LEFT ATRIAL SHAPE AND FUNCTION AFTER ENDOVASCULAR DEVICE AND
SURGICAL CLOSURE OF ASDS IN CHILDREN
Sokolov Alexandr Anatolievich MD1
Varvarenko Viktor Ivanovich MD1
Krivoshchekov Evgeny Vladimirovich MD1
Smorgon Andrey Vladimirovich MD1
Cardiology Research Institute, Tomsk National Research Medical Center,
Russian Academy of Sciences
ADDRESS FOR CORRESPONDENCE:
634012, Russian, Tomsk, Kievskay st. 111-А, Cardiology Research
Institute, Tomsk National Research Medical Center, Russian Academy of
Sciences
Tel: +7 (3822) 55-83-67, +7 (3822) 55-36-10
CORRESPONDING AUTHOR:
Smorgon Andrey Vladimirovich MD, e-mail:sav.ssmu@gmail.com
634017, Russian, Tomsk, Andrey Kraychkov st.17-227
Tel: +79069481206
AUTHOR CONTRIBUTIONS
All authors helped craft and critically revise themanuscript. All
authors approved the final version of the manuscriptand can be held
accountable for the integrity of the work.
CONFLICT OF INTERESTS
All authors declare that there are no conflict of interests.
FUNDING STATEMENT:
There is no funding for this study.
DATA AVAILABILITY STATEMENT
The data that support the findings of this study are available on
rea-sonable request from the corresponding author. The data are not
pub-licly available due to institutional data protection and ethical
restrictions
Abstract
Retrospective analysis of echocardiograms was performed in 756 children
who received endovascular device or surgical ASD closure from 2006 to
2016 in the Cardiac Center in Tomsk Russia. 564 patients had an
endovascular closure and 192 had surgical correction. Follow-up duration
was from 1 day to 10 years, mean 3.6 yrs for the device group and 4.2
yrs for the surgery group. The control group consisted of 3393
age-matched healthy patients.
In patients with endovascular closure of an ASD, 35% had a change in
the shape of the left atrium in early follow-up. Changes in the shape of
the left atrium at early follow-up were more often observed in the
device group and in children of a younger age. The left atrial changes
were a decrease in sphericity and an increase in ellipsoidy. Changes in
the shape of the left atrium persisted in 22% after transcatheter
correction in the long-term. The change in shape of the left atrium
after the placement of ASD devices was accompanied by activation of the
mechanical function of the atrium and an increase in the filling
pressure of the left ventricle. These changes were not accompanied by
any disturbance in the contractility and volume of the heart chambers.
In the group with surgical correction of ASD, the contractility and
volume of the heart chambers did not significantly differ from those in
the device closure group.
Introduction
Atrial septal defects (ASDs) account for 10-15% of all patients with
congenital heart defects (CHD). Endovascular device closure is currently
accepted as the treatment of choice in most patients with secundum ASD.
Its efficacy and complication rates are comparable to surgery. However,
in some patients who have contraindications for using an endovascular
approach, surgical treatment is still needed. [1].
ASD occluder devices and surgically placed patches may increase the
rigidity of the septum. These interventions, while eliminating the
interatrial shunt, may limit septal mobility, and possibly disrupt the
mechanical function of the left atrium (LA). The purpose of this study
was to study the effect of surgical and endovascular device closure of
ASDs on the size, shape and function of the LA and left ventricle (LV)
in children.
Subjects
We retrospectively studied consecutive echocardiograms from children who
received endovascular device or surgical ASD closure between 2006 and
2016 at the Cardiac Center in Tomsk, Russia. In total, 756 patients with
ASD were evaluated. Seventy-five percent (564 patients) had endovascular
device closure. Various devices were utilized (Nit-Occlud, Amplatzer,
Occlutech), the LA side of the devices ranged from 14 to 38 mm (25.6 +
4.1). Twenty-five percent (192 patients) had surgical ASD closure with a
pericardial patch. Follow-up duration was1 day to 10 years (yrs) (mean
3.6 yrs for the device group and 4.2 yrs for the surgery group). The
control group consisted of 3393 healthy age-matched children. Patient
demographics and follow-up intervals are demonstrated in Table 1. The
surgical group included patients with contraindications for endovascular
correction, in most cases because of a deficient rim.
Methods
Institutional review board approval was obtained for analysis of the
echocardiography database, with no requirement to obtain informed
consent. International Review Board approval was not sought. The trial
was not registered with Clinicaltrials.gov.
Echocardiographic images were obtained using commercially available
ultrasound equipment (iE33, Philips Ultrasound). Standard echo measures
of chamber sizes and volumes were evaluated and indexed to body surface
area. These measurements were compared to previously published normative
data. Doppler echocardiographic evaluation of mitral inflow velocities
and A wave duration were used in the assessment of left ventricular
diastolic function. E/A ratio transmitral flow and mean septal and
lateral mitral annular tissue Doppler diastolic velocities and peak
duration were evaluated. To reduce the effect of heart rate, diastole
duration as a percentage of the duration of the R-R interval was used.
Diastolic time expressed as percent of cardiac cycle (D%) calculated by
the formula: D%=((R-R)-ET) / RR x 100, where D%- diastole duration,
ET- ejection time. Diastolic timing intervals were measured from
transmitral flow and named DF (diastole flow). Mitral annular tissue
Doppler was named MD (mechanical diastole).
Left atrial shape index (LASI) was calculated as the ratio of the
anteroposterior and transverse size to vertical: LASI = (W1 + W2) / 2* H
* 100. Where W1 = anteroposterior size measured in parasternal short
axis, W2 = width measured in apical 4-chamber projection, and H = height
of the LA measured from the posterior LA wall to the mitral annulus in
the apical 4-chamber projection. (Fig.1). an increase in the index close
to 100 was regarded as an increase in sphericity, a decrease in
ellipsoidity. Left atrial force (LAEF) was determined by the Manning
method [5, 6, 7].
LAVi-left atrial volume index and RAVi-right atrial volume index were
calculated as volume/BSA. Atrial volumes was calculated by standard
methods using 4 and 2 chamber projections. An atrial index (Ai) was
defined as RAV\LAV, using unindexed values. [8]
Since various size occluders were used, the ratio of the smallest size
of the left atrium (w1) and the diameter of the LA side disc was
calculated. LASI in the control group was evaluated by a frequency
table. Only 5% of controls had an LASI < 65 and we defined
that as the “cut of point” value between normal and abnormal (Table 2,
Fig. 2).
Continuous variables were presented as mean +/- standard deviation.
Categorical data were represented by frequencies and percentages.
Clinical and procedural data were compared with paired and unpaired
t-tests. Categorical data used applied tests that were two-sided. P
< 0.05 was considered statistically significant.
Results
Patients in the surgical group had significantly larger left to right
shunt (Qp/Qs) than patients in the device group (2,97 + 0.47 versus 2.10
+ 0.64, p = 0.01). The RAVi in the surgical group was larger (Table 3).
During follow-up, the device group LASI was significantly decreased, and
LASI before device or surgical closure were similar but both were
significantly different from the control group. Patients with ASD had
LASI < 65 in 10,6% of cases (Fig.3). After closing the ASD,
the percentage of patients who had an abnormal LASI (<65)
increased in both groups but was more pronounced in the device group
(Fig.3) . During follow-up LASI was decreased from the first day to
several years after device implantation. But, there was no significant
difference between the surgery group and control group at late
follow-up. The device group had a decreased LASI compared to controls
(Fig.2). There was no significant change in the surgical group (Fig.2).
The number of patients with an abnormal shape of the LA in the surgical
group decreased during the observation period. In the device group, LASI
was stable from 6 months post-procedure throughout the follow-up period.
(Fig.3). There was no difference between surgery and device groups in
respect to chamber volumes, contractility, and right ventricular
systolic pressure at all data collection points.
We then evaluated the possible significance of changing LASI to chamber
volumes and function. All device patients were divided into two groups.
A reshaped group defined as: (RS) – LASI ≤ 65 any point after
implantation, and a saved shape group that had an LASI > 65
(Table 5).
Chamber Volumes
At 1-5 days after ASD closure, LV volume increased significantly and
right-sided chamber sizes decreased in both surgical and device groups.
After ASD closure the following data were obtained: LVEDV and LVEF were
unchanged in both groups, LA volume decreased significantly in the
device group (Table 2) and RVSP and RA volumes decreased. The LAEF in
the device group with “reshaped” LA remained maximal during short-term
(1-5 days, mean 3,4+1,3) and long-term (2 -10 mean 3,6+3,5years) (Fig 4)
follow-up.
Other echo parameters in these patients were not different between the
surgery group and the patients who had “saved shape” group. Only
mechanical diastole in the “reshape” subgroup was longer compared to
controls (Table 4)
In the early period (1-5 days) after ASD closure in patients in both the
surgical and device groups, the volume of the RA decreased significantly
but the Ai was unchanged (Table 3). At the same time, the LVEDVi in the
device group increased, while in the surgical group it decreased in
comparison with the preoperative period. The RVSP in both groups
decreased significantly (p <0.05) while the contractility of
the LV remained unchanged. The patients in the device group with a
increased LASI at the time of implantation of the device were
significantly younger than patients with a preserved LASI (2,06+0,47 and
2,98+0,64 yrs, p=0.02).
Long-term follow-up
The surgical and device closure groups were compared in long-term
follow-up from 2.1 to 10 years. Patient age in the groups was the same
9.6 + 6.9 years (surgery) and 9.0 + 4.5 years (device). Mean follow-up
in the surgery group was 4.3 years and 3.6 years in device the group.
The LASI was lower in the device group (74,0 +0,3) versus the surgery
group (70,0 + 2). A LASI < 65 (significantly different from
the norm) in the device group was found in 22,5%, of the device group,
8.0% of the surgical group and 16.6% of the overall study cohort. The
indexed LV diastolic volume in the groups did not differ (surgical: 49,9
+/- 10,8 ml/m^2; device: 49,3 +/- 9,6 ml/m^2, p = 0.61).
Similarly, ejection fraction was the same in the surgical and device
groups (71% +/- 5%) (Table 5).
The LACF (left atrial ejection force) was significantly lower in the
surgery group than in the device group (Figure 5). But, the contraction
force of the LA in the device group did not differ from the control
group.
It should be noted that in patients who lost form of the LA after ASD
closure (34.4% of total), the strength of the contraction of the LA was
higher than the group average and amounted to 9.51 + 4.7 kdynes
/cm/m^2, while in those with impaired LA form after surgery, the
strength of the contraction of the LA was not significantly different
from the entire surgery group (6.5 + 4.4 kdynes/cm/m^2) or the
control group (6.6 + 4.8 kdynes/cm/m^2).
Discussion
In this study, 35% of children with device closure of an ASD had a
change in the shape of the LA - a decrease in sphericity and an increase
in ellipsoidity. The first mechanisms of LA remodeling after ASD
closure, specifically changes in shape and force of contraction, may
turn out to be unfavorable factors for the patient in the future.
Similar changes were found in adult patients with interatrial adiposity.
These remodeling processes were associated with increased LA global
kinetic energy and ejection force at the hemodynamic level, which may
serve to compensate for functional LA deterioration in asymptomatic
patients [ 10]. It is hoped that these changes are not significant
for the lives of our young patients. In the long-term after surgical and
endovascular treatment of ASDs, the main hemodynamic parameters and
indexed chamber volumes were not abnormal (Table 5).
It is interesting that loss of LA shape after ASD device closure was
found in the youngest children. There are several problems encountered
during device closure in small children. The inherent design of several
commercially available devices, with excessive disc width, may increase
the risk for erosion and cause the device to encroach on adjacent
cardiac structures [11]. But the stiffness of these devices may have
a detrimental effect on the LA shape. This topic has not been well
researched. It is possible that device size or stiffness may restriction
growth of the LA in the antero-posterior direction. It is controversial
if interatrial septum length is a limiting factor for sizing the device.
[12.]. Our data suggest that device oversizing may have a negative
long-term effect on LA shape.
Patients in the device group with an increased LASI were significantly
younger than patients with a preserved LASI (2,06+0,47 versus 2,98+0,64
yrs, respectively, p=0.02). The calculated ratio of the minimum size of
the interatrial septum and the LA disc of the device had a significant
negative correlation at 6 and 12 months of follow-up (r = -0.62 and
-0.55, p = 0.01). This meant that the larger the device with respect to
the size of the septum, the greater the change in the shape of the LA.
There is an opinion that ASD device occlusion should performed in
infants and young children only if the disk diameter is smaller than the
diameter of the atrial septum. [13.] In our study, we used large
oversized devices and in small children this may change LA shape.
The increased left ventricular filling pressure after ASD closure should
not be regarded as a negative factor. Most likely this was due to
increased volume entering the left ventricle after ASD closure. It is
not known if the initial mechanisms of LA remodeling, changes in shape
and force of contraction, will turn out to be unfavorable factors in the
future. Similar changes were found in adult patients with interatrial
adiposity. These remodeling processes were associated with increased LA
global kinetic energy and ejection force at the hemodynamic level, which
may serve to compensate for those functional deteriorations of LA in
asymptomatic patients [10].
At long-term follow-up, left ventricular filling pressure was normal in
the device group. Recent studies have shown that LA dysfunction after
ASD device closure is more common in children. In adult patients LA
contractility improves after ASD closure [14]. In addition, the size
of the ASD device was negatively correlated with contractility of the
LA. These results imply that ASD occlusion devices adversely affect LA
function and may be important in choosing other treatment strategies.
Depression of LA function was detected by speckle tracking in adult
patients immediately after device implantation, but this resolved by one
month after intervention [15,16]. It is unknown if the changes in LA
shape that we observed after ASD device closure impact the lives of
young patients.
Conclusions
Endovascular device closure of ASDs was accompanied by a change in LA
shape - a decrease in sphericity and an increase in ellipsoidity. These
changes were more frequent in younger children. Changes in LA shape
persisted in 22% of patients after ASD device closure. The LA shape
after ASD closure device placement was accompanied by activation of the
mechanical function of the atrium and an increase in the filling
pressure of the left ventricle. These changes were not accompanied by
any disturbance in the contractility and volume of the heart chambers.
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