(Chest. 2000;117:1546-1550.)
© 2000
American College of Chest Physicians
Effect of Atrial Fibrillation on Pulmonary Venous Flow Patterns Assessed by Doppler Transesophageal Echocardiography*
Ting-Hsing Chao, MD;
Liang-Miin Tsai, MD;
Wei-Chuan Tsai, MD;
Yi-Heng Li, MD;
Li-Jen Lin, MD and
Jyh-Hong Chen, MD, PhD
*
From the Section of Cardiology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan.
Correspondence to: Liang-Miin Tsai, MD, Professor of Medicine, Section of Cardiology, Department of Internal Medicine, National Cheng Kung University Medical College and Hospital, 138 Sheng-Li Road, Tainan 704, Taiwan
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Abstract
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Study objectives: To investigate the effect of atrial
fibrillation (AF) on pulmonary venous flow (PVF) patterns in a cohort
with nonrheumatic AF.
Design and settings: A
prospective and controlled study undertaken at a tertiary referral
medical center.
Patients and measurements: The
echocardiographic parameters of left superior PVF as assessed by
Doppler transesophageal echocardiography in 40 patients with chronic AF
(group 1) were compared to those of 33 volunteers with sinus rhythm
(group 2) and well-matched baseline characteristics.
Results: All group 1 patients presented with single
systolic forward flow (SFF) patterns. In contrast, single and double
SFF patterns were found equally in group 2. With regard to reverse flow
(RF), most group 1 patients (33 of 40) had an early systolic RF and
none had atrial RF; however, most group 2 subjects (29 of 33) had an
atrial RF. Some of the group 1 patients (17%) had a late systolic RF
in the absence of significant mitral regurgitation. In group 1, the SFF
appeared later and disappeared earlier than in group 2. The mean
systolic peak velocity and time-velocity integral (TVI) of the SFF were
significantly lower in group 1 compared to group 2. The diastolic peak
velocity and TVI were not significantly different between groups.
Conclusions: Our data indicate that AF independently and
significantly affects the PVF and leads to characteristic flow patterns
different from sinus rhythm. The presence of AF reduces SFF in addition
to the absence of atrial RF. These changes in the flow patterns should
be taken into account while interpreting the implications of PVF in the
presence of AF.
Key Words: atrial fibrillation pulmonary venous flow transesophageal echocardiography
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Introduction
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The
flow patterns of the pulmonary veins have been described in
healthy1
2
3
and diseased hearts.4
5
Some
Doppler echocardiography parameters of pulmonary venous flow
(PVF) have been reported to be implicated in the detection of the
presence of severe mitral regurgitation6
and in the
estimation of the level of left ventricular end-diastolic
pressure7
in patients with sinus rhythm. Although the PVF
patterns in patients with chronic atrial fibrillation (AF) have been
presented in a few studies,8
9
10
the effect of AF on the
PVF is still poorly understood. Previous studies may have been limited
by a heterogeneous population, small sample size, and less control.
Recently, several factors have been reported to affect the PVF. These
include age,11
12
left ventricular function,4
heart rate,2
13
14
respiration,2
12
and
severity of mitral regurgitation.8
15
16
It is necessary
to control these confounding factors when evaluating the PVF patterns
with AF. The purpose of this study was to investigate the effect of AF
on PVF under a well-controlled design.
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Materials and Methods
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Study Population
This study included a total of 40 patients with chronic
nonrheumatic AF (group 1) and 33 volunteers with sinus rhythm and no
major cardiovascular complications (group 2). In group 2, those with
uncomplicated hypertension were not excluded. All patients in group 1
had an AF rhythm, which was found to persist over 30 days as documented
by serial ECGs, and none had physical or echocardiographic evidence of
rheumatic mitral stenosis or a prosthetic mitral valve. The underlying
etiologies of AF were hypertension in 19 patients, coronary artery
disease in 2 patients, hyperthyroidism in 2 patients, and lone AF in 17
patients. None of group 2 had a history of tachycardia or documented AF
on ECGs. Patients who had contraindication of transesophageal
echocardiography (TEE) or who could not tolerate this procedure were
excluded. In addition, patients with poor TEE images or significant
mitral regurgitation were also excluded. Informed consent was obtained
from all study subjects before enrollment.
Echocardiograhy
Both transthoracic echocardiography and TEE studies were
performed in all subjects. Transthoracic echocardiography was performed
with a 2.0- or 2.5-MHz phased-array transducer and a commercially
available ultrasound system (Sonos 1500; Hewlett-Packard; Andover, MA).
Subjects were examined in the left lateral semirecumbent position
during quiet respiration. M-mode echocardiographic measurements were
made as recommended by the American Society of
Echocardiography,17
and five consecutive beats were
averaged. The left ventricular ejection fraction was calculated using
the method described by Teichholz et al.18
Mitral
regurgitation was evaluated and graded by color flow
imaging.19
A grade of moderate or severe mitral
regurgitation was considered significant. A 5-MHz multiplane probe
(model 21364A; Hewlett-Packard) was used to perform TEE in the left
lateral decubitus position. All subjects fasted for > 4 h before the
TEE study. IV or IM sedation with diazepam (2.5 to 5 mg) and topical
pharyngeal anesthesia with 2% lidocaine (Xylocaine) spray were
administered before insertion of the transesophageal probe. Pulmonary
veins were visualized by rotating and tilting the transducer far
leftwards to the upper portion of the left atrium. PVF velocity
profiles were obtained by pulsed-wave Doppler echocardiography with the
sample volume placed in the left upper pulmonary vein, approximately
0.5- to 1-cm proximal to the entrance into the left atrium. The peak
flow velocities and flow time-velocity integrals (TVIs) of the systolic
forward flow (SFF), diastolic forward flow (DFF), and reverse flow (RF)
were measured and averaged over five consecutive cardiac cycles during
end expiration. The TVI of the biphasic SFF pattern was determined by
calculating the whole systolic component of the forward flow, and the
highest point of the SFF was chosen as the peak of the biphasic SFF. In
addition, we also calculated the separate TVI of the early and late
components of the SFF in normal subjects with the biphasic SFF pattern.
Statistical Analysis
Results were expressed as mean ± SD. All analyses were
performed with a software program (SPSS for Windows; SPSS; Chicago,
IL). Continuous variables were compared with an unpaired Students
t test, and categorical variables were compared with a
2 test, with Yates correction between groups.
A significance level of p
0.05 by two-tailed analysis was used in
all tests.
 |
Results
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The underlying clinical and echocardiographic characteristics in
both groups are shown in Table 1
. There were no significant differences between groups regarding age,
sex, left ventricular end-diastolic and end-systolic diameters,
ejection fraction, and the presence of hypertension, mitral
regurgitation, or tachycardia (> 100 beats/min).
PVF Patterns
The PVF patterns of the two groups are listed in Table 2
, and examples are illustrated in Figure 1
. The forward flow consisted of two components, including SFF (which
appeared as a monophasic [single] or biphasic [double] wave) at
systole and DFF at diastole. The end of the SFF was almost always
accompanied with the beginning of the DFF. All of group 1 presented
single SFF patterns. In contrast, single and double SFF patterns were
found in group 2 with almost equal distributions (17 single and 16
double). RF waves appeared in both groups. The onset of the RF that
appeared just after the end of the DFF was correlated with P wave on
the ECG, suggestive of atrial contraction. Such an RF was called atrial
RF. Early systolic RF occurred in the early stage of systole and just
after the peak of the R wave on the ECG, whereas late systolic RF
appeared in the late half of systole. In group 2, most had atrial RF
(88%), and the remainder of the group had early systolic RF (12%). In
contrast, none of the patients with AF had atrial RF, and all of them
had systolic RF (83% at early systole and 17% at late systole).

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Figure 1.. The Doppler echocardiography flow patterns of the
pulmonary vein showing biphasic SFF with atrial reversal in sinus
rhythm (upper panel) and monophasic SFF with early
systolic reversal in AF (lower panel). The cyclic
changes of respiration (arrow) were recorded simultaneously. S = SFF
(S1 = early component, S2 = late component); D = DFF;
AR = atrial reversal; ESR = early systolic reversal.
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Doppler Echocardiography Parameters of the PVF
The Doppler echocardiography parameters of the PVF are shown in
Tables 3
, 4
. In control subjects with biphasic SFF, both peak velocity and TVI were
larger in late SFF than early SFF. The peak velocity and TVI of the SFF
were reduced markedly in group 1 compared to group 2; however, the DFF
was not significantly different. The TVI of the SFF in group 1 was
significantly less than that of the late SFF in control subjects who
had biphasic SFF pattern (4.2 ± 2.5 cm vs 7.5 ± 2.9 cm;
p < 0.001). In group 2, the peak velocity and TVI of the SFF were
greater than those of the DFF. In contrast, inverse relations of these
parameters were found in group 1. In group 1, the deceleration time and
duration of the SFF were shorter, and the onset of SFF was delayed in
comparison with those in group 2. With regard to the DFF, the
deceleration time and duration were not significantly different between
the two groups, but the onset of the DFF was earlier in group 2.
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Discussion
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Since the advent of TEE, PVF patterns can be assessed easily and
clearly.1
Blood flow in the pulmonary veins is inversely
related to pressure events in the left atrium.20
21
In
normal individuals with sinus rhythm, PVF patterns consist of a
biphasic or triphasic forward flow wave and an atrial
RF.22
23
Previous reports showed that early SFF is
influenced by atrial relaxation, late SFF by downward displacement of
mitral leaflets to the left ventricle during ventricle contraction, DFF
by rapid filling during ventricle relaxation, and atrial RF by atrial
contraction.22
Several clinical factors have been reported to affect the PVF patterns
in normal or diseased hearts. First, the effect of old age is greater
on SFF velocity than DFF velocity, and the amplitude of atrial RF is
increased in the elderly.11
12
Second, in sinus
tachycardia, the RF wave may disappear,2
the peak velocity
ratio of SFF/DFF may increase,13
and the SFF and DFF will
fuse.14
Third, spontaneous respiration has little effect
on the PVF,2
12
but straining during the Valsalva maneuver
markedly decreases the peak velocity and TVI of the SFF and
DFF.2
Fourth, decreased mitral annular motion due to lower
left ventricular ejection fraction in dilated cardiomyopathy reduces
the SFF component.4
Fifth, mitral regurgitation may reduce
the amplitude of SFF and contribute to the presence of late systolic
RF.8
15
16
Finally, mitral stenosis may decrease the SFF
component24
25
and prolong DFF.24
Our study
uniquely identifies the actual and independent effect of AF on PVF by
carefully controlling each of the above-mentioned confounding factors.
The PVF patterns in AF have been presented in a few
studies8
9
10
; however, the reported results are
inconsistent. Castello et al8
reported that peak SFF
velocities in patients with AF were not significantly reduced, as
compared to those in sinus rhythm, whereas peak DFF velocities were
significantly higher in AF. In contrast, Ren et al9
indicated that the SFF parameters were significantly different between
those with sinus rhythm and AF patients.
In our study, the flow patterns of the pulmonary veins were
significantly different between patients with AF and the normal control
subjects. The loss of atrial RF and early SFF in all patients with AF
is suggestive of the absence of the atrial contraction and relaxation,
respectively. Accordingly, most of the SFF in AF originated from the
contribution of downward displacement of mitral leaflets to the left
ventricle at systole. In control subjects, the mean TVI of late SFF was
higher than that of early SFF, suggesting that the contribution of the
downward displacement of mitral leaflets was more than that of the
atrial relaxation with regard to the SFF. The decreased TVI of SFF in
patients with AF was probably due to the loss of the atrial relaxation,
as well as the reduced amplitude of the downward displacement of mitral
leaflets. The smaller TVI of SFF in AF patients compared to late
systolic TVI in the control subjects suggests a decreased mitral
movement in AF. A recent study reported that late SFF could also be
caused by forward propagation of right ventricular
pressure26
; whether this mechanism could be affected by AF
remains unknown. The peak velocity and TVI ratios of SFF/DFF were
< 1.0 in patients with AF and > 1.0 in the control group. This
discrepancy was primarily due to the differences of SFF. With regard to
the atrial functions, our results suggest that the presence of AF may
cause marked impairment of the atrial pumping and reservoir functions,
but not the conduit function.
The end of SFF was always accompanied by the beginning of DFF in all
echocardiography studies, suggesting that the end of the recoil of the
mitral annulus toward the atrium coincided with the onset of
transmitral filling.4
In patients with AF, the
deceleration time of SFF was shorter, and the onset and peaking of DFF
were earlier compared with control group. We postulate that the absence
of the atrial contraction during the late stage of mitral filling in AF
may increase the blood volume and, hence, create a higher pressure
burden in the left atrial cavity during ventricular systole. This may
lead to the reduced deceleration time of SFF and the early onset of
DFF.
Systolic RF was present in all AF patients (83% with early and 17%
with late systolic RF), but in only 12% of the normal control subjects
(all with early systolic RF). The possible mechanisms for systolic RF
might be that the mitral valve leaflets remain in a semi-open position
during systole in humans with AF.27
Paraskevaidis et
al10
observed that systolic RF appears in concordance with
the abnormal motion of the mitral annulus toward the left atrium during
early systole, due probably to the absence of atrial relaxation. In
terms of late systolic RF, some studies have addressed the clinical
importance of these flow patterns accounting for the existence of
clinically significant mitral regurgitation.8
15
16
As
observed in one report,28
we found some AF patients
to have late systolic RF, and none of these patients had significant
mitral regurgitation. Therefore, late systolic RF is not reliable in
predicting severe mitral regurgitation in the presence of AF.
Several limitations should be mentioned. First, the number of our study
subjects was not large enough to represent the general population of AF
patients. Second, we evaluated only the flow patterns of the left
superior pulmonary vein. Third, the intracardiac pressures were not
measured; therefore, the implication of PVF on hemodynamics such as
atrial pressure could only be postulated.
In conclusion, our results indicate that AF significantly affects the
PVF and leads to characteristic flow patterns distinct from sinus
rhythm. The absence of atrial contraction and relaxation contributes
largely to the changes of PVF in AF. The clinical implications of PVF
as reported in sinus rhythm should be interpreted cautiously when
applied to patients with AF.
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Footnotes
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Abbreviations: AF = atrial
fibrillation; DFF = diastolic forward flow; PVF = pulmonary venous
flow; RF = reverse flow; SFF = systolic forward flow;
TEE = transesophageal echocardiography; TVI = time-velocity
integral
These results have been presented in part at the Eighth Asian-Pacific
Conference on Doppler and Echocardiography, Taipei, Taiwan, May 1314,
1999.
Received for publication August 31, 1999.
Accepted for publication January 25, 2000.
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