|
 
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| ORIGINAL ARTICLE |
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| Year : 2017 | Volume
: 2
| Issue : 1 | Page : 40-48 |
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Effect of transcatheter closure of secundum atrial septal defect on cardiac electric remodeling
Shaimaa Ahmed Mostafa1, Abdrabu Abdelhakim2, Tarek Helmy Aboelazm1, Osama Sanad Arafa1, Ahmed M Elemam2
1 Department of Cardiovascular Disease, Faculty of Medicine, Benha University, Benha 13511, Egypt
2 Department of Cardiology, National Heart Institute, Cairo, Egypt
| Date of Web Publication | 19-Jun-2017 |
Correspondence Address:
Shaimaa Ahmed Mostafa
Department of Cardiovascular Disease, Faculty of Medicine, Benha University, Benha 13511
Egypt
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2352-4197.208453
Purpose: This study aimed to investigate the intermediate- and short-term effects of transcatheter secundum atrial septal defect (ASD) closure on cardiac electric remodeling in children and adults. Methods: Fifty patients with secundum ASD referred for possible transcatheter device closure were subjected to history taking, proper physical examination, electrocardiographic assessment, and transthoracic echocardiographic examination and were evaluated before the ASD closure, 1 day, 3 months, and 6 months after closure. Results: During the 6-month follow-up, electrocardiographic parameters of remodeling were improved. P dispersion decreased from 49.73 ± 9.01 ms to 30.53 ± 5.08 ms (P = 0.004), QT dispersion decreased from 67.60 ± 5.31 to 51.13 ± 5.73 ms (P = 0.003), QRS duration decreased from 134.40 ± 4.97 ms to 116.20 ± 3.47 ms (P = 0.002), and PR interval decreased from 188.87 ± 6.06 ms to 168.00 ± 6.16 ms (P = 0.002). Electric remodeling was associated with remodeling of the cardiac chambers. At the end of follow-up, the right ventricular (RV) end-diastolic dimension decreased from 25.67 ± 5.50 mm to 17.80 ± 2.70 mm (P = 0.001) the left ventricular end-diastolic dimension increased from 33.17 ± 6.44 mm to 37.53 ± 5.15 mm (P = 0.002), mean pulmonary artery pressure decreased from 16.97 ± 3.37 mmHg to 9.22 ± 1.37 mmHg (P = 0.000), and RV systolic pressure decreased from 30.77 ± 4.69 mmHg to 18.8 ± 2.11 mmHg. After 6 months, 93.3% of the patients had normal RV size. Conclusion: Transcatheter ASD device closure leads to a significant improvement in the right-sided chambers' dimension and function and can reverse electrical changes in atrial and ventricular myocardium in children and adults after correcting hemodynamic status in short- and intermediate-term follow-up. Keywords: Atrial septal defect, chambers' remodeling, electric remodeling
How to cite this article:
Mostafa SA, Abdelhakim A, Aboelazm TH, Arafa OS, Elemam AM. Effect of transcatheter closure of secundum atrial septal defect on cardiac electric remodeling. Int J Heart Rhythm 2017;2:40-8 |
How to cite this URL:
Mostafa SA, Abdelhakim A, Aboelazm TH, Arafa OS, Elemam AM. Effect of transcatheter closure of secundum atrial septal defect on cardiac electric remodeling. Int J Heart Rhythm [serial online] 2017 [cited 2023 Jun 3];2:40-8. Available from: https://www.ijhronline.org/text.asp?2017/2/1/40/208453 |
| Introduction | |  |
Atrial septal defect (ASD) is the second most common congenital lesion in adults (behind bicuspid aortic valves). They represent approximately 7% of all cardiac anomalies.[1] These defects are often undetected until adulthood due to the lack of prominent clinical symptoms initially. If untreated, an ASD can eventually result in the right ventricular (RV) heart failure, pulmonary hypertension, atrial arrhythmias or paradoxical embolization, and ischemic cerebral events.
Often, atrial tachyarrhythmias may coexist or precede symptoms. The incidence of arrhythmias increases with age as well as an increase in pulmonary pressures.[2] However, it is still unclear whether atrial arrhythmias improve with the closure of the defect, although some trials have shown that atrial flutter may improve with ASD closure as opposed to atrial fibrillation, which usually remains unchanged following closure.[2] As a result, the development of an atrial tachyarrhythmia alone does not constitute an immediate need for ASD closure.
Recently, the definition of “significant ASD” has been changed. Nowadays, significant ASD, according to the ESC Guidelines, is defined as shunt with signs of RV volume overload despite the QP: QS ratio.[3] Patients with significant shunt (signs of right ventricle volume overload) and pulmonary vascular resistance <5 wood units should undergo ASD closure regardless of symptoms. However, the closure of the ASD in patients with insignificant shunt with QP:QS ratio <1.5 and lack of pulmonary overload and hypertension is controversial.
Historically, ASDs have been closed surgically. More recently, these procedures have been accomplished with minimally invasive surgical techniques as well as a percutaneous transcatheter technique. The latter technique has been increasing in popularity due to the avoidance of cardiac surgery and the associated risks.
ASD repair with the transcatheter technique has been shown to have a high closure rate.[4] Unfortunately, anatomy of the defect often limits their use. Currently, transcatheter closure is limited to secundum-type defects which are <36 mm in size.
Patients with severe fixed pulmonary hypertension may actually do worsen with ASD closure due to the need for partial right-to-left shunting of blood to decrease right-sided pressures.[5] Early diagnosis and follow-up of ASDs offers the best opportunity to avoid late complications from pulmonary hypertension, heart failure, arrhythmia, and stroke.
This study aimed to investigate the intermediate- and short-term effects of transcatheter secundum ASD (at the site of fossa ovalis in the middle of the interatrial septum, astium premium at the lower part of the septum was excluded) closure on cardiac remodeling in children and adults.
| Methods | | |
Patients
The study included fifty patients who were referred to the Department of Cardiology, National Heart Institute (Cairo, Egypt), for the possibility of elective percutaneous closure of their secundum ASD from April 2014 to April 2015. All patients signed informed consent, and the study was approved by the local Ethical Committee.
The inclusion criteria include: (1) Secundum ASD with a left-to-right shunt, (2) ASD diameter ≤36 mm, (3) presence of 4 mm or more septal rims, (4) and increased RV volume load (QP/QS ratio >1.5 and/or RV dilation).
The exclusion criteria include: (1) Sinous venosus and primum ASD types, (2) ASD >36 mm or <4 mm, (3) absence of an indication or contraindication of ASD closure as QP/QS <1.5 mm or pulmonary vascular resistance >8 woods, (4) nonsinus rhythm at the time of electrocardiogram (ECG) recording, (5) and use of antiarrhythmic drugs.
Diagnosis and treatment process
Patients enrolled in the study underwent the following processes.
History taking and clinical examination
Thorough history taking and physical examination with emphasis on the New York Heart Association class, signs of pulmonary hypertension (accentuated second heart sound), and signs of RV volume overload.
Twelve-lead surface electrocardiogram
A standard 12-lead ECG was recorded at a rate of 50 mm/s (to show all ECG criteria and small P waves) and a calibration of 1 mV/cm for all the patients as a baseline before the procedure and during the follow-up period. ThePwave, PR interval, QRS duration, and QT dispersion times were measured.
Transthoracic echocardiography
All patients underwent full echocardiographic study using general electric ViVid 5 echocardiography machine using 3.5–5.0 MH-phased array transducers for children and 2.5 MH-phased array transducers for adults. In agitated infants and children, sedation with chloral hydrate (50 mg/kg) 15 min prior to the study was done.
Sequential analysis
A sequential analysis was performed to determine the situs, atrioventricular (AV) and ventriculo-arterial connections, great vessel relation and abnormalities, state of cardiac valves, and venous connections.
The interatrial septum
The atrial septum was visualized from multiple aspects to assess the size, shape, number, and location of the defect as well as its relationship to adjacent structures. Particular care was taken to assess the relationship of the defect to the superior and inferior vena cava, the pulmonary veins, and the coronary sinus [Figure 1].
Left atrial dimensions and right atrial dimensions
Left and right atria were measured in two dimensions in both transverse and longitudinal axes [Figure 2]. | Figure 2: Apical 4-chamber view with measurement of the left atrial dimension in both horizontal and vertical dimensions.
Click here to view |
Tricuspid valve and right ventricular systolic pressure
- Apical 4-chamber view: The tricuspid valve was examined regarding mobility of the leaflets and presence of tricuspid regurgitation (TR)
- If TR was present, a continuous wave Doppler was applied to the TR jet after being properly aligned to determine the TR velocity and hence, the RV systolic pressure (RVSP) was calculated according to the modified Bernoulli equation which states RVSP = (TR velocity) 2 + P (RA), where TR velocity is the maximal velocity of the TR jet (in meters per se cond) and PRA is an estimate of right atrial pressure [6]
- Parasternal long-axis view (RV inflow): the tricuspid valve was re-assessed using this view and the RVSP was calculated again and the maximum value obtained from two views was taken [6]
- Tricuspid annular plane systolic excursion (TAPSE): By placing the M-mode cursor through the lateral annulus of the tricuspid valve, the maximum excursion was measured and recorded. Normally, value <16 mm indicates RV systolic dysfunction
- In parasternal long-axis view (RV outflow): the pulmonary valve was examined, and if pulmonary regurgitation (PR) was present, a continuous wave Doppler was applied to the PR jet after being properly aligned to determine the PR peak velocity and hence, the mean pulmonary artery pressure (PAP) was calculated according to the modified Bernoulli equation as follows,
MPAP = 4 × (peak PR velocity)2 + RAP
- Parasternal short-axis view (at the level of the aortic valve): the pulmonary valve was re-examined and the PR was re-measured, if present, for the mean PAP to be calculated according to the modified Bernoulli equation, and the maximum value obtained from the two views was taken.[7]
Right ventricular dimensions and size
The RV end-diastolic dimension (RVEDD) was evaluated using the following method. In the parasternal short-axis view, M-mode was applied and the RVEDD was measured and categorized accordingly into normal, mildly, moderately, and severely dilated right ventricle (reference values; RV diameter: 1.8–3.4 cm by M-mode).[6]
Left ventricular dimensions and systolic function
Parasternal short-axis view M-mode was applied, and the left ventricular (LV) dimensions were measured including LV end-diastolic dimension (LVEDD normal values: 3.9–5.3 in women and 4.2–5.9 in men), and ejection fraction was obtained by a cut through the tip of papillary muscles.[6]
Transesophageal echocardiography
Most of the patients had full transesophageal echocardiographic examination under general anesthesia in the cath lab before starting the procedure and during the procedure for assessment of the ASD and rims.
Atrial septal defect transcatheter device closure
Informed consent was obtained from each patient or patient's parents before the procedure. The procedure was performed under both echocardiographic and fluoroscopic guidance.
Transesophageal echocardiography (TEE) or transthoracic echocardiography (TTE) was used to document complete occlusion of the defect, both prior to and following the release of the device from the delivery cable. If device position was not certain or questionable after all these maneuvers, the device was recaptured entirely or partly and repositioned following similar steps. Once device position was verified, the device was released by counterclockwise rotation of the delivery cable using a pin vice. There was often a notable change in the angle of the device as it was released from the slight tension of the delivery cable and it self-centers within the ASD and aligns with the interatrial septum.
Postcatheterization care
Patients received a dose of an appropriate antibiotic during the catheterization procedure and two further doses at 8-h intervals postcatheterization. Patients were also asked to take endocarditis prophylaxis, when necessary, for 6 months after the procedure, as well as aspirin 5 mg/kg daily in children for 6 months, and adults were kept on both asprin 75–150 mg and clopidogrel for 6 months.
Follow-up
All patients were evaluated by ECG and echocardiography at 24 h, 3 months, and 6 months after the procedure.
The success criteria were as follows: (1) No residual shunts, (2) no encroachment upon nearby structure, (3) decrease in PAP, and (4) improvement in cardiac remodeling.
Statistical analysis
All data were collected, tabulated, and statistically analyzed using a PC. The data were entered into the Statistical Package for Social Science Program version 20 (Germany). The quantitative data were presented as mean and SD for the parametric data and as median and interquartile range for the nonparametric data while the qualitative data were presented as a number and percentage. Chi-square test was used to compare between two groups with qualitative data whereas paired sample t-test was used to compare between two paired groups with quantitative data. The confidence interval was set to be at 95%, and P< 0.05 was considered statistically significant.[8]
| Results | | |
Patient characteristics
This study included fifty patients undergoing ASD transcatheter device closure in National Heart Institute Hospital from April 2014 to April 2015, 27 men (54%) and 23 women (46%) with age ranging from 2.5 to 49 years (mean: 6 years). The weight of patients ranged from 10 to 125 kg with a mean of 33 ± 27 kg. The body surface area ranged from 0.6 to 2.3 with a mean of 1.02 ± 0.48.
The ASD diameter using TTE ranged from 7 to 35 mm (mean 16 ± 7 mm), and using TEE, it ranged from 10 to 36 mm (mean: 19 ± 7 mm).
The aortic rim ranged from 2 to 10 mm (mean: 4.95 ± 2.06 mm), the mitral rim ranged from 4 to 15 mm (mean: 9.50 ± 2.71 mm), the SVC rim ranged from 5 to 15 mm (mean: 10.60 ± 2.65 mm), the inferior vena cava rim ranged from 6 to 19 mm (mean: 10.43 ± 3.09 mm), and the pulmonary vein rim ranged from 5 to 14 mm (mean: 10.3 ± 2.58 mm).
Twenty patients (20/50, 40%) underwent ASD closure under TTE guidance while thirty patients (30/50, 60%) underwent ASD closure under TEE guidance. TEE guidance decreased the fluro time.
Thirty-seven patients underwent closure using Amplatzer device St. Jude Medical (37/50, 74%) and 13 patients underwent closure using Occlutech device (Germany) (13/50, 26%). Amplatzer device size ranged from 12 to 36 mm while Occlutech device size used ranged from 12 to 34 mm. The study showed a highly statistically significant linear correlation between ASD size by TTE (r = 0.937) and TEE (r = 0.966) (P = 0.000).
All the patients studied had successful ASD device closure after 24 h but only two patients had trivial residual shunting (6.6%) which disappeared after 3 months.
Echocardiographic remodeling after atrial septal defect closure
All echocardiographic parameters of remodeling were improved after 24 h including those of the right-sided chambers' dimension and function, left-sided chambers' dimension and function, and PAP, and also after 3 months of follow-up and at 6-month follow-up.
There was a highly significant improvement when comparing the echocardiographic parameters measured before versus those at 24 h, 3 months, and 6 months after device closure. The LVEF, LVEDD, left atrial dimension (LAD) 1, LAD2, and TAPSE showed a significant increase while the RVEDD, right atrial dimension (RAD) 1, RAD2, RVSP, and mean PAP showed a significant decrease [Table 1] and [Figure 3]. | Table 1: Echocardiographic results before, or 24 hours, 3 month and 6 month after device closure (n=50, mean±SD (range))
Click here to view |
 | Figure 3: Echocardiographic results before (1), and 24 h (2), 3 months (3), 6 months (4) after atrial septal defect device closure.
Click here to view |
Before closure, eight patients had normal RV (16.%), thirty patients had mildly dilated RV (60%), and 12 patients had moderately dilated RV (24%); 24 h after closure, 31 patients had normal RV (62%), 13 had mildly dilated RV (26%), and six patients had moderately dilated RV (12%). Three months after closure, 45 patients had normal RV (90%) and five had mildly dilated RV (10%), and there were no patients having moderately dilated RV (P = 0.105). At 6 months, 49 patients had normal RV (98%) and one had mildly dilated RV (2%), and there were no patients having moderately dilated right ventricle [Table 2]. | Table 2: Comparison the quantitative RV measurement of 24 hours, 3 months, and 6 months after closure with before
Click here to view |
Electrocardiographic remodeling after atrial septal defect closure
All ECG parameters representing the electrical remodeling showed statistically significant improvement after 24 h of ASD closure except for QT minimum and P minimum; after 3 months, all parameters showed statistically significant improvement compared to before ASD closure and 24 h after closure except for QT minimum; and at 6 months of follow-up, all parameters showed statistically significant improvement [Table 3] and [Figure 4]. | Table 3: ECG changes at 24 hour, 3 months, and 6 months after ASD closure (n=50, mean±SD (range))
Click here to view |
 | Figure 4: Electrocardiogram changes at before (1), and 24 h (2), 3 months (3), 6 months, (4) and after atrial septal defect closure.
Click here to view |
| Discussion | | |
ASDs account for 5%–10% of all congenital heart defects. These defects should be closed when diagnosed during childhood or adulthood because they lead to right atrial and ventricular volume load, arrhythmias, and paradoxical embolism.[9]
Transcatheter closure of ASD has become an important alternative to surgical repair in the management of patients with secundum-type ASD.[10] As a result of ASD closure, the right heart is protected from volume load, leading to reduction in both PAP and right heart cavity dimensions. Thus, significant symptomatic improvement with decrease in arrhythmic events was observed in these patients.[11]
The current study evaluated the effect of transcatheter closure of secundum ASD in adults and children on the electric and echocardiographic remodeling in intermediate- and short-term follow-up for 6 months.
This study included fifty patients who underwent transcatheter ASD device closure (27 men and 23 women) in National Heart Institute from April 2014 to April 2015, with age range from 2 to 65 years and median of 6 years. All patients had successful device closure (100%) with two patients having a residual trivial shunt after 24 h (6.6%) that disappeared after 3 months of device closure (P = 0.313).
In the current study, the ASD diameter by TTE ranged from 7 to 35 mm (mean [16.13 ± 6.51] mm) and by TEE from 10 to 36 mm (mean [18.67 ± 6.63] mm) whereas the ASD size ranged from 8 to 33 mm (mean [18.78 ± 6.38] mm). Thirty-seven patients underwent closure using Amplatzer device (74%) and 13 patients underwent closure using Occlutech device (26%), and Amplatzer device size ranged from 12 to 36 mm whereas Occlutech device size ranged from 12 to 34 mm. The study showed a highly statistically significant linear correlation between ASD size by TTE (r = 0.937) and TEE (r = 0.966) (P = 0.000).
Comparing the ECG parameters measured before closure and those after 24 h, 3 months, and 6 months of closure in the present study showed a highly significant reduction in the values ofP maximum, Pdispersion, QT maximum, QT dispersion, QRS duration, and the PR interval while significant reduction in theP minimum appeared at 3 months but QT minimum did not show significant change during follow-up.
As a noninvasive marker, P-wave dispersion is especially useful in predicting atrial arrhythmias.[23] Arrhythmias, particularly atrial fibrillation and flutter, are significant causes of morbidity among patients with ASD.
A few studies evaluating ECG variables among patients with secundum-type ASD have demonstrated an increase in P-wave dispersion.[24] After comparing 62 patients with secundum-type ASD and 47 healthy individuals, it was reported thatP maximum, P minimum, andPdispersion times were prolonged for patients with secundum-type ASD due to mechanical and electrical changes in the atrial myocardium.
The reasons for the increase in P-wave duration in patients with ASD may be increased atrial stretch, atrial dilation, or atrial conduction disturbance; a reduction inPdispersion after surgical ASD closure was also demonstrated.
Kaya et al.[12] were the first to demonstrate statistically significant reductions inP maximum andPdispersion after transcatheter closure of ASD. Transcatheter ASD closure can reverse electrical and mechanical changes in the atrial myocardium and result in a reduction inP maximum andPdispersion.
It is known that QT dispersion increases the risk of cardiac events and arrhythmia. In previous studies, QT dispersion increased in various cardiac diseases such as arrhythmia, myocardial infarction, heart failure, and cardiomyopathy.[25]
However, to date, the relationship of QT dispersion and arrhythmias is not clear. An early decrease in QRS duration after surgical ASD closure [25] and a significant decrease in QT dispersion after transcatheter ASD closure were demonstrated.[26] These mechano-electrical changes reflect better intra-atrial and intraventricular conduction properties after volume unloading of both right heart chambers and can potentially decrease the substrate for late atrial arrhythmias.
We showed highly statistically significant reduction in QT maximum and QT dispersion values. However, there was no significant reduction in the QT minimum value in the 3-month follow-up that maybe related to changes in the intraventricular conduction properties, but at the 6-month follow-up period, there was a significant reduction in the QT minimum to a mean of 547.13 ± 12.20 (P = 0.004).
Only a few reports in the literature relate to the prevalence of cardiac arrhythmias after ASD closure, and these reports are somewhat conflicting.[24] Reductions in the right heart volume overload and improvements in the right atrium and ventricular diameters after percutaneous ASD closure decrease the prevalence of cardiac arrhythmias.[27]
However, some studies demonstrated the increased prevalence of atrial arrhythmias due to unknown causes after surgical ASD closure,[24] suggesting that older age and mean PAP are risk factors for persistent atrial arrhythmias and the development of new atrial arrhythmias after surgical ASD closure.
In another study comparing surgical and transcatheter methods, the investigators reported a higher occurrence of cardiac arrhythmias in the surgical group although the difference did not reach statistical significance.[27]
Wilson et al.[4] documented the presence of arrhythmias (most frequently atrial fibrillation and atrial flutter) in 26 of 211 patients (12%) before transcatheter ASD closure. During a mean follow-up period of 1.8 years, arrhythmias had resolved in 16 patients and new arrhythmias had occurred in six patients after ASD closure.
Kaya et al.[12] assessed arrhythmias over a longer follow-up period (2-years). Before ASD closure, three patients had paroxysmal atrial fibrillation, one patient had supraventricular tachycardia, and two patients had frequent atrial extra beats. After ASD closure, arrhythmias were eliminated in five patients, and only one patient had ongoing paroxysmal atrial fibrillation, indicating the greatest likelihood of remaining free of arrhythmia. A prospective study reported patients without a history of arrhythmia and those younger than 40 years at the time of ASD closure.[28]
Atrial arrhythmias also may develop in the late period after ASD closure. A long-term follow-up study reported complete AV block in one patient 4.5 years after ASD closure.[29] Atrial tachyarrhythmias resolved after ASD closure, suggesting that atrial size can play a role in the mechanism of tachycardia. Therefore, regular follow-up evaluation by Holter ECG is recommended for these patients.
All echocardiographic parameters of remodeling were improved after 24 h of ASD closure, including those of the right-sided chambers' dimension and function, left-sided chambers' dimension and function, and PAP, and also after 3 months of follow-up and after 6 months.
Our results are in agreement with that of Oliveira and Moura et al.[13] who studied 120 patients with hemodynamically significant ASD closure using Occulotech device; over a follow-up period of 3 years, all patients had significant reduction or normalization of the RV size and function by TAPSE without residual shunt.
Furthermore, another research team found decreased right heart volume load and improvement of RV function by TAPSE after ASD closure using the transcatheter device closure and so reduction in PAP and right heart cavity dimensions was established.[14] Previous studies have shown a significant cardiac remodeling early after percutaneous ASD closure.[15],[10]
Du et al.[16] also showed that after transcatheter closure of the ASD, RV volume overload decreased within 24 h.
Cardiac remodeling occurs quite quickly after ASD device closure.[17] Reduced right atrial and ventricular volumes are apparent within 24 h, and probably earlier.
Another study showed that the reverse remodeling process appears to continue for at least 1 year and it is more advanced in the right ventricle than in the right atrium.[18] Furthermore, the magnitude of right atrial remodeling is inversely related to patients' age at the time of closure, as demonstrated in another study that reported persistent right atrial dilation in up to 64% of patients who underwent late ASD closure, which in turn was associated with elevation of brain natriuretic peptide levels and RV diastolic dysfunction.[19] All these data clearly support for early and timely closure of ASDs at the time of diagnosis.
One study found statistically significant reductions in RVEDD, function by TAPSE, and systolic PAP. Another study reported a 30% reduction in the RVEDD/LVEDD ratio (an indicator of cardiac geometry) 6 months after transcatheter closure of ASD.[16] The improvement of cardiac geometric remodeling after ASD transcatheter device closure resulted in the increase in LV ejection fraction.[20],[21]
A study including 38 patients who underwent successful ASD closure showed a highly statistically significant reduction in RAD (P = 0.004) and RV dimension (P < 0.001) in a follow-up period of 3–6 months [4] which is similar to our study.
The current study also evaluated RV dimensions quantitatively. Kort et al.[22] investigated RV size quantitatively by subjective TTE assessment. Before closure, 3% of the cohort had a normal RV size, 35% had a mildly dilated RV, 54% had a moderately dilated RV, and 7% had a severely dilated RV. At the last follow-up evaluation, RV had returned to normal for 75%, 19% had persistent mildly dilated RV, 5% had a moderately dilated RV, and 1% had a severely dilated RV.
A study showed that only 29% of patients had persistent RV enlargement 1 year after percutaneous ASD closure. Another report showed that only 33% of the patients had persistent RV enlargement at a 2-year follow-up assessment.[12] In agreement with other studies, our study confirmed that the RV generally returns to normal size and function by TAPSE after ASD closure in children and adults.
A previous study reported that persistent RV enlargement continues in approximately 50%–70% of both adults and children after surgical treatment despite elimination of right heart volume load.[19] This situation can be explained by a few mechanisms including myocardial changes due to long-term volume load, functional abnormalities due to cardiopulmonary bypass, and geometric modifications of the heart due to opening of the pericardium.
One research team investigated the phenomenon of persistent RV enlargement after surgical ASD closure and showed the importance of early treatment specifically for patients older than 40 years.
| Conclusion | | |
Transcatheter ASD device closure leads to significant improvement in right-sided chamber dimension and function and can reverse electrical changes in atrial and ventricular myocardium in children and adults after correcting hemodynamic status in short- and intermediate-term follow-up.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3]
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