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Transcript
Original Article
Doppler Echocardiography and Hemodynamic Parameters in
Congenital Heart Disease with Increased Pulmonary Flow
Zilma Verçosa de Sá Ribeiro, Jeane Mike Tsutsui, Rogério dos Anjos Miranda, Samira Mohry, Wilson Mathias,
Antonio Augusto Lopes
Instituto do Coração (InCor) - HC-FMUSP, São Paulo, SP - Brazil
Abstract
Background: The prediction of pulmonary hemodynamic data from non-invasive assessment could exempt some
patients with congenital cardiac septal defects from preoperative invasive assessment (catheterization).
Objective: To determine, in simultaneous assessment, whether data obtained from Doppler echocardiography could
predict aspects of pulmonary hemodynamics in such patients.
Methods: Echocardiographic parameters related to systolic and systemic pulmonary flow and pulmonary venous flow
were related to hemodynamic data in 30 consecutive patients with cardiac septal defects (aged 4 months to 58 years,
median 2.2 years, mean pulmonary artery pressure between 16 and 93 mmHg).
Results: The velocity-time integrals of systolic flow in right ventricle outflow tract (VTIRVOT ≥ 22 cm) and pulmonary
venous flow (VTIVP ≥ 20 cm) predicted PVR/SVR ≤ 0.1 levels (pulmonary vascular resistance and systemic vascular
resistance ratio), with a specificity of 0.81 and odds ratio above 1.0. For VTIRVOT ≥ 27 cm and VTIPV ≥ 24 cm values, the
specificity was higher than 0.90 and odds ratio 2.29 and 4.47 respectively. The ratio between pulmonary and systemic
flows (Qp/Qs ≥ 2.89 and ≥ 4.0, echocardiographic estimates) was useful in predicting Qp/Qs > 3.0 values through
catheterization (specificity of 0.78 and 0.91, odds ratio 1.14 and 2.97, respectively).
Conclusion: In patients with cardiac septal defects, Doppler echocardiography is able to identify those at increased flow
and low pulmonary vascular resistance. (Arq Bras Cardiol 2010;94(5):557-564)
Key words: Echocardiography, Doppler; heart defects, congenital; heart catheterization.
Introduction
Currently, most patients, particularly pediatric patients,
with congenital cardiac septal defects that cause increased
flow and pressure in the pulmonary region are referred to
corrective procedures based on non-invasive assessment only.
This is due to the advancement of correction techniques,
especially surgeries, plus the development of postoperative
care, resulting in the possibility of treating early in the first
months of life. There is evidence that in infants undergoing
early correction of septal defects, particularly under 9 months
of age, pulmonary vascular resistance, evaluated one year
after it, returns to normal levels, regardless of the severity of
vascular lesions observed in lung biopsy samples1. Thus, in
most cases, the invasive assessment of pulmonary vascular
resistance becomes unnecessary.
Nevertheless, some situations fall out of this rule.
The following conditions have been linked to persistent
Mailing address: Antonio Augusto Lopes •
Av Dr. Eneas de Carvalho Aguiar 44 - Cerqueira César - 05403-000 - São
Paulo, SP - Brazil
E-mail: [email protected]
Manuscript received May 14, 2009; revised manuscript received August 26,
2009, accepted on October 20, 2009.
557
pulmonary hemodynamic changes even after successful
correction of cardiac septal defects, requiring a diagnostic
evaluation in greater depth, even through invasive methods:
1) patients older than two; 2) presence of certain abnormal
conditions such as common arterial trunk, atrioventricular
septal defects and transposition of great arteries associated
with ventricular septal defects; 3) no history of congestive
lung associated with deficits in weight gain. In these
situations, despite the development of noninvasive methods
for assessing the pulmonary hemodynamics, particularly
Doppler echocardiography and magnetic resonance 2-4,
there is consensus on the need to measure pulmonary
vascular resistance through cardiac catheterization5 and the
characterization of its behavior in vasodilator stimuli6-10. In
the absence or, if necessary, in the presence of vasodilator
stimuli, the final pulmonary vascular resistance is expected
to lie below 6.0 Wood units m2 and pulmonary and systemic
resistance ratio should be smaller than 0.3.
There have been efforts to try to estimate pulmonary
hemodynamic variables through echocardiography data,
especially in patients with congenital heart disease, aiming
at the progressive replacement of invasive assessment with
noninvasive assessment. Pressure, blood flow and pulmonary
vascular resistance have been estimated through a variety
Ribeiro et al
Echo/pulmonary hemodynamics
Original Article
of echocardiographic indexes11-15. However, the use of such
measures in clinical practice is still quite limited, especially
in view of the great variability of the correlation coefficients
between echocardiographic and hemodynamic data, when
different authors are compared. Thus, echocardiography
is still limited in its ability to provide timely hemodynamic
data usually obtained through catheterization. High values
of correlation coefficients are found in studies with limited
number of congenital heart disease included, thus not
allowing generalizations.
This study, conducted in patients with three types of cardiac
septal defects known to cause increased flow and pulmonary
pressures, was targeted at answering the following question:
would it be possible, through noninvasive assessment
(echocardiography), to identify with acceptable accuracy
patients in situations of increased pulmonary blood flow
without a considerable increase in vascular resistance in that
territory, so that cardiac catheterization could be avoided
even in the presence of clinical suspicion of pulmonary
hypertension? The study was then designed to perform such
assessment prospectively.
Methods
Case series
The following patients were found to be eligible for this
study: patients with congenital heart defects, namely atrial
septal defect, ventricular septal defect or atrioventricular
septal defect in preoperative evaluation at the Unit of Pediatric
Cardiology and Adult Congenital Heart Diseases, Instituto
do Coração, Hospital das Clínicas, Medical School of the
University of São Paulo. We only included patients whose
clinical and echocardiographic initial assessment suggested,
for some reason, the need for cardiac catheterization as a
diagnostic complementation, as in the defects cited, invasive
assessment is not generally necessary. In our routine, factors
that usually lead to the prescription of catheterization in
patients with heart defects are: age above 18 months,
associated syndromes, absence of pulmonary congestion
signs, peripheral oxygen saturation periods below 90% and
presence of bidirectional flow through the septal defects.
Beyond these criteria, catheterization was occasionally
prescribed for anatomical clarifications (for example, on
pulmonary venous drainage) in cases of persistent doubts
with noninvasive assessment. Exclusion criteria were patients
with cardiac arrhythmias, anatomic defects that would lead
to inaccurate measurements (pulmonary stenosis or atrial
septal defects), or that would require oxygen concentrations
above 30% in the air inhaled during cardiac catheterization.
All patients or their guardians signed an informed consent
before taking part in the entry. The protocol was approved
by the Scientific and Ethics Committee of the Instituto do
Coração (nSDC2277/03/071) and by the Ethics Committee
of the Hospital das Clínicas (n.573/03).
congestion, oxygen saturation periods below 90% and the flow
direction (from left to right, from right to left or bidirectional)
through the septal defect.
Ecocardiographic assessment
Parallel to the assessment of structural heart defects,
Doppler echocardiography was used to analysis of variables
potentially relatable to hemodynamic data. Echocardiography
was performed simultaneously with cardiac catheterization
in the hemodynamic laboratory, under sedation or general
anesthesia when required, and supply of oxygen in inhaled
air ranging from 21% to 30% in concentration. The survey
was conducted with use of HDI5000 model equipment
(Philips Medical System, Andover, MA, USA) equipped
with 2.5MHz and 5MHz transducers. Echocardiographic
measurements were made as recommended by the American
Society of Echocardiography16.
All flow variables on the right were obtained with pulsedwave Doppler positioned in the right ventricle outflow tract,
just below the pulmonary valve. By recording the pulmonary
systolic flow curve, the following variables were recorded
(average value of three consecutive heartbeats): acceleration
time (ACt), ejection time (ET), right ventricle pre-ejective
period (PEP); velocity-time integral of total systolic flow in the
right ventricle outflow tract (VTIRVOT), ACt/ET; PEP/ET and PEP/
VTIRVOT indexes. The velocity-time integral value corresponding
to the pulmonary venous flow was also determined (VTIPV).
The pulmonary and systemic flow ratio (Qp/Qs) was obtained
by assessing each of them through the following equation:
Q (l/min) = V x a x 60 s/min x (1000 ml/l)-1
where Q is blood flow, V is the average velocity of the
pulmonary or aortic flow (Doppler, cm/s), and “a” is the
cross-sectional area (aortic or pulmonary, cm2). Finally, the
overall assessment of right ventricular function was made
by determining the myocardial performance index (MPI) as
previously described17,18.
Cardiac catheterization
Right and left heart catheterization was performed by
introducing catheter through femoral vein puncture, requiring
intravenous anesthetics (midazolam, fentanyl, ketamine) and
occasionally inhalation (sevoflurane) in pediatric patients.
Pulmonary artery pressures were recorded (PBPS, PBPD and
PBPM, respectively, systolic, diastolic and mean), as well
as pulmonary wedge pressure (PWP) and systemic arterial
pressures (SAP S, SAP D and SAP M, respectively, systolic,
diastolic and mean). After obtaining blood samples for blood
gas analysis, pulmonary and systemic blood flows were
calculated by the Fick principle. Subsequently, from the values
of pressures and flows, pulmonary and systemic vascular
resistance indexes were determined. Both blood flows and
vascular resistances in the lungs and systemic circulation were
expressed as ratios (respectively, Qp/Qs and PVR/SVR).
General diagnostic data
Statistical analysis
Data obtained were age, sex, type of structural heart defect,
associated syndromes, presence or absence of pulmonary
The results for the variables analyzed were expressed
as median and limits. Mean and standard deviation results
Arq Bras Cardiol 2010;94(5):557-564
558
Ribeiro et al
Echo/pulmonary hemodynamics
Original Article
were also determined in the case of satisfactory adherence
to normal distribution. The potential association between
hemodynamic and echocardiographic variables was
tested by adjusting mathematical models. Therefore, the
transformation of explanatory variables and response variables
was necessary. The suitability of adjusted models to predict
the extent of hemodynamic variables, was checked by
obtaining the coefficient of determination (r2). The possibility
of predicting hemodynamic data by category, by means of
echocardiographic data, was checked by adjusting the logistic
regression models. In this case, the prediction suitability was
examined by building operating characteristics curves (ROC).
Cut-off values were determined for predicting variables
(echocardiographic variables), taking into account the best
sensitivity and specificity ratio, but giving priority to the
latter. The prioritization of specificity was due to the fact that
the study aimed to safely identify patients with most benign
pulmonary hemodynamic change. Thus, we focused only on
cut-off values with sensitivity around or above 0.80. In all
procedures, we adopted the value 0.05 as significance level.
Results
The study included 30 patients with ages ranging between
0.41 and 58.2 (median 2.2 years), of which 75% were below
10 years. The sex ratio was 1:1. The mean pulmonary artery
pressure ranged between 16 and 93 mmHg (median 28
mmHg) upon catheterization. Individual diagnostic data
are displayed in Table 1. With respect to clinical data that
could point out to the possibility of high pulmonary vascular
resistance (over 18 months, associated syndromes, no
pulmonary congestion, peripheral oxygen saturation periods
below 90% and bidirectional flow through the cardiac septal
defect) the number of patients with none, one, two, three,
four or five of these characteristics were respectively 1, 4,
17, 5, 3 and 0.
Echocardiographic and hemodynamic findings
Findings of echocardiographic and hemodynamic measures
that can be obtained in all 30 patients are summarized in
tables 2 and 3, respectively. The number of patients with Qp/
Qs > 3.0 upon echocardiography and through catheterization
were respectively 12 and 15, suggesting that the study cohort
includes a subgroup of individuals in a condition of clear
increased pulmonary blood flow (compatible with low vascular
resistance). Table 2 shows that there were ACt variable records
below 65 ms, and ACt/ET variable records below 0.26, noting
that these limits generally identify patients with PBPM over
40 mmHg2. Values below 16.0 cm to VTIRVOT19 and VTIPV also
suggested the absence of increased pulmonary blood flow in
some cases. MPIRV values greater than 0.3220 were suggestive
of right ventricular dysfunction in some patients.
Point estimation of hemodynamic data
Table 4 shows that among the various attempts to determine
a potential interdependence between echocardiographic
and hemodynamic variables it was possible to develop six
predictive models with statistical significance, all non-linear.
However, based on coefficient of determination values (r2),
559
Arq Bras Cardiol 2010;94(5):557-564
the point prediction of hemodynamic data was not considered
satisfactory (Fig. 1).
Interval estimation of hemodynamic data
The echocardiographic variables VTIRVOT, VTIPV, Qp/Qs, PEP/
ET, and PEP/VTIRVOT were tested for their ability to predict levels
to hemodynamic variables Qp/Qs and PVR/SVR. Table 5 shows
sensitivity, specificity and odds ratio values for the models
whose development was possible with statistical significance.
It was not possible to identify, from the echocardiogram,
patients with high pulmonary vascular resistance (eg, PVR/SVR
> 0.5). However, through the echocardiographic variables
Qp/Qs, VTIRVOT and VTIPV, we could identify patients under
hemodynamics of clear increased pulmonary flow (Qp/Qs
> 3.0 upon catheterization) and low vascular resistance
levels (PVR/SVR ≤ 0.1). The concordance level between
echocardiography and catheterization, as measured by the
percentage of correctly classified cases, was 70%, 73% and
73% respectively, in predicting Qp/Qs > 3.0 and in the PVR/
SVR ≤ 0.1 ratio, from the variables VTIRVOT and VTIPV. Table
5 provides two potential “cut-off values” for each of the
echocardiographic variables, suggesting that, for the purposes
of clinical use, the specificity should be prioritized. Figure
2 shows the operating characteristic curves corresponding
to the prediction (interval) of hemodynamic data from the
echocardiographic variables arranged in Table 5. Note that the
variable VPPV was slightly more robust in its predictive capacity.
Patients’ ages, ranging from 0.41 to 58.2, did not influence
the results, even when tested alone or in combination with
echocardiographic indexes in multiple regression models.
Discussion
The findings of this study show a significant association
between echocardiographic and hemodynamic data (cardiac
catheterization) in patients with congenital cardiac septal
defects. There was sufficient precision to point estimation.
Basically, we could identify, through Doppler echocardiography
(e.g., VTIRVOT ≥ 22 cm, VTIPV ≥ 20 cm and Qp/Qs ≥ 2.89) in
patients under unquestionable condition of increased blood
flow (Qp/Qs > 3.0) and low levels of pulmonary vascular
resistance (PVR/SVR ≤ 0.1). Although echocardiographic
variables could have been tested for their ability to predict
other hemodynamic levels (e.g., Qp/Qs > 1.5 and PVR/SVR <
0.3), our goal was not looking for ways to exempt individuals
in borderline situations from catheterization. However, not
so significant sensitivity levels suggest that, according to the
criteria proposed, some patients in situations of increased
pulmonary flow would still be assessed invasively.
Attempts to assess hemodynamic data (especially
pulmonary data) through Doppler echocardiography begin
with the determination of pressures. Thus, the systolic pressure
in the right ventricle (and by implication, the PBPS, provided
that there is no obstruction in the ventricular outflow tract)
has been estimated through modified Bernoulli equation,
using maximum velocity of tricuspid regurgitation flow21,22.
PBPM and PBPD have been estimated by the same principle,
but using the initial and final velocities of the pulmonary
regurgitation flow. Alternatively, the latter can be predicted
Ribeiro et al
Echo/pulmonary hemodynamics
Original Article
Table 1 - Diagnoses in 30 patients with congenital heart disease
Patient No
1
Age
(years)
Gender
Anomaly
(ies)
PBPM
Qp/Qs
Syndromes Pulmonary
congestion
Sat O2 < 90%
Direction of
flow (*)
58.2
F
ASD / AR
16
1.43
--
not found
no
E-D
2
50.9
F
ASD
16
3.10
--
not found
no
E-D
3
49.8
F
ASD
23
5.09
--
not found
no
E-D
4
37.5
F
ASD
19
3.03
--
not found
no
E-D
5
1.9
M
AVSD
27
2.35
Down
found
no
E-D
6
1
M
AVSD
33
1.75
Down
found
yes
Bidirectional
7
2
M
VSD / MS
40
4.70
--
found
no
Bidirectional
8
0.66
M
AVSD
25
3.17
Down
found
no
Bidirectional
9
0.66
M
VSD
21
2.92
--
found
no
Bidirectional
10
0.91
M
VSD
42
4.00
--
found
no
Bidirectional
11
1.4
F
AVSD
44
3.90
--
found
yes
Bidirectional
12
2.4
F
VSD / IM
93
1.73
--
found
no
Bidirectional
13
1.3
F
VSD
35
5.14
--
found
no
Bidirectional
14
4
F
VSD
28
1.95
--
found
no
Bidirectional
15
0.41
M
VSD / ASD
28
5.38
--
found
no
E-D
16
1.58
M
VSD
24
3.30
--
found
no
Bidirectional
17
2.75
F
VSD
43
4.33
--
found
no
Bidirectional
18
0.75
M
VSD
33
2.58
--
found
no
Bidirectional
19
0.75
F
VSD / ASD
19
4.58
Down
found
no
Bidirectional
20
1
F
AVSD
25
4.57
--
found
yes
Bidirectional
21
6
F
AVSD
26
6.25
Down
found
yes
Bidirectional
22
36
M
AVSD
73
1.40
--
not found
yes
Bidirectional
23
2.58
F
VSD
32
5.21
Down
found
no
Bidirectional
24
0.83
M
AVSD
50
1.63
Down
found
yes
Bidirectional
25
46.2
F
VSD
82
0.82
--
not found
yes
D-E
26
11
F
VSD
22
4.17
--
found
no
Bidirectional
27
7.5
M
ASD
20
2.05
Aaskorg
found
no
E-D
28
1
M
AVSD / CoAo
48
1.55
Down
found
yes
Bidirectional
29
44.7
M
ASD
33
0.92
--
not found
no
Bidirectional
30
54
M
ASD
19
3.81
--
not found
No
E-D
ASD - atrial septal defect; VSD - ventricular septal defect; CoAo - coarctation of the aorta; AVSD - atrioventricular septal defect; AR - aortic regurgitation; MS - mitral
stenosis; PBPM - mean pulmonary artery pressure measured during catheterization; Qp/Qs - ratio between pulmonary and systemic blood flow upon catheterization; Sat O2
<90% - recorded periods of oxygen saturation below 90%. (*) Direction of flow through the cardiac septal defect. Bidirectional flow in both directions; D-E - predominantly
from right to left; E-D - predominantly left to right.
using regression models, taking as independent variables
the ACt or ACt/ET (PBPM) or PEP/ET indexes (PBPD)2,11. All
these propositions have constraints. Pulmonary and tricuspid
regurgitation are not always present. When present, these
do not always reflect pressure increases, as it is the case of
valve regurgitation by anatomical abnormality in patients with
atrioventricular septal defect. For these reasons, the pressure
record through regurgitation flows was not considered in this
study. It was possible to develop a regression model to predict
the PBPD from the PEP/ET ratio, with a weak coefficient of
determination, though. It should be noted that for the purposes
of making decisions regarding the prescription of corrective
treatment (usually surgery) in these patients, blood pressure
levels per se have not been taken into account.
More informative than the pressures are the numerical
value of pulmonary blood flow (Qp) and its relation to
systemic flow (Qp/Qs). In the absence of respiratory disorders
or systemic vasodilatation which may alter the Qp/Qs ratio,
that has been routinely used as a measure of pulmonary blood
flow in cardiac septal defects, mainly because its calculation
depends only on blood gas data not requiring the measured
value of oxygen consumption. After catheterization, Qp/Qs
Arq Bras Cardiol 2010;94(5):557-564
560
Ribeiro et al
Echo/pulmonary hemodynamics
Original Article
Table 2 - Echocardiographic variables analyzed in the study
PEP
(ms)
ACt (ms)
ET (ms)
VTIRVOT
(cm)
VTIPV (cm)
ACt/ET
Mean 82.1
233.4
19.6
18.9
0.34
Standard
deviation
26.8
51.7
7.5
5.9
0.08
Median PEP/ET
PEP/VTIRVOT
(ms/cm)
Qp/Qs
MPIRV
78.5
70.5
233.5
18.9
18.8
0.36
0.3
4.1
2.3
0.26
Lower limit
42
40
109.4
5.5
7.1
0.18
0.15
1.2
0.3
0.08
Upper limit
140
140
335
38.2
35.2
0.54
1
21.7
7.4
2.6
MPIRV - right ventricle myocardial performance index; PEP - pre-ejection period; Qp/Qs - pulmonary flow and systemic flow ratio: Act - acceleration time, ET - ejection time;
VTIPV - velocity-time integral of right superior pulmonary venous flow; VTIRVOT - velocity-time integral of systolic flow in the right ventricle outflow tract. Mean and standard
deviation are presented only for variables with satisfactory adherence to normal layout.
Table 3 - Hemodynamic variables analyzed in the study
PBPS
(mmHg)
POC
(mmHg)
SAPS
(mmHg)
SAPD
(mmHg)
PBPM
(mmHg)
Qp/Qs
Mean 11.6
88.8
51.4
62.1
3.2
Standard
Deviation
3.7
33.1
22.1
24
1.6
10.5
77.5
44.5
55.5
3.1
0.09
Median PBPD
(mmHg)
50
PBPM
(mmHg)
18
28
PVR/SVR
Lower limit
30
10
16
4
45
25
32
0.8
0.02
Upper limit
130
130
93
20
150
90
110
6.6
0.86
PBPD - diastolic pulmonary arterial pressure; PBPM - mean pulmonary arterial pressure; PBPS - systolic pulmonary artery pressure; SAPD - diastolic blood pressure; PBPM mean systemic arterial pressure; SAPS - systolic blood pressure; PWP - pulmonary wedge pressure; Qp/Qs - pulmonary flow and systemic flow ratio; PVR/SVR - pulmonary
vascular resistance and systemic vascular resistance ratio. Mean and standard deviation are presented only for variables with satisfactory adherence to normal layout.
Table 4 - Point estimation of hemodynamic variables from
echocardiographic data (*)
values greater than 1.5 and values above 1.7 or 2.0 have
been considered as suggesting “increased pulmonary flow”
respectively in ventricular and atrial septal defects.
Response
variable [y]
(catheterization)
r2
P value
PBPS
--
--
PEP/ET
PBPD
0.29
0.0019
ACt/ET
PBPM
--
--
PEP/ET
PVR/SVR
0.21
0.0102
ACt/ET
PVR/SVR
--
--
PEP/VTIRVOT
Explanatory variable
[x] (echocardiogram)
PEP/VTIRVOT
PVR/SVR
0.18
0.0202
Qp/Qs
Qp/Qs
0.21
0.0104
VTIRVOT
PVR/SVR
0.22
0.0094
VTIPV
PVR/SVR
0.38
0.0003
PBPD - pulmonary arterial pressure (mmHg), PBPM - mean pulmonary arterial
pressure (mmHg), PBPS - pulmonary artery systolic pressure (mmHg); PEP
- pre-ejection period (ms); Qp/Qs - pulmonary flow and systemic flow ratio; r2
- coefficient of determination; PVR/SVR - pulmonary vascular resistance and
systemic vascular resistance ratio; Act - acceleration time (ms); ET - ejection
time (ms); VTIPV - velocity-time integral of right superior pulmonary venous
flow (cm); VTIRVOT - systolic flow velocity-time integral of right ventricle outflow
tract (cm). (*) The six models we have tried to develop (see coefficients of
determination) were all exponential, of y=EXP (a+bx) type, and the explanatory
variable (x) used in the form of natural logarithm or root.
561
Arq Bras Cardiol 2010;94(5):557-564
Several methods have been proposed to estimate, through
Doppler echocardiography, the ratio between flows. These
methods involve the use of flow velocities in ventricle outflow
tracts, as well as the cross-sectional area of the pulmonary
artery and aorta23, as performed in this study. The Qp/Qs
ratio can be determined with echocardiographic analysis
of flows in different heart positions, for greater accuracy
in estimating septal defects in different locations, that is,
pre-tricuspid, post-tricuspid or interatrial24. The same ratio
can be estimated in patients with ventricular septal defects
by analyzing the flow velocity through such septal defect,
considering its diameter25. However, clinical practice use of
Qp/Qs index analyzed by echocardiography has been limited
mainly due to the diversity of correlation coefficients with
catheterization findings. Coefficients greater than 0.90 are
reported in literature, but in case series involving a limited
number of heart defects. Therefore, generalization was not
possible26. In most reports, the correlation coefficients are
between 0.80 and 0.85 using different methods12,24,25. In
this study, despite attempts to adjust several models, based
on echocardiography, an acceptable point prediction for
the Qp/Qs ratio determined by catheterization could not
be established. However, it was possible to determine that
Ribeiro et al
Echo/pulmonary hemodynamics
PVR/SVR
Original Article
VTIRVOT (cm)
VTIPV (cm)
Figure 1 - Point estimation of the pulmonary and systemic vascular resistance ratio (PVR/SVR, cardiac catheterization) from the velocity-time integral of pulmonary
flow, determined by echocardiography with Doppler positioned in the right ventricle outflow tract (VTIRVOT, systolic flow) or pulmonary tract (VTIPV). The data correspond
to patients with congenital cardiac septal defects (n = 30). The nonlinear models have the format y = EXP (a+b(lnX)).
Table 5 - Interval estimation of hemodynamic variables from the echocardiographic data
Predictor
(echocardiogram)
Variable estimated
(catheterization)
Sensitivity Specificity
Odds ratio
Qp/Qs³ 2.89
Qp/Qs > 3.0
0.6
0.78
1.14
Qp/Qs ≥ 4.0
Qp/Qs > 3.0
0.33
0.91
2.97
VTIRVOT ≥ 22 cm
PVR/SVR ≤ 0.1
0.57
0.81
1.23
VTIRVOT ≥ 27 cm
PVR/SVR ≤ 0.1
0.15
0.94
2.29
VTIPV ≥ 20 cm
PVR/SVR ≤ 0.1
0.65
0.81
1.21
VTIPV ≥ 24 cm
PVR/SVR ≤ 0.1
0.32
0.93
4.47
P value (*)
0.0263
0.0476
0.0092
Sensitivity
Qp/Qs - pulmonary flow and systemic flow ratio; PVR/SVR - pulmonary vascular resistance and systemic vascular resistance ratio; VTIPV - velocity-time integral of right
superior pulmonary venous flow (cm); VTIRVOT - systolic flow velocity-time integral in the right ventricle outflow tract (cm). (*) Related to coefficient β of the predictor in the
logistic model adjusted.
1 - Specificity
Figure 2 - Operating characteristic curves (ROC) for predicting hemodynamic data from echocardiographic variables. Dashed line: prediction of values PVR/SVR ≤
0.1 (pulmonary vascular resistance and systemic vascular resistance ratio upon catheterization) from the echocardiographic variable VTIPV (velocity-time integral of
pulmonary venous flow); solid line: prediction of values Qp/Qs > 3.0 (pulmonary and systemic blood flow ratio upon catheterization) from the same variable (Qp/Qs) upon
echocardiography; dotted line: prediction of values PVR/SVR ≤ 0.1 from the echocardiographic variable VTIRVOT (velocity-time integral of systolic flow in the right ventricle
outflow tract). We can note a slight superiority of the VTIPV, as a predictor, in relation to others. The areas under the curves are, respectively, 0.80, 0.75 and 0.72, and the
total area is assumed as 1.0. The data correspond to patients with congenital cardiac septal defects (n = 30).
Arq Bras Cardiol 2010;94(5):557-564
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Ribeiro et al
Echo/pulmonary hemodynamics
Original Article
patients with Qp/Qs ≥ 2.89 estimated by echocardiography
have odds ratios greater than 1.0 on the possibility of
being in a range above 3.0 for the Qp/Qs ratio determined
by catheterization. For patients with Qp/Qs ≥ 4.0 on
echocardiography (that occurred in six individuals in this
study), the specificity of this prediction hit 0.91, with odds
ratio of 2.97. Thus, for decision-making purposes, the interval
prediction of the ratio between the flows seemed safer.
Alternatively, the pulmonary and systemic flows can
be predicted indirectly through the velocity-time integral
(VTI) determined in ventricular outflow tracts by Doppler
echocardiography. In the absence of septal defects that
may produce increased pulmonary blood flow, the variable
VTIRVOT has values around 16 cm, which seems to be stable
across different age groups. However, it is inversely related
to heart rate 19. Patients with increased pulmonary flow
associated with cardiac septal defects usually present VTIRVOT
values above 20 cm. In this study, the velocity-time integral
was more useful in predicting the pulmonary vascular
resistance than the flow itself.
In addition to the pressures (pulmonary pressures) and
blood flows, attempts have been made to estimate the
pulmonary vascular resistance using variables deriving from
Doppler echocardiography. Among the latter are the ratio
between tricuspid regurgitant jet velocity and velocity-time
integral on the right (TRV/VTIRVOT), in addition to PEP, ET, PEP/
ET, PEP/VTIRVOT, ACt and the PEP/ACt ratio and the total systolic
time 3,11,13,27,28. Despite reports of correlation coefficients with
hemodynamic data in excess of 0.90, there are a number
of difficulties in interpreting and applying these results. The
most important one is the exclusion of patients from the final
analysis, on the grounds of technical difficulties in determining
echocardiographic or hemodynamic data 11,13,27. As the
exclusion criteria are not clearly explained in advance, the
interpretation of findings is impaired. Other problems include
the use of regression procedures in data whose distribution
would clearly not allow it3 and the use of very small case
series28. Another limitation of the use of these correlations is
that findings obtained from case series that do not include
patients with congenital heart disease3,27,28 are not applicable
to situations of clinical practice involving patients with cardiac
septal defects by promoting communication between the
systemic and pulmonary circulations.
In the strict context of congenital heart disease, it is worth
discussing some predictions based on intervals. Hirschfeld et
al11 used the cutoff value < 0.30 for the PEP/ET variable in
identifying patients with low pulmonary vascular resistance
(below 3.0 Wood units, which generally corresponds to
the PVR/SVR ratio between 0.15 and 0.18). They found an
association between PEP/ET > 0.40 values and pulmonary
vascular resistance above 5.0 units11. Ebeid et al13 found
associations of PEP/VTIRVOT variable values below 0.40,
between 0.40 and 0.60 and above 0.60 seconds/meter,
respectively, with pulmonary resistance levels below 3.0,
between 3.0 and 7.5 and above 7.5 Wood units13. In this
study, in terms of point prediction, the highest coefficient of
determination was obtained for the association between the
variables VTIPV and PVR/SVR, still not sufficiently robust. The
563
Arq Bras Cardiol 2010;94(5):557-564
variables VTIRVOT and VTIPV were able to mark out the subgroup
of individuals with low pulmonary vascular resistance. Indeed,
patients with VTIPV ≥ 24 cm (six cases in this series) may be
considered patients with PVR/SVR below 0.1 with a specificity
of 0.93 and odds ratio of 4.47.
The value of the variable VTIPV, in this study, represents
an increase compared to previous publications. The
echocardiographic parameters determined through the
analysis of systolic flow in the right ventricle outflow tract
cannot be used to check the pulmonary hemodynamics in
patients with localized septal defects beyond the pulmonary
valve. This would be the case of patent ductus arteriosus and
aortopulmonary window. Such patients are usually excluded
from the analysis13. The analysis of variable VTIPV would then
be useful in these situations in the absence of anatomic or
functional barriers to pulmonary venous drainage.
Contrary to the findings of Hirschfeld and Ebeid11,13, in
this study it was not possible, based on echocardiographic
data, to identify, with acceptable accuracy, patients with high
pulmonary vascular resistance (e.g., individuals with PVR/SVR
> 0.5). It should be noted, however, that such identification
would be have a limited value in clinical practice, particularly
with regard to the characterization of the need for cardiac
catheterization. These patients (especially pediatric patients)
are generally over the age of one year, without clinical signs of
pulmonary congestion, despite the presence of cardiac septal
defects. The flow through the defect is often bidirectional,
and may be predominantly from right to left, and in some
periods, peripheral oxygen saturation is below 90%. In
these circumstances, whatever is the estimate in relation
to pulmonary hemodynamics by noninvasive methods, the
patient will invariably be referred to catheterization in order
to determine an accurate measurement of pulmonary vascular
resistance and its behavior to vasodilator stimuli.
The main limitations of this study include a relatively
small sample, and the fact that patients were aged within
broad limits, which could bring some questions about the
applicability of findings in pediatric patients and adults.
It should be noted, however, that the influence of age on
prediction models developed has not been shown. Levels
of sensitivity coupled with cut-off values chosen suggest that
if these values are adopted, some patients with favorable
hemodynamics (increased pulmonary blood flow and not
high pulmonary vascular resistance) will still depend on
diagnostic catheterization.
In summary, the findings produced by this study show that
besides clinical data known and widely used in taking decisions
on the operability in patients with cardiac septal defects, some
echocardiographic indicators can be placed. Thus, patients
with Qp/Qs ≥ 2.89, VTIRVOT ≥ 22 cm and VTIPV ≥ 20 cm,
determined through Doppler echocardiography, may be
considered as having a positive pulmonary hemodynamics
and exempt from preoperative invasive assessment.
Acknowledgments
To Mrs. Roseli Polo for the technical assistance in preparing
this manuscript.
Ribeiro et al
Echo/pulmonary hemodynamics
Original Article
Potential Conflict of Interest
No potential conflict of interest relevant to this article was
reported.
Sources of Funding
There were no external funding sources for this study.
Study Association
This article is part of the thesis of doctoral submitted by
Zilma Verçosa de Sá Ribeiro, from FMUSP.
References
1. Rabinovitch M, Keane JF, Norwood WI, Castaneda AR, Reid L. Vascular
structure in lung tissue obtained at biopsy correlated with pulmonary
hemodynamic findings after repair of congenital heart defects. Circulation.
1984; 69 (4): 655-67.
2. Kitabatake A, Inoue M, Asao M, Masuyama T, Tanouchi J, Morita T, et al.
Noninvasive evaluation of pulmonary hypertension by a pulsed Doppler
technique. Circulation. 1983; 68 (2): 302-9.
3. Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. A
simple method for noninvasive estimation of pulmonary vascular resistance.
J Am Coll Cardiol. 2003; 41 (6): 1021-7.
4. Beerbaum P, Körperich H, Barth P, Esdorn H, Gieseke J, Meyer H. Noninvasive
quantification of left-to-right shunt in pediatric patients: phase-contrast cine
magnetic resonance imaging compared with invasive oximetry. Circulation.
2001; 103 (20): 2476-82.
5. Lopes AA, O’Leary PW. Measurement, interpretation and use of
hemodynamic parameters. In: Lopes AA, Rabinovitch M (editors). Statements
on the management of pulmonary hypertension associated with congenital
heart disease. Cardiol Young. 2009; 19 (5): 431-5.
6. Berner M, Beghetti M, Spahr-Schopfer I, Oberhansli I, Friedli B. Inhaled
nitric oxide to test the vasodilator capacity of the pulmonary vascular bed in
children with long-standing pulmonary hypertension and congenital heart
disease. Am J Cardiol. 1996; 77 (7): 532-5.
7. Atz AM, Adatia I, Lock JE, Wessel DL. Combined effects of nitric oxide and
oxygen during acute pulmonary vasodilator testing. J Am Coll Cardiol. 1999;
33 (3): 813-9.
8. Yasuda T, Tauchi N, Baba R, Nishibata K, Hatano T, Nakamura S, et al. Inhalation
of low-dose nitric oxide to evaluate pulmonary vascular reactivity in children
with congenital heart disease. Pediatr Cardiol. 1999; 20 (4): 278-82.
9. Turanlahti MI, Laitinen PO, Pesonen EJ. Preoperative and postoperative
response to inhaled nitric oxide. Scand Cardiovasc J. 2000; 34 (1): 46-52.
10.Balzer DT, Kort HW, Day RW, Corneli HM, Kovalchin JP, Cannon BC, et al.
Inhaled Nitric Oxide as a Preoperative Test (INOP Test I): the INOP Test Study
Group. Circulation. 2002; 106 (12 Suppl. 1): I76-81.
11.Hirschfeld S, Meyer R, Schwartz DC, Kofhagen J, Kaplan S. The
echocardiographic assessment of pulmonary artery pressure and pulmonary
vascular resistance. Circulation. 1975; 52 (4): 642-50.
12.Sanders SP, Yeager S, Williams RG. Measurement of systemic and
pulmonary blood flow and QP/QS ratio using Doppler and two-dimensional
echocardiography. Am J Cardiol. 1983; 51 (6): 952-6.
13.Ebeid MR, Ferrer PL, Robinson B, Weatherby N, Gebland H. Doppler
echocardiographic evaluation of pulmonary vascular resistance in children
with congenital heart disease. J Am Soc Echocardiogr. 1996; 9 (6): 822-31.
14.Rivera IR, Moisés VA, de Paola AA, Carvalho AC. Echocardiographic
assessment of the pulmonary venous flow: an indicator of increased
pulmonary flow in congenital cardiac malformations. Arq Bras Cardiol. 2002;
78 (6): 537-44.
15.Selimovic N, Rundqvist B, Bergh CH, Andersson B, Petersson S, Johansson
L, et al. Assessment of pulmonary vascular resistance by Doppler
echocardiography in patients with pulmonary arterial hypertension. J Heart
Lung Transplant. 2007; 26 (9): 927-34.
16.Henry WL, DeMaria A, Gramiak R, King DL, Kisslo JA, Popp RL, et al. Report
of the American Society of Echocardiography Committee on Nomenclature
and Standards in Two-dimensional Echocardiography. Circulation. 1980; 62
(2): 212-7.
17.Tei C. New non-invasive index for combined systolic and diastolic ventricular
function. J Cardiol. 1995; 26 (2): 135-6.
18.Eidem BW, O’Leary PW, Tei C, Seward JB. Usefulness of the myocardial
performance index for assessing right ventricular function in congenital heart
disease. Am J Cardiol. 2000; 86 (6): 654-8.
19.Evangelista A, García del Castillo H, González-Alujas T, Brotons C, GarcíaDorado D, Soler-Soler J. Normal values of valvular flow velocities determined
by Doppler echocardiography: relations with heart rate and age. Rev Esp
Cardiol. 1996; 49 (3): 189-95.
20.Yeo TC, Dujardin KS, Tei C, Mahoney DW, Mcgoon MD, Seward JB. Value of
a Doppler - derived index combining systolic and diastolic time intervals in
predicting outcome in primary pulmonary hypertension. Am J Cardiol. 1998;
81 (9): 1157-61.
21.Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure
by Doppler ultrasound in patients with tricuspid regurgitation. Circulation.
1984; 70 (4): 657-62.
22.Chan KL, Currie PJ, Seward JB, Hagler DJ, Mair DD, Tajik AJ. Comparison of
three Doppler ultrasound methods in the prediction of pulmonary artery
pressure. J Am Coll Cardiol. 1987; 9 (3): 549-54.
23.Snider AR, Serwer GA, Ritter SB. Methods for obtaining quantitative
information from the echocardiographic examination. In: Snider AR, Gersony
RA, Serwer GA, Ritter SB. (eds). Echocardiography in pediatric heart disease.
2nd ed. Missouri: Mosby 1997. p. 133-234.
24.Vargas Barron J, Sahn DJ, Valdez-Cruz LM, Lima CO, Goldberg SJ, Grenadier
E, et al. Clinical utility of two-dimensional Doppler echocardiographic
techniques for estimating pulmonary to systemic blood flow ratios in children
with left ti right shunting atrial septal defect, ventricular septal defect or patent
ductus arteriosus. J Am Coll Cardiol. 1984; 3 (1): 169-78.
25.Sabry AF, Reller MD, Silberbach GM, Rice MJ, Sahn DJ. Comparison of four
Doppler echocardiographic methods for calculating pulmonary-to-systemic
shunt flow ratios in patients with ventricular septal defect. Am J Cardiol. 1995;
75 (8): 611-4.
26.Cloez JL, Schmidt KG, Birk E, Silverman NH. Determination of pulmonary
to systemic blood flow ratio in children by a simplified Doppler
echocardiographic method. J Am Coll Cardiol. 1988; 11 (4): 825-30.
27.Scapellato F, Temporelli PL, Eleuteri E, Corrà U, Imparato A, Giannuzzi P.
Accurate noninvasive estimation of pulmonary vascular resistance by Doppler
echocardiography in patients with chronic failure heart failure. J Am Coll
Cardiol. 2001; 37 (7): 1813-9.
28.Vlahos AP, Feinstein JA, Schiller NB, Silverman NH. Extension of Dopplerderived echocardiographic measures of pulmonary vascular resistance to
patients with moderate or severe pulmonary vascular disease. J Am Soc
Echocardiogr. 2008; 21 (6): 711-4.
Arq Bras Cardiol 2010;94(5):557-564
564