvasively. Pulmonary vascular resistance (PVR) is a hemodynamic variable that contributes to the management of patients with advanced cardiovascular and pulmonary conditions. Pulmonary vascular resistance is calculated invasively by the ratio of transpulmonary pressure gradient to transpulmonary flow (Qp)[18]. Therefore, noninvasive determination of PVR is possible using variables that are routinely obtained by Doppler echocardiography. Increased SPAP may be secondary to increased transpulmonary flow or abnormal PVR. Peak tricuspid regurgitant velocity (TRV) and right ventricular outflow time-velocity integral (TVI RVOT) can be used to estimate PVR. The ratio of TRV: RVOT TVI has been shown to correlate with PVR with a correlation coefficient of r=0.93 (95% confidence interval 0.87–0.96) [19]. Patients with TRV/ RVOT TVI <0.2 are likely to have low PVR values (<2 WU), and pulmonary vascular disease may be excluded despite increased SPAP by Doppler [19]. A value higher than 0.2 demands further invasive workup. In conclusion, a “normal” SPAP combined with a small flow but high PVR could be abnormal in fact. There are some reasons for which right heart catheterization, although invasive, remains the gold standard for accurately assessing PAP. Despite many advantages, Doppler echo is limited by load dependency and reproducibility or by the fact that it is not reliable enough to reflect minor therapeutic improvement. As a rule, Doppler echo overestimates PASP and mean PAP, which may lead to unnecessary catheterizations. A useful approach to keep invasive procedures to a minimum is to noninvasively assess RV function. DOPPLER ECHOCARDIOGRAPHY FOR RIGHT VENTRICULAR FUNCTION EVALUATION Quantifying right ventricular systolic function is not always easy to do and several approaches have been suggested, including the Doppler derived Tei index or myocardial performance index (MPI) [20]. This index is defined as the isovolumic contraction time (ICT) and isovolumic relaxation time (IRT) divided by the ejection time (ET). An increased right ventricular myocardial performance index is a sensitive and specific marker of pulmonary hypertension. MPI may be of value in patients in whom TR is either not present or cannot be quantified to assess for pulmonary hypertension. Normal value of Tei index is 0.28 ± 0.04, increased Tei index being correlated with RV dysfunction. The MPI also appears to provide powerful prognostic information. However, the short absolute values of the times used 11 Doppler flow patterns and pulmonary hypertension in the index confer a high degree of measurement error and elevated RAP may limit its accuracy [21]. The estimation of the Tei index is based on separate PW recordings from tricuspid (with tissue Doppler) and RV outflow (with conventional PW Doppler) (Fig. 14A,B) at different HR. 119 Tissue Doppler imaging (TDI) is a relatively new echocardiographic tool in the assessment of myocardial function. The method is available in most modern ultrasound systems and can provide accurate information on myocardial motion throughout the cardiac cycle. In contrast to traditional pulsed Doppler B A Fig. 14. – The estimation of Tei index based on separate PW recordings from tricuspid with traditional Doppler on different cardiac cycles (A) and from RV outflow with tissue Doppler velocity on the same cardiac cycle (B). In both cases, MPI is calculated as the ratio (a–b)/b. echocardiography, which detects high velocity with low amplitudes, offline TDI detects low velocity with high amplitudes. Tissue velocities can be displayed with spectral pulsed or colour-encoded Doppler visualized with 2D, M-mode or Doppler signals. TDI is proposed to be less preload dependent compared to the traditional pulsed Doppler technique. Pulsed TDI is simpler and more robust to use, with high temporal resolution. The major disadvantages of pulsed TDI are poor spatial resolution due to movement of the heart, while the sample volume is fixed and apical velocities from the apical long axis projection are difficult to measure [22]. TDI determines the timing, direction, and velocity of RV wall motion. The PW approach measures online peak velocities. Colour DTI is an alternative approach to measuring myocardial motion and can be used off-line, therefore is favoured for simultaneous wall motion analysis, exercise and stress echocardiography. It is important to note that offline TDI analysis provides mean values compared to pulsed TDI which provides peak velocities. Thus, it is important to emphasize that the velocities measured by color TDI are lower (approximately by 25%) than maximal velocities measured online [23]. Other proposed measures of RV systolic and diastolic functions that have been explored include right ventricular fractional area change (RV FAC) and RV wall stress, tricuspid annular plane systolic excursion (TAPSE; a measurement of systolic elevation of tricuspid annular plane), tricuspid deceleration duration, E/E’ ratio. In some of these cases, the amount of data built to date is small and one cannot make any conclusion on their potential value in the future [24]. CONCLUSIONS In conclusion, Doppler echocardiography provides several complementary methods and indices to assess RV hemodynamics for a comprehensive evaluation of PH. Doppler echocardiography may noninvasively characterize each component of flowpressure-resistance interactions both at rest and during exercise. The development of new ultrasound imaging equipment has decreased the number of 120 Carmen Ginghină et al. technically inadequate studies and has simultaneously increased the accuracy of echo PAP estimation in everyday clinical practice. 12 Acknowledgements. This work was partially supported by the Romanian National Research Programme II of the UEFISCSU, grant ID_246/2008. Hipertensiunea arterială pulmonară este definită ca un grup de boli, caracterizate prin creşterea progresivă a presiunii în circulaţia pulmonară, ceea ce conduce la creşterea presiunii în artera pulmonară, la apariţia fenomenelor de insuficienţă cardiacă dreaptă şi riscul de moarte prematură. Dată fiind lipsa de specificitate a simptomelor şi semnelor iniţiale, hipertensiunea arterială pulmonară este adesea diagnosticată în stadiile avansate. Astfel, deşi evaluarea clinică este esenţială în cazul pacienţilor suspectaţi de hipertensiune pulmonară, ecocardiografia este instrumentul cheie de screening în cadrul algoritmului de diagnostic, deoarece, în comparaţie cu metodele invazive, are avantajul de a fi sigură, portabilă şi reproductibilă. De aceea, evaluarea ecocardiografică Doppler este metoda cea mai utilizată la pacienţii cu hipertensiune pulmonară. Ea aduce date importante despre severitatea, etiologia posibilă şi consecinţele hipertensiunii pulmonare, atât în faza iniţială, cât şi ulterior, în perioada de urmărire în vederea estimării progresiei, prognosticului şi pentru monitorizarea răspunsului terapeutic. Ecocardiografia Doppler permite estimarea noninvazivă a presiunii arteriale pulmonare sistolice (PAPS), medii şi diastolice, cuantificarea funcţiei ventriculului drept (VD) precum şi evaluarea rezistenţelor vasculare pulmonare (RVP). Corresponding author: Carmen Ginghina, MD, PhD, FESC, FACC 100, V. Lascar Str. 020506 Bucharest, Romania E-mail: [email protected] REFERENCES 1. SIMMONNEAU G., GALIE N., RUBIN L. et al., Clinical classification of pulmonary arterial hypertension. J. Am. Coll. Cardiol., 2004; 43:55-12. 2. JAE K. OH, JAMES B. SEWARD, A. JAMIL TAJIK, Pulmonary Hypertension and Pulmonary Vein Stenosis. The Echo Manual- third edition, 2007; 9: 143. 3. YOCK P.G. and POPP R.L., Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation, 1984; 70:657–662. 4. HINDERLITER A.L., WILLIS IV P.W., LONG W.A. et al., Frequency and severity of tricuspid regurgitation determined by Doppler echocardiography in primary pulmonary hypertension. Am. J. Cardiol., 2003; 91:1033–1037. 5. KIRCHER B.J., Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am. J. Cardiol.,1990; 66(4): 493–6. 6. NAGEH M.F., KOPELEN H.A., ZOGHBI W.A. et al., Estimation of mean right atrial pressure using tissue Doppler imaging. Am. J. Cardiol., 1999; 84:1448–51. 7. SHERIF F., NAGUEH, HELEN A., KOPELEN, WILIAM A., ZOGHBI, Relation of Mean Right Atrial Pressure to Echocardiographic and Doppler Parameters of Right Atrial and Right Ventricular Function. Circulation, 1996; 93:1160–1169. 8. OMMEN S.R., NISHIMURA R.A., HURRELL D.G. et al., Assessment of right atrial pressure with two-dimensional and Doppler echocardiography: a simultaneous catheterization and echocardiographic study. Mayo Clin. Proc., 2000; 75:24–9. 9. GHIO S., RECUSANI F., SEBASTIANI R. et al., Doppler velocimetry in superior vena cava provides useful information on the right circulatory function in patients with congestive heart failure. Echocardiography, 2001; 18:469–477. 10. ABBAS A., LESTER S., MORENO F.C. et al., Noninvasive assessment of right atrial pressure using Doppler tissue imaging. J. Am. Soc. Echocardiogr., 2004; 17:1155–60. 11. LEE K., ABBAS A., KHANDHERIA B., LESTER S., Echocardiographic Assessment of Right Heart Hemodynamic Parameters.J. Am. Soc. Echocardiogr., 2006; 20(6): 773–782. 13 Doppler flow patterns and pulmonary hypertension 121 12. TORBICKI A., KUZYNA M., CIURZYNSKI M., PRUSZCZYK P., PACHO R., KUCH-WOCIAL A., SZULC M., Proximal pulmonary emboli modify right ventricular ejection pattern. Eur. Respir. J., 1999; 13:616–621. 13. FURUNO Y., NAGAMOTO Y., FUJITA M., KAKU T., SAKURAI S., KUROIWA A., Reflection as a cause of mid-systolic deceleration of pulmonary flow wave in dogs with acute pulmonary hypertension: comparison of pulmonary artery constriction with pulmonary embolisation. Cardiovasc. Res., 1991; 25:118–124. 14. HARDZIYENKAL M., REESINK H.J., BOUMA B.J. et al., A novel echocardiographic predictor of in-hospital mortality and mid-term haemodynamic improvement after pulmonary endarterectomy for chronic thrombo-embolic pulmonary hypertension. Eur. Heart J., 2007, 28, 842–849. 15. MASUYAMA T., KODAMA K., KITABATAKE A., SATO H., NANTO S. et al., Continuous-wave Doppler echocardiographic detection of pulmonary regurgitation and its application to noninvasive estimation of pulmonary artery pressure. Circulation, 1986, 74:484–492. 16. RISTOW B., AHMED S., WANG L. et al., Pulmonary regurgitation end-diastolic gradient is a Doppler marker of cardiac status: Data from the Heart and Soul Study. J. Am. Soc. Echocardiogr., 2005; 18:885–891. 17. LEE R.T., LORD C.P., PLAPPERT T. et al., Prospective Doppler echocardiographic evaluation of pulmonary artery diastolic pressure in the medical intensive care unit. Am. J. Cardiol., 1989; 64:1366–70. 18. WILLARD J.E.L., RICHARD A., HILLIS L.D., Cardiac catheterization. In: Kloner R.A., editor. The Guide to Cardiology. 3rd ed. Greenwich, CT: Le Jacq Communications, 1995:151. 19. ABBAS A., FORTUIN D.F., SCHILLER N.B. et al., A simple method for noninvasive estimation of pulmonary vascular resistance. J. Am. Coll. Cardiol., 2003; 41:1021–7. 20. VONK M.C., SANDER M.H., Van Den HOOGEN F.H.J. et al., Right ventricle Tei-index: A tool to increase the accuracy of non-invasive detection of pulmonary arterial hypertension in connective tissue diseases. Eur. J. Echocardiogr., 2007, 8(5):317– 321. 21. TEI C., DUJARDIN K.S., HODGE D.O., KYLE R.A., TAJIK A.J. and SEWARD J.B., Doppler index combining systolic and diastolic myocardial performance: clinical value in cardiac amyloidosis. J. Am. Coll. Cardiol., 1996; 28:658–664. 22. HATLE L., SUTHERLAND G.R., Regional myocardial function – a new approach. Eur. Heart J., 2000; 21:1337–57. 23. ISSAZ K., MUNOZ del ROMERAL L., LEE E., SCHILLER N.B., Quantitation of the motion of the cardiac base in normal subjects by Doppler echocardiography. J. Am. Soc. Echocardiogr., 1993; 6:166–76. 24. QUAIFE R.A., CHEN M.Y., LYNCH D., BADESH D.B. et al., Importance of right ventricular end-systolic regional wall stress in idiopathic pulmonary arterial hypertension: a new method for estimation of right ventricular wall stress. Eur. J. Med. Res., 2006; 11:214–220. Received March 10, 2009 122 Carmen Ginghină et al. 14