Download Pulmonary venous flow by doppler echocardiography: revisited 12

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Heart failure wikipedia , lookup

Electrocardiography wikipedia , lookup

Hypertrophic cardiomyopathy wikipedia , lookup

Echocardiography wikipedia , lookup

Lutembacher's syndrome wikipedia , lookup

Atrial septal defect wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Dextro-Transposition of the great arteries wikipedia , lookup

Transcript
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.