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Journal of the American College of Cardiology © 2003 by the American College of Cardiology Foundation Published by Elsevier Science Inc. Vol. 41, No. 8, 2003 ISSN 0735-1097/03/$30.00 doi:10.1016/S0735-1097(03)00126-8 STATE-OF-THE-ART PAPER Pulmonary Venous Flow by Doppler Echocardiography: Revisited 12 Years Later Tomotsugu Tabata, MD, FACC, James D. Thomas, MD, FACC, Allan L. Klein, MD, FACC Cleveland, Ohio In 2003, pulmonary venous flow (PVF) evaluation by Doppler echocardiography is being used daily in clinical practice. Twelve years ago, we reviewed the potential uses of PVF in various conditions. Some of its important uses in cardiology have materialized, while others have not and have been supplanted by newer approaches. Current applications of measuring PVF have included: differentiating constrictive pericarditis from restriction, estimation of left ventricular (LV) filling pressures, evaluation of LV diastolic dysfunction and left atrial (LA) function, and grading the severity of mitral regurgitation (MR). However, there have been a number of controversies raised in the use of PVF profiles. Using transthoracic echocardiography, there may be technical issues in measuring the atrial reversal flow velocity. The use of PVF in the evaluation of the severity of MR is not always specific and can be affected by atrial fibrillation (AF) and elevated mean LA pressure. Mitral valvuloplasty and radiofrequency ablation for AF, which are the newer applications of PVF in monitoring invasive procedures, are mentioned. This article reviews the important clinical role of Doppler evaluation of PVF, discusses its limitations and pitfalls, and highlights its newer applications. (J Am Coll Cardiol 2003;41:1243–50) © 2003 by the American College of Cardiology Foundation In 2003, evaluation of pulmonary venous flow (PVF) by Doppler echocardiography is being performed daily. Since the 1970s, PVF was measured invasively using flow meters and was closely related to the pulmonary capillary and left atrial (LA) pressures (1) (Table 1). Pulmonary venous flow was recorded as forward flow during ventricular systole and early diastole with a reversed flow during atrial systole. These flow waves were noted to be reciprocal to the LA pressure waves (2). Noninvasive assessment of the PVF was first reported by Keren et al. (3,4) using pulsed-wave Doppler transthoracic echocardiography (TTE). However, PVF by TTE could be recorded with only systolic and diastolic waves. Using transesophageal echocardiography (TEE), a complete PVF profile could be clearly recorded because of the posterior approach providing unimpeded interrogation of cardiac structures (5). In 1991, we reviewed the physiology and technique of measuring PVF and described its potential utility in various disease states (6). The PVF profile was proposed as being useful for: differentiating constrictive pericarditis from restrictive cardiomyopathy (7,8); estimating left ventricular (LV) filling pressures (9 –11); and evaluating LV diastolic dysfunction (12) and LA function (13,14), severity of mitral regurgitation (MR) (15,16), and stenosis (17,18). Some of its important uses in cardiology have materialized, while others have not. The purpose of this article, therefore, is to review the place of PVF using Doppler echocardiography, discuss its From the Cardiovascular Imaging Center, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio. Manuscript received December 18, 2001; revised manuscript received November 12, 2002, accepted November 27, 2002. limitations and pitfalls, as well as mention its newer applications. Anatomy and physiology of PVF. Between the lung capillaries and the LA, there are the intra- and extraparenchymal pulmonary veins. There are usually four pulmonary veins including the right and left upper and lower veins. The right and left pulmonary veins connect, respectively, medially and laterally to the superior and posterior LA walls (19). The lower veins run below the inferior border of the right and left bronchi, and the upper veins run anterior to their bronchi. The right pulmonary veins run behind the superior vena cava and right atrium and join the LA adjacent to the atrial septum (19). Recently, the relationship between LA pressure and Doppler-derived PVF has been carefully evaluated (20,21). Pulmonary venous pressure varies according to its proximity to the pulmonary arteries and LA. It resembles the pulmonary artery pressure closer to the pulmonary capillaries and the LA pressure closer to the venoatrial junction (20). The flow in the pulmonary veins is pulsatile, and its waveform shows an inverse relationship to LA pressure (20,21). IMAGING TECHNIQUE Characteristics of the normal PVF by TEE. The right pulmonary veins can best be seen at a 45° to 60° angle, and the transducer should be rotated clockwise. In this view, the right upper and lower pulmonary veins appear as a “y” shape. To obtain the left upper and lower veins, the angle should be set at 110°, and the transducer should be rotated counterclockwise. The left lower veins can be visualized by advancing the probe from the position used for the left upper veins (22). 1244 Tabata et al. Pulmonary Venous Flow Revisited Abbreviations and Acronyms AF ⫽ atrial fibrillation AR ⫽ pulmonary venous atrial reversal wave AV ⫽ atrioventricular D ⫽ pulmonary venous early diastolic wave LA ⫽ left atrial/atrium LV ⫽ left ventricle/ventricular MR ⫽ mitral regurgitation PVF ⫽ pulmonary venous flow S1 ⫽ pulmonary venous first systolic wave S2 ⫽ pulmonary venous second systolic wave TEE ⫽ transesophageal echocardiography TTE ⫽ transthoracic echocardiography The pulsed-wave Doppler PVF velocity pattern can be recorded by placing the sample volume 1 to 2 cm into the orifice of the pulmonary veins. The normal PVF usually shows a tri- or quadriphasic pattern consisting of a pulmonary venous first systolic wave (S1), pulmonary venous second systolic wave (S2), pulmonary venous early diastolic wave (D), and pulmonary venous atrial reversed flow wave (AR) (16,23) (Fig. 1). Table 2 shows the LA and ventricular factors that influence PVF (6,20,21,24,25). The S1 occurs during LA pressure “a” to “c” and “c” to “x” descent, and the S2 occurs during LA pressure increase between the “x” pressure nadir and the “v” pressure peak (6). There is a direct correlation between the mitral inflow E-wave velocity and the D wave velocity (6). Characteristics of the normal PVF by TTE. There have been attempts to obtain better quality recordings of PVF by TTE (26,27). One study reported that the measurement of PVF by TTE was feasible and accurate compared with TEE recordings (26). Another study suggested that it was possible to obtain high-quality recordings of PVF in 90% of the patients by TTE with current machine technology, sonographer education, and daily practice (27). Contrast injection may improve the PVF profile (28). It is the authors’ opinion that the TTE recordings of PVF, especially the atrial reversal, may be limited even with the improvement of transducers. In contrast, TEE can provide clear PVF tracings in most of the patients with JACC Vol. 41, No. 8, 2003 April 16, 2003:1243–50 more laminar-appearing spectral signals (6). However, TEE may be limited due to its semi-invasive approach, but would be recommended in patients with complex diastolic dysfunction and in assessing hemodynamics. Physiologic factors influencing normal PVF velocities. There are many physiologic variables that will affect PVF including age, preload, LV function, atrioventricular (AV) conduction, and heart rate (6,20,29,30 –34). The aging process will influence PVF, and there are published normal values with 95% confidence intervals (29). Increased or decreased preload may change the S2 and AR velocities reflecting the Frank-Starling mechanism (30). Thus, PVF can provide a relatively noninvasive means to assess directional changes in LV preload. There is a significant correlation between S2 velocity and LA pressure in patients with a normal cardiac index (31). The change induced by volume loading in the S2/D ratio positively correlates with the change in LA pressure in normal LV function. This indicates that the S2/D ratio can estimate the LA reservoir function (32,33). In the absence of LV dysfunction, PVF can provide an estimate of mean LA pressure and is determined largely by atrial function (32,34). Evaluation of LV diastolic function. Diastolic dysfunction has been evaluated noninvasively using the Doppler mitral inflow velocity (6); PVF was the first to provide additional information for differentiating pseudonormal from normal LV filling (6,9,35). Normal PVF. The effects of age on PVF in normal subjects have been described previously (29). In healthy older subjects, the PVF shows a greater systolic than diastolic flow, and there are increased atrial reversals compared with younger normal subjects. Abnormal PVF. RELAXATION ABNORMALITY. In patients with impaired LV relaxation, the mitral inflow E velocity decreases with a longer deceleration time, reflecting a decreased early diastolic LV filling rate. The mitral inflow A velocity increases because of the complementary mechanisms. Corresponding to these changes, the pulmonary venous systolic fraction and the S2/D ratio increases, and the deceleration time of the D wave prolongs so that the LA Table 1. History of the Clinical Application of PVF Skagseth (1), Rajagopalan et al. (2) Keren et al. (3,4) Seward et al. (5) Schiavone et al. (7), Klein et al. (8), Klein et al. (43) Kuecherer et al. (9), Appleton et al. (35) Rossvoll et al. (10), Yamamoto et al. (11), Dini et al. (28) Klein et al. (6) Oki et al. (13,14) Klein et al. (46), Castello et al. (15) Klein et al. (17), Tabata et al. (18), Stojnic et al. (56) Klein et al. (6,46) Robbins et al. (63), Scanavacca et al. (64), Sohn et al. (66) Invasive assessment of PVF Noninvasive assessment of PVF by TTE Technique for recording PVF by TEE Differentiation of constrictive pericarditis from restrictive cardiomyopathy Assessment of the LV filling pressures Estimation of the LV end-diastolic pressure Evaluation of the diastolic dysfunction Evaluation of the LA function Assessment of mitral regurgitation severity Evaluation of mitral stenosis Monitoring mitral valve procedures Pulmonary vein stenosis after catheter ablation LA ⫽ left atrial; LV ⫽ left ventricular; PVF ⫽ pulmonary venous flow; TEE ⫽ transesophageal echocardiography; TTE ⫽ transthoracic echocardiography. Tabata et al. Pulmonary Venous Flow Revisited JACC Vol. 41, No. 8, 2003 April 16, 2003:1243–50 1245 Figure 1. Pulmonary venous flow velocity profile in a 60-year-old normal subject. Pulmonary venous systolic wave is usually greater than early diastolic wave. Note the pulmonary venous first systolic wave (S1) and pulmonary venous second systolic wave (S2). AR ⫽ pulmonary venous atrial reversal wave; D ⫽ pulmonary venous early diastolic wave. reservoir volume during ventricular systole could compensate for the impaired early LV filling (36,37) (Fig. 2A). The mitral inflow pattern changes in relation to myocardial function and hemodynamic status, such as preload. An increase in LA pressure normalizes the abnormal mitral inflow pattern and masks the LV relaxation abnormality (6). The mitral inflow E-wave velocity increases, and the A-wave velocity decreases. There are a number of methods to differentiate “pseudonormalization” from a normal mitral inflow pattern (37,38). The classic way was by observing a normal or decreased S2 (“blunted” systolic pattern) and increased D velocities resulting in decreased systolic fraction and S2/D ratio and with a large atrial reversal ⬎35 cm/s (6,38) (Fig. 2B). Another method was by decreasing preload with the Valsalva maneuver (38). The main limitation using PVF in assessing the pseudonormal pattern is the difficulty of accurately recording the atrial reversal velocity. PSEUDONORMALIZATION. RESTRICTIVE PHYSIOLOGY. The primary abnormality in patients with restrictive cardiomyopathy, such as in advanced cardiac amyloidosis, is increased chamber stiffness. In patients with a restrictive mitral inflow pattern (a deceleration time ⬍150 ms), the PVF shows a lower S2 and higher D velocities (severely blunted systolic flow) and increased atrial reversals (unless atrial systolic failure), suggesting decreased LV operating compliance (12) (Fig. 2C). Pulmonary venous flows have been used to clinically estimate mean LA pressure; LA pressure has been shown to have a negative correlation with pulmonary venous systolic fraction and S2/D ratio in those patients with pseudonormal and restrictive physiology (9,39). A systolic fraction ⱕ55% was found to be 91% sensitive and 87% specific in predicting a mean LA pressure ⬎15 mm Hg (40). However, S2 velocity is not only affected by LA pressure, but also by LV contractility (41). There is a negative correlation between the S2 velocity and the LA pressure in patients with a low cardiac index because of the decrease in the systolic descent of the mitral annulus (31,32,41). On the other hand, the difference between the PVF-AR wave duration and the mitral inflow atrial-wave duration has been reported to correlate with an increase in LV pressure during atrial contraction and LV end-diastolic pressure (10,28). The PVF-AR wave duration (exceeding mitral inflow A-wave duration by 30 ms) is reported to provide high sensitivity (82%) and specificity (92%) for the detection of LV end-diastolic pressure ⬎20 mm Hg (11,28). PVF in pericardial disease. CONSTRICTIVE PERICARDITIS. The hemodynamic characteristics of constriction show markedly elevated atrial and ventricular pressures and an early diastolic “dip-and-plateau” pattern (42). The respiratory variation of the Doppler flow velocities has been reported in the differentiation between constriction and restriction (7,43,44). In restrictive cardiomyopathy, PVF ESTIMATION OF LV FILLING PRESSURES. Table 2. Left Atrial and Ventricular Factors Influence on Each Wave of PVF Ventricular Function First systolic wave Second systolic wave Early diastolic wave Atrial reversal wave LV contraction RV contraction Ventricular relaxation Ventricular chamber stiffness Ventricular chamber stiffness LV ⫽ left ventricular; PVF ⫽ pulmonary venous flow; RV ⫽ right ventricular. Atrial Function Atrial relaxation Reservoir function Atrial compliance Conduit function Booster pump function Atrial compliance 1246 Tabata et al. Pulmonary Venous Flow Revisited JACC Vol. 41, No. 8, 2003 April 16, 2003:1243–50 Figure 2. Pulmonary venous flow (PVF) (top) and mitral inflow (bottom) velocity profiles recorded by transesophageal echocardiography in patients with left ventricular diastolic dysfunction. (A) Relaxation abnormality pattern. The peak pulmonary venous systolic velocity (S) increased. The peak pulmonary venous early diastolic velocity (D) decreased, and its deceleration time increased corresponding to the change in mitral inflow early diastolic wave (E). (B) Pseudonormal pattern. The PVF shows a markedly increased atrial reversal wave (AR) and a normal S to D velocity ratio with normalized mitral inflow velocity pattern. The deceleration time of the D wave is shortened. (C) Restrictive pattern. The PVF shows a markedly decreased S to D velocity ratio with markedly shortened deceleration times of the D and E waves. A ⫽ mitral inflow late diastolic wave. Panels B and C from Klein AL, Canale MP, Rajagopalan N, et al. Role of transesophageal echocardiography in assessing diastolic dysfunction in a large clinical practice: a 9-year experience. Am Heart J 1999;138:880 –9; reproduced with permission. shows blunting of the S2 velocity and decreased S2/D ratio throughout the respiratory cycle (Fig. 3A). In contrast, marked respiratory change in PVF was observed in constrictive pericarditis (Fig. 3B). The S2 and D velocities increased, especially the D velocity, during expiration, and decreased during inspiration. This is explained by incomplete transmission of the inspiratory fall of intrathoracic pressure to the LA (44). Those changes were more prominent compared with changes in mitral inflow velocities (44). The combination of the S2/D ratio ⬎0.65 in inspiration and a respiratory variation of D velocity ⬎40% correctly classified 86% of patients with constrictive pericarditis (43). Similar respiratory variation can also be observed even in patients with constrictive pericarditis and atrial fibrillation (AF) regardless of the irregular cycle lengths (45) (Fig. 3C). PVF in mitral valve diseases. MITRAL REGURGITATION. Twelve years ago, PVF was suggested to estimate the severity of MR (15,16,46,47). As the degree of MR increases, the S2 velocity decreases, thus causing systolic blunting and then late systolic flow reversal and, finally, pan-systolic reversal occurs, while the D velocity increases (46) (Fig. 4A). A qualitative grading system for MR was proposed using PVF. Normal systolic flow was seen in patients with 1⫹ or 2⫹ MR, whereas blunted and reversed systolic flows were detected in patients with 3⫹ and 4⫹ MR, respectively. Reversed systolic flow was seen in 93% of the patients with 4⫹ MR (46) (Fig. 4B). The sensitivity and specificity of reversed systolic flow for severe MR were reported as 90% to 100% by Castello et al. (15) and 82% and 100%, respectively, by Kamp et al. (47). Mitral regurgitation was the most common cause of large LA pressure “v” wave (48), and the “v” wave size and regurgitant volume showed a significant relationship in determining pulmonary venous reversed systolic flow (49). Furthermore, the changes in D velocity were closely related to changes in the “v” wave in MR under altered loading conditions (50). The best correlation of the S2/D ratio was found with the LA pressure “v” wave (r ⫽ ⫺0.76), the “v-y” descent (r ⫽ ⫺0.73), and the “a/v” ratio (r ⫽ 0.71). On the other hand, there were significant problems in using PVF in the grading of MR. A large “v” wave is neither highly sensitive nor specific for severe MR (51). Increased LA compliance may be associated with trivial “v” wave in the presence of severe MR (48). In addition, there are a number of other physiologic and technical factors influencing either the S2 or D velocities, such as mitral stenosis, presence of LV dysfunction, and presence of AF (10,23,35). The decrease in the velocity time integral of PVF is more prominent for any given volume of MR at a higher LA pressure (52). Jet directions and jet areas may also influence the effect of MR on PVF patterns (53). There are some patients with discordance between the left and right upper PVF patterns. Both PVF patterns must be evaluated when assessing the severity of MR (54) because the left PVF Tabata et al. Pulmonary Venous Flow Revisited JACC Vol. 41, No. 8, 2003 April 16, 2003:1243–50 1247 Figure 3. Pulmonary venous flow (PVF) velocity profiles recorded by transesophageal echocardiography with respiratory monitoring. (A) Patient with cardiac amyloidosis shows pseudonormal pattern characterized by slight blunting of pulmonary venous systolic wave (S) throughout the respiratory cycle with a large atrial reversal. (B) Patient with constrictive pericarditis and sinus rhythm shows a marked respiratory variation. Both the pulmonary venous systolic and early diastolic (D) flow velocities decreased from expiration to inspiration. (C) Patient with constrictive pericarditis and atrial fibrillation also shows similar respiratory variation in the PVF. Both the S and D velocities increased at the onset of expiration, even with a short RR interval, and decreased at the onset of inspiration with a long RR interval. Exp ⫽ expiration; Insp ⫽ inspiration. usually shows blunted systolic flow, and the right PVF shows reversed systolic flow— depending on jet direction (46). Despite these limitations and pitfalls, reversed systolic flow is a highly specific marker of severe MR, whereas the normal PVF is useful to confirm the presence of mild-tomoderate MR. The blunted PVF pattern must be inter- preted cautiously in the clinical practice as a marker for the severity of MR (53,55). The characteristics of the PVF pattern in patients with mitral stenosis and normal sinus rhythm are lower S2, D, and AR velocities (18,56). The pressure MITRAL STENOSIS. Figure 4. (A) Simultaneous recording of the pulmonary venous flow (PVF) using transesophageal echocardiography and left atrial pressure (LAP) in patients with 4⫹ mitral regurgitation (MR). The pulmonary venous systolic wave (S) was blunted, and late systolic reversal flow (SRF) was observed corresponding to the large LAP “v” wave. (B) Relationship between LAP and PVF in 2⫹, 3⫹, and 4⫹ MR. As MR grade increases, the “v” wave and “v-y” descent increase, and the “a” wave and “a-x” descent decrease, which is consistent with decrease in S wave, increase in D and SRF waves. ECG ⫽ electrocardiogram. From Klein AL, Savage RM, Kahan F, et al. Experimental and numerically modeled effects of altered loading conditions on pulmonary venous flow and left atrial pressure in patients with mitral regurgitation. J Am Soc Echocardiogr 1997;10:41–51; reproduced with permission. 1248 Tabata et al. Pulmonary Venous Flow Revisited JACC Vol. 41, No. 8, 2003 April 16, 2003:1243–50 Figure 5. Pulmonary vein stenosis induced by radiofrequency ablation for atrial fibrillation. Left upper pulmonary vein stenosis (arrow) is seen by two-dimensional echocardiography (left), and the peak velocities of pulmonary venous systolic (S) and early diastolic (D) waves are markedly increased (right). Ao ⫽ ascending aorta; AR ⫽ pulmonary venous atrial reversal wave; LA ⫽ left atrium; LPV ⫽ left upper pulmonary vein. half time of the D wave is longer and correlated with that in the mitral inflow E-wave because of the gradual decay of the AV pressure gradient (17,56). We observed the blunted PVF pattern in 61% of the patients with mitral stenosis (17). In patients with severe mitral stenosis, LA filling shows a diastolic preponderance (57). The LA contribution to the LV filling and AR velocity correlates positively with the mitral valve area and negatively with the mean LA pressure in patients with sinus rhythm (58). Patients with mitral stenosis and AF have a predominantly blunted systolic pattern. The S2 velocity markedly decreases in the presence of AF due to loss of timed atrial function, and the early diastolic phase is the main LA filling phase (17,56). Effects of rhythm disorder. Rhythm disorders may definitely influence the use of PVF in clinical practice. The AR and S1 waves are generated by active LA contraction and relaxation, respectively (14,59); because of the loss in effective LA function, both of them disappear in patients with rhythm disorders, such as AF and asynchronous AV conduction (23,60). Those velocities are small immediately after restoration to sinus rhythm from AF due to temporal LA stunning, but subsequently increase over time (59,61). In AF, the onset of the S2 wave is delayed, and the S2 velocity and systolic fraction are reduced with increased D velocity (23,41). The S2 velocity is especially lower in patients with LV dysfunction than in those with lone AF. The S2 velocity and LA pressure “v” wave are relatively constant in patients with lone AF, whereas they change corresponding to the preceding cardiac cycle lengths in patients with LV dysfunction (62). PVF as a monitor during invasive procedures. MITRAL VALVE DISEASE. In the operating room, we have assessed residual MR during mitral valve repair and demonstrated the return to normal PVF after a successful procedure (46). Similarly, in patients with severe mitral stenosis, successful mitral valvuloplasty could be associated with an immediate increase in S2 velocity (57). A new use of monitoring PVF is the detection of pulmonary vein stenosis after radiofrequency catheter ablation for AF. The focal origin of AF has been recently reported to be mainly inside of the pulmonary veins, and catheter ablation has been demonstrated to interrupt chronic incessant AF. However, the progressive veno-occlusive pulmonary syndrome with pulmonary hypertension as a consequence of pulmonary vein stenosis was reported to be a major complication of this procedure (63). Using TEE, the site of stenosis in all four pulmonary veins could be observed two-dimensionally and the severity estimated by the increased PVF velocities (Fig. 5). This complication should be acutely treated by balloon dilation (64). Future status of PVF evaluation. From the available evidence, there are certain indications for the routine use of PVF by Doppler echocardiography. First, it will be useful in assessing LV diastolic dysfunction using an integrated approach with mitral inflow, as well as estimating LV filling pressures (6,9,10,35) especially in patients with decreased LV systolic function (65). On the other hand, tissue Doppler echocardiography and color M-mode Doppler may be more useful in patients with normal LV systolic function (65). Second, it will continue to be key in differentiating constriction from restriction by noting the enhanced respiratory variation of the diastolic flow (43,45). Third, it will play a major contribution in the evaluation of the severity of MR (66). Finally, evaluation of the orifice of all four pulmonary veins and its flow characteristics by TEE (67) or intracardiac ultrasound (68,69) will play an increasing role in radiofrequency ablation for AF. RADIOFREQUENCY ABLATION. JACC Vol. 41, No. 8, 2003 April 16, 2003:1243–50 Conclusions. Pulmonary venous flow revisited 12 years later is still “alive and well” and will continue to play an important role in clinical practice. Reprint requests and correspondence: Dr. Allan L. Klein, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Desk F-15, Cleveland, Ohio 44195. E-mail: [email protected]. REFERENCES 1. Skagseth E. Pulmonary vein flow pattern in man during thoracotomy. Scand J Thorac Cardiovasc Surg 1976;10:36 –42. 2. Rajagopalan B, Friend JA, Stallard T, Lee GD. Blood flow in pulmonary veins. I. Studies in dog and man. Cardiovasc Res 1979;13: 667–76. 3. Keren G, Sherez J, Megidish R, Levitt B, Laniado S. Pulmonary venous flow pattern—its relationship to cardiac dynamics: a pulsed Doppler echocardiographic study. Circulation 1985;71:1105–12. 4. Keren G, Bier A, Sherez J, Miura D, Keefe D, LeJemtel T. Atrial contraction is an important determinant of pulmonary venous flow. J Am Coll Cardiol 1986;7:693–5. 5. Seward JB, Khandheria BK, Oh JK, et al. Transesophageal echocardiography: technique, anatomic correlations, implementation, and clinical applications. Mayo Clin Proc 1988;63:649 –80. 6. Klein AL, Tajik AJ. Doppler assessment of pulmonary venous flow in healthy subjects and in patients with heart disease. J Am Soc Echocardiogr 1991;4:379 –92. 7. Schiavone WA, Calafiore PA, Salcedo EE. Transesophageal Doppler echocardiographic demonstration of pulmonary venous flow velocity in restrictive cardiomyopathy and constrictive pericarditis. Am J Cardiol 1989;63:1286 –8. 8. Klein AL, Cohen GI. Doppler echocardiographic assessment of constrictive pericarditis, cardiac amyloidosis, and cardiac tamponade. Cleve Clin J Med 1992;59:278 –90. 9. Kuecherer HF, Muhiudeen IA, Kusumoto FM, et al. Estimation of mean left atrial pressure from transesophageal pulsed Doppler echocardiography of pulmonary venous flow. Circulation 1990;82:1127–39. 10. Rossvoll O, Hatle LK. Pulmonary venous flow velocities recorded by transthoracic Doppler ultrasound: relation to left ventricular diastolic pressures. J Am Coll Cardiol 1993;21:1687–96. 11. Yamamoto K, Nishimura RA, Burnett JC Jr., Redfield MM. Assessment of left ventricular end-diastolic pressure by Doppler echocardiography: contribution of duration of pulmonary venous versus mitral flow velocity curves at atrial contraction. J Am Soc Echocardiogr 1997;10:52–9. 12. Klein AL, Hatle LK, Burstow DJ, et al. Doppler characterization of left ventricular diastolic function in cardiac amyloidosis. J Am Coll Cardiol 1989;13:1017–26. 13. Oki T, Fukuda N, Iuchi A, et al. Left atrial systolic performance in the presence of elevated left ventricular end-diastolic pressure: evaluation by transesophageal pulsed Doppler echocardiography of left ventricular inflow and pulmonary venous flow velocities. Echocardiography 1997; 14:23–32. 14. Oki T, Fukuda N, Ara N, et al. Evaluation of left atrial active contraction and relaxation in various myocardial diseases by transesophageal pulsed Doppler echocardiography of left ventricular inflow and pulmonary venous flow. Am J Noninvas Cardiol 1994;8:140 –5. 15. Castello R, Pearson AC, Lenzen P, Labovitz AJ. Effect of mitral regurgitation on pulmonary venous velocities derived from transesophageal echocardiography color guided pulsed Doppler imaging. J Am Coll Cardiol 1991;17:1499 –506. 16. Klein AL, Stewart WJ, Bartlett J, et al. Effects of mitral regurgitation on pulmonary venous flow and left atrial pressure: an intraoperative transesophageal echocardiographic study. J Am Coll Cardiol 1992;20: 1345–52. 17. Klein AL, Bailey AS, Cohen GI, et al. Effects of mitral stenosis on pulmonary venous flow as measured by Doppler transesophageal echocardiography. Am J Cardiol 1993;72:66 –72. Tabata et al. Pulmonary Venous Flow Revisited 1249 18. Tabata T, Oki T, Fukuda N, et al. Transesophageal pulsed Doppler echocardiographic study of pulmonary venous flow in mitral stenosis. Cardiology 1996;87:112–8. 19. Edwards WD. Applied anatomy of the heart. In: Brandenburg RO, Fuster V, Giuliani ER, McGoon DC, editors. Cardiology: Fundamentals and Practice. Chicago, IL: Year Book Medical Publishers, 1987:58. 20. Appleton CP. Hemodynamic determinants of Doppler pulmonary venous flow velocity components: new insights from studies in lightly sedated normal dogs. J Am Coll Cardiol 1997;30:1562–74. 21. Smiseth OA, Thompson CR, Lohavanichbutr K, et al. The pulmonary venous systolic flow pulse—its origin and relationship to left atrial pressure. J Am Coll Cardiol 1999;34:802–9. 22. Oh JK, Seward JB, Tajik AJ. Transesophageal echocardiography. In: Oh JK, Seward JB, Tajik AJ, editors. The Echo Manual. Philadelphia, PA: Lippincott Raven, 1999:23–36. 23. Bartzokis T, Lee R, Yeoh TK, Grogin H, Schnittger I. Transesophageal echo-Doppler echocardiographic assessment of pulmonary venous flow patterns. J Am Soc Echocardiogr 1991;4:457–64. 24. Masuda Y, Toma Y, Ogawa H, et al. Importance of left atrial function in patients with myocardial infarction. Circulation 1983;67:566 –71. 25. Oki T, Tabata T, Yamada H, et al. Assessment of abnormal left atrial relaxation by transesophageal pulsed Doppler echocardiography of pulmonary venous flow velocity. Clin Cardiol 1998;21:753–8. 26. Masuyama T, Nagano R, Nariyama K, et al. Transthoracic Doppler echocardiographic measurements of pulmonary venous flow velocity patterns: comparison with transesophageal measurements. J Am Soc Echocardiogr 1995;8:61–9. 27. Jensen JL, Williams FE, Beilby BJ, et al. Feasibility of obtaining pulmonary venous flow velocity in cardiac patients using transthoracic pulsed wave Doppler technique. J Am Soc Echocardiogr 1997;10: 60 –6. 28. Dini FL, Michelassi C, Micheli G, Rovai D. Prognostic value of pulmonary venous flow Doppler signal in left ventricular dysfunction: contribution of the difference in duration of pulmonary venous and mitral flow at atrial contraction. J Am Coll Cardiol 2000;36:1295–302. 29. Klein AL, Burstow DJ, Tajik AJ, Zachariah PK, Bailey KR, Seward JB. Effects of age on left ventricular dimensions and filling dynamics in 117 normal persons. Mayo Clin Proc 1994;69:212–24. 30. Keren G, Milner M, Lindsay J Jr., Goldstein S. Load dependence of left atrial and ventricular filling dynamics by transthoracic and transesophageal Doppler echocardiography. Am J Card Imaging 1996;10: 108 –16. 31. Castello R, Vaughn M, Dressler FA, et al. Relation between pulmonary venous flow and pulmonary wedge pressure: influence of cardiac output. Am Heart J 1995;130:127–34. 32. Hoit BD, Shao Y, Gabel M, Walsh RA. Influence of loading conditions and contractile state on pulmonary venous flow: validation of Doppler velocimetry. Circulation 1992;86:651–9. 33. Akita S, Ohte N, Hashimoto T, Kobayashi K, Narita H. Effects of volume loading on pulmonary venous flow patterns in dogs with normal left ventricular function. Angiology 1995;46:393–9. 34. Gentile F, Mantero A, Lippolis A, et al. Pulmonary venous flow velocity patterns in 143 normal subjects aged 20 to 80 years old: an echo 2D color Doppler cooperative study. Eur Heart J 1997;18:148 – 64. 35. Appleton CP, Galloway JM, Gonzalez MS, Gaballa M, Basnight MA. Estimation of left ventricular filling pressures using twodimensional and Doppler echocardiography in adult patients with cardiac disease: additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction. J Am Coll Cardiol 1993;22:1972–82. 36. Masuyama T, Lee JM, Yamamoto K, Tanouchi J, Hori M, Kamada T. Analysis of pulmonary venous flow velocity patterns in hypertensive hearts: its complementary value in the interpretation of mitral flow velocity patterns. Am Heart J 1992;124:983–94. 37. Torrecilla EG, Garcia Fernandez MA, Bueno H, Moreno M, Delcan JL. Pulmonary venous flow in hypertrophic cardiomyopathy as assessed by the transesophageal approach: the additive value of pulmonary venous flow and left atrial size variables in estimating the mitral inflow pattern in hypertrophic cardiomyopathy. Eur Heart J 1999;20: 293–302. 1250 Tabata et al. Pulmonary Venous Flow Revisited 38. Rakowski H, Appleton CP, Chan KL, et al. Canadian consensus recommendations for the measurement and reporting of diastolic dysfunction by echocardiography: from the Investigators of Consensus on Diastolic Dysfunction by Echocardiography. J Am Soc Echocardiogr 1996;9:736 –60. 39. Hofmann T, Keck A, van Ingen G, Simic O, Ostermeyer J, Meinertz T. Simultaneous measurement of pulmonary venous flow by intravascular catheter Doppler velocimetry and transesophageal Doppler echocardiography: relation to left atrial pressure and left atrial and left ventricular function. J Am Coll Cardiol 1995;26:239 –49. 40. Kuecherer H, Ruffmann K, Kuebler W. Determination of left ventricular filling parameters by pulsed Doppler echocardiography: a noninvasive method to predict high filling pressures in patients with coronary artery disease. Am Heart J 1988;116:1017–21. 41. Keren G, Sonnenblick EH, LeJemtel TH. Mitral annulus motion: relation to pulmonary venous and transmitral flows in normal subjects and in patients with dilated cardiomyopathy. Circulation 1988;78: 621–9. 42. Shabetai R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 1970; 26:480 –9. 43. Klein AL, Cohen GI, Pietrolungo JF, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol 1993;22:1935–43. 44. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989;79:357–70. 45. Tabata T, Kabbani SS, Murray RD, Thomas JD, Abdalla I, Klein AL. Difference in the respiratory variation between pulmonary venous and mitral inflow Doppler velocities in patients with constrictive pericarditis with and without atrial fibrillation. J Am Coll Cardiol 2001;37: 1936 –42. 46. Klein AL, Obarski TP, Stewart WJ, et al. Transesophageal Doppler echocardiography of pulmonary venous flow: a new marker of mitral regurgitation severity. J Am Coll Cardiol 1991;18:518 –26. 47. Kamp O, Huitink H, vanEenige MJ, Visser CA, Roos JP. Value of pulmonary venous flow characteristics in assessment of severity of native mitral valve regurgitation: an angiographic correlated study. J Am Soc Echocardiogr 1992;5:239 –46. 48. Fuchs RM, Heuser RR, Yin FC, Brinker JA. Limitations of pulmonary wedge V waves in diagnosing mitral regurgitation. Am J Cardiol 1982;49:849 –54. 49. Teien DE, Jones M, Shiota T, Yamada I, Sahn DJ. Doppler evaluation of severity of mitral regurgitation: relation to pulmonary venous blood flow patterns in an animal study. J Am Coll Cardiol 1995;25:264 –8. 50. Klein AL, Savage RM, Kahan F, et al. Experimentally and numerically modeled effects of altered loading conditions on pulmonary venous flow and left atrial pressure in patients with mitral regurgitation. J Am Soc Echocardiogr 1997;10:41–51. 51. Pichard AD, Kay R, Smith H, Rentrop P, Holt J, Gorlin R. Large V waves in the pulmonary wedge pressure tracing in the absence of mitral regurgitation. Am J Cardiol 1982;50:1044 –50. 52. Passafini A, Shiota T, Depp M, et al. Factors influencing pulmonary venous flow velocity patterns in mitral regurgitation: an in vitro study. J Am Coll Cardiol 1995;26:1333–9. JACC Vol. 41, No. 8, 2003 April 16, 2003:1243–50 53. Pieper EP, Hellemans IM, Hamer HP, et al. Value of systolic pulmonary venous flow reversal and color Doppler jet measurements assessed with transesophageal echocardiography in recognizing severe pure mitral regurgitation. Am J Cardiol 1996;78:444 –50. 54. Klein AL, Bailey AS, Cohen GI, et al. Importance of sampling both pulmonary veins in grading mitral regurgitation by transesophageal echocardiography. J Am Soc Echocardiogr 1993;6:115–23. 55. Pu M, Griffin BP, Vandervoort PM, et al. The value of assessing pulmonary venous flow velocity for predicting severity of mitral regurgitation: a quantitative assessment integrating left ventricular function. J Am Soc Echocardiogr 1999;12:736 –43. 56. Stojnic BB, Radjen GS, Perisic NJ, Pavlovic PB, Stosic JJ, Prcovic M. Pulmonary venous flow pattern studied by transesophageal pulsed Doppler echocardiography in mitral stenosis in sinus rhythm: effect of atrial systole. Eur Heart J 1993;14:1597–601. 57. Jolly N, Arora R, Mohan JC, Khalilullah M. Pulmonary venous flow dynamics before and after balloon mitral valvuloplasty as determined by transesophageal Doppler echocardiography. Am J Cardiol 1992;70: 780 –4. 58. Oki T, Iuchi A, Tabata T, et al. Left atrial contribution to left ventricular filling in patients with mitral stenosis: combined analysis of transmitral and pulmonary venous flow velocities. Echocardiography 1998;15:43–50. 59. Iuchi A, Oki T, Fukuda N, et al. Changes in transmitral and pulmonary venous flow velocity patterns after cardioversion of atrial fibrillation. Am Heart J 1996;131:270 –5. 60. Ren WD, Visentin P, Nicolosi GL, et al. Effect of atrial fibrillation on pulmonary venous flow patterns: transesophageal pulsed Doppler echocardiographic study. Eur Heart J 1993;14:1320 –7. 61. Tabata T, Oki T, Iuchi A, et al. Evaluation of left atrial appendage function by measurements of changes in flow velocity patterns after electrical cardioversion in patients with isolated atrial fibrillation. Am J Cardiol 1997;79:615–20. 62. Oki T, Tabata T, Yamada H, et al. Evaluation of left atrial filling using systolic pulmonary venous flow velocity measurements in patients with atrial fibrillation. Clin Cardiol 1998;21:169 –74. 63. Robbins IM, Colvin EV, Doyle TP, et al. Pulmonary vein stenosis after catheter ablation of atrial fibrillation. Circulation 1998;98:1769 – 75. 64. Scanavacca MI, Kajita LJ, Vieira M, Sosa EA. Pulmonary vein stenosis complicating catheter ablation of focal atrial fibrillation. J Cardiovasc Electrophysiol 2000;11:677–81. 65. Nagueh SF, Zoghbi WA. Clinical assessment of LV diastolic filling by Doppler echocardiography. ACC Curr J Rev 2001;10:45–9. 66. Thomas L, Foster E, Hoffman JI, Schiller NB. The mitral regurgitation index: an echocardiographic guide to severity. J Am Coll Cardiol 1999;33:2016 –22. 67. Sohn RH, Schiller NB. Left upper pulmonary vein stenosis 2 months after radiofrequency catheter ablation of atrial fibrillation. Circulation 2000;101:e154 –5. 68. Packer DL, Stevens CL, Curley MG, et al. Intracardiac phased-array imaging: methods and initial clinical experience with high resolution, under blood visualization: initial experience with intracardiac phasedarray ultrasound. J Am Coll Cardiol 2002;39:509 –16. 69. Saad EB, Cole CR, Marrouche NF, et al. Use of intracardiac echocardiography for prediction of chronic pulmonary vein stenosis after ablation of atrial fibrillation. J Cardiovasc Electrophysiol 2002; 13:986 –9.