Browse

Journals By Subject

Life Sciences, Agriculture & Food
Chemistry
Medicine & Health
Materials Science
Mathematics & Physics
Electrical & Computer Science
Earth, Energy & Environment
Architecture & Civil Engineering
Education
Economics & Management
Humanities & Social Sciences
Multidisciplinary

Books

Publish Conference Abstract Books
Upcoming Conference Abstract Books
Published Conference Abstract Books
Publish Your Books
Upcoming Books
Published Books

Proceedings

Events

Events
Five Types of Conference Publications

Join

Join as Editorial Board Member
Become a Reviewer

Information

For Authors
For Reviewers
For Editors
For Conference Organizers
For Librarians
Article Processing Charges
Special Issue Guidelines
Editorial Process
Manuscript Transfers
Peer Review at SciencePG
Open Access
Copyright and License
Ethical Guidelines
Submit an Article
Research Article | | Peer-Reviewed

Epidemiological Profile, Diagnostic Approach and Associated Complications of Ventricular Septal Defect in a Pediatric Population

Mohammad Moniruzzaman*
Published in American Journal of Pediatrics (Volume 11, Issue 3)
Received: 30 June 2025     Accepted: 10 July 2025     Published: 28 July 2025
Views:       Downloads:
Download PDF
Abstract

Ventricular septal defect (VSD) is the most common congenital heart defect in children, associated with important considerations for disease epidemiology, diagnosis, and long-term outcomes. VSD results from a deficiency in growth or the failure of alignment or fusion of the components of the ventricular septum. This study aimed to describe the epidemiological profile, diagnostic approach, and associated complications of VSD in a pediatric population. This cross-sectional study was conducted in the Department of Pediatric Cardiology, Combined Military Hospital, Dhaka, Bangladesh, from January 2018 to December 2018. This study included 46 pediatric patients less than 12 years old with isolated VSD. The mean age of the participants was 2.78 ± 3.44 years, with a slight male predominance (male-to-female ratio of 1.09:1). Most patients (60.87%) were under one year of age. A family history of congenital heart disease was reported in 13.04% of cases. Common presenting symptoms included feeding difficulty (69.57%), cough (60.87%), poor weight gain (54.35%), and head sweating (50%). Respiratory distress was the most frequently observed clinical sign (71.74%), followed by tachycardia (47.83%) and failure to thrive (41.30%). Echocardiography was the definitive diagnostic tool, performed in all cases. Other investigations included ECG (82.61%), chest X-ray (76.09%), and cardiac catheterization (8.70%). Perimembranous VSD was the most prevalent type (67.39%), and the majority of defects were small in size (58.70%). Pulmonary hypertension was the most common complication, noted in 58.70% of patients, followed by aortic cusp prolapse (23.91%) and aortic regurgitation (17.39%). Ventricular septal defect remains a significant pediatric cardiac condition, predominantly affecting infants. Early diagnosis, with the help of a clinical picture and widely and easily accessible diagnostic tools like echocardiography (ECHO), will help initiate timely treatment and decrease mortality. Pulmonary hypertension was the most frequent complication, followed by aortic cusp prolapse and aortic regurgitation.

Published in American Journal of Pediatrics (Volume 11, Issue 3)
DOI 10.11648/j.ajp.20251103.18
Page(s) 166-172
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2025. Published by Science Publishing Group
Previous article
Keywords

Ventricular Septal Defect, Echocardiography, Pulmonary Hypertension

1. Introduction
Congenital heart disease (CHD) refers to structural and functional abnormalities of the heart present at birth. These abnormalities may involve the heart itself or the adjacent great blood vessels and can be detected either at birth or later in life.
[1]
The current global prevalence of CHD is estimated at approximately 8 cases per 1,000 live births, representing about 1.35 million affected newborns each year.
[2]
Ventricular septal defect (VSD) is the most common type, accounting for up to 40% of all cardiac malformations.
[3, 4]
A VSD is a defect in the septum that separates the right and left ventricles, and is often described colloquially as a “hole in the heart”.
[5]
They result from either a deficiency in the growth of the septum or a failure in the alignment or fusion of its parts.
[6]
Isolated VSD accounts for approximately 25–45% of all congenital heart diseases.
[7, 8]
The most widely accepted and practical classification of VSD was proposed by Soto et al. (1980), which categorizes VSD into perimembranous, muscular, and doubly committed subarterial (DCSA) types.
[9]
Perimembranous defects are the most common, accounting for around 80% of ventricular septal defects.
[10]
These are often associated with aneurysms or pouches of the septal leaflet of the tricuspid valve, which can partially or completely occlude the defect.
[11]
Muscular VSD accounts for 5–20% of cases and generally has a better prognosis, as they tend to close spontaneously earlier than perimembranous defects.
[12]
Doubly committed subarterial VSD represents 5–7% of cases in surgical and autopsy series.
[13]
Initial screening tools like chest X-ray and electrocardiogram (ECG) play a supportive role in diagnosing ventricular septal defects (VSDs); however, echocardiography remains the gold standard for definitive diagnosis. It not only confirms the presence of a VSD but also assesses the degree of hemodynamic disturbance and guides the decision between medical, surgical, or transcatheter intervention.
[14]
On chest X-ray, findings such as cardiomegaly and increased pulmonary vascular markings are commonly seen in moderate to large VSDs, while small defects may present with a normal radiographic appearance. Similarly, ECG results are usually normal in small VSDs but may show left atrial and left ventricular hypertrophy in moderate cases, and biventricular hypertrophy in larger defects.
[15, 16]
Echocardiographic assessment, particularly through two-dimensional imaging and color Doppler, is highly effective in pinpointing the location of defects within the ventricular septum.
[17]
This modality also assists in evaluating left atrial and ventricular dilation, which typically correlates with defect size.
[18]
Furthermore, echocardiography can reveal aneurysmal tissue formation, which may aid in the spontaneous closure of the VSD.
[19]
Doppler studies are valuable for visualizing shunting across the defect, with peak Doppler flow velocities being inversely proportional to VSD size. Higher velocities generally indicate smaller defects.
[14]
Although advanced imaging techniques like CT and MRI are helpful in assessing other congenital heart diseases, they are rarely necessary for diagnosing VSDs. Historically, cardiac catheterization and selective cineangiography were essential for preoperative evaluation. However, with advances in echocardiographic techniques, these invasive procedures are now typically reserved for selected cases, particularly those where elevated pulmonary vascular resistance is suspected.
[17]
The natural history of VSD is associated with various complications, among which pulmonary hypertension and prolapse of the aortic valve cusp are particularly notable. This complication occurs more frequently in doubly committed sub-arterial VSDs and less commonly in perimembranous outlet types.
[20]
Aortic cusp prolapse can progress to secondary aortic insufficiency, which is observed in approximately 5% of patients with VSD.
[21]
When the aortic leaflet prolapses, it can partially close a moderate or large VSD, thus limiting the left-to-right shunt. Although the prevalence of this complication increases with age, it can also manifest in children younger than six years of age.
[8]
Aortic regurgitation may also develop, with its severity varying among individuals. The anatomical and hemodynamic characteristics of DCSA ventricular septal defects significantly influence the risk of developing aortic valve deformities and subsequent aortic regurgitation.
[8]
Deformities in the aortic cusp can predict progressive aortic regurgitation.
[8]
Aortic regurgitation tends to be progressive, and even mild regurgitation or isolated aortic valve prolapse without regurgitation is considered an indication for surgical intervention.
[22]
Perimembranous outlet VSDs are also associated with infundibular hypertrophy, which can lead to progressive right ventricular outflow tract obstruction requiring surgical management.
[23]
Although infective endocarditis is rare in children under two years of age, it remains a concern.
[23]
Additionally, discrete fibrous subaortic stenosis may occasionally occur in association with VSDs, most frequently with perimembranous types, and can appear after either spontaneous or surgical closure of the defect.
[23, 24]
Therefore, in this study, we aimed to describe the epidemiological profile, diagnostic approach, and associated complications of VSD in a pediatric population.
2. Materials and Methods
This cross-sectional study was conducted in the Department of Pediatric Cardiology, Combined Military Hospital, Dhaka, Bangladesh, from January 2018 to December 2018. In this study, we included 46 pediatric patients less than 12 years of age with Doppler ECHO findings showing isolated VSD, a defect in the ventricular wall.
The following criteria were used to determine eligibility for enrollment as study participants:
Inclusion Criteria
a) Patients aged less than 12 years;
b) Patients having an isolated Ventricular Septal Defect;
c) Patients having minor associated anomalies, like a small patent ductus arteriosus, a small secundum atrial septal defect, and mild mitral regurgitation.
Exclusion Criteria
a) Patients with incomplete medical records;
b) Patients having VSD with other complex congenital structural heart disease;
c) Patients whose parents or guardians were not willing to participate in the study.
Data Collection Procedure: The legal guardians or parents of neonates were invited to participate in the current study. Informed written consent was obtained after the study procedure was explained. This cross-sectional study used a structured questionnaire to gather relevant data. The questionnaire included socio-demographic and clinical data at baseline, along with investigation findings and associated complications. Treatment, whether medical or surgical, was selected based on the patient's categorization.
Statistical Analysis: The qualitative data from this study were presented as frequency distributions and percentages, while the quantitative data were expressed in terms of mean and standard deviation. The data were analyzed using SPSS 25 (Statistical Package for Social Sciences) for Windows Version 10. This study was approved by the ethical review committee of the Directorate General Medical Service (DGMS), Dhaka Cantonment.
3. Results
Figure 1 presents the age distribution of the study subjects (n = 46). The majority of participants were under 1 year of age (60.87%), followed by 21.74% aged 6–12 years, and 17.39% were aged 1–5 years.
Figure 1. Age Distribution of Study Subjects (n = 46).
Table 1. Demographic and epidemiological characteristics of the study population (n = 46).

Variable

Number

Percentage (%)

Age (Mean ±SD, years)

2.78 ± 3.44

Sex

Male

24

52.17

Female

22

47.83

Residence

Urban

28

60.87

Rural

18

39.13

Family History of CHD

Present

6

13.04

Absent

40

86.96
Table 1 shows that the mean age of the children was 2.78 ± 3.44 years. Of the total participants, 52.17% were male and 47.83% were female. The male and female ratio was 1.09:1 in our study. A majority (60.87%) of the children were from urban areas, while the remaining 39.13% resided in rural settings. Family history of congenital heart disease (CHD) was present in 13.04% of the participants, whereas 86.96% reported no family history of CHD.
Table 2. Baseline findings of study participants (n = 46).

Baseline Findings

Number

Percentage (%)

Symptoms

Head sweating

23

50.00

Dyspnea on exertion

22

47.83

Cough

28

60.87

Feeding difficulty

32

69.57

Poor weight gain

25

54.35

Asymptomatic

14

30.43

Signs

Respiratory distress

33

71.74

Tachycardia

22

47.83

Fever

11

23.91

Failure to thrive (FTT)

19

41.30

Precordium Findings

Bulge of the precordium

17

36.96

Cardiomegaly

16

34.78

Thrill

33

71.74

P2 palpable

5

10.87

Loud P2

7

15.22

Pansystolic murmur

32

69.57

Ejection systolic murmur

13

28.26
Table 2 summarizes the baseline findings of the study participants (n = 46). Among symptoms, feeding difficulty was reported in 69.57% of participants, cough in 60.87%, poor weight gain in 54.35%, and head sweating in 50%. Notably, 30.43% of participants were asymptomatic. Regarding the clinical signs, respiratory distress was observed in 71.74% of subjects, tachycardia in 47.83%, fever in 23.91%, and failure to thrive in 41.30%. In terms of precordium findings, thrill was mostly present in 71.74% of cases, followed by pansystolic murmur in 69.57%, bulge of the precordium in 36.96%, cardiomegaly in 34.78%, and an ejection systolic murmur in 28.26% of subjects.
Table 3. Diagnostic modalities used for VSD detection in study subjects (n=46).

Diagnostic Tool

Number

Percentage (%)

Chest X-ray

35

76.09

ECG

38

82.61

Echocardiography

46

100.00

Cardiac Catheterization

4

8.70
Table 3 outlines the diagnostic tools used among the study population. Echocardiography was performed in all cases (100%), which is the most universally applied diagnostic modality for VSD detection. Electrocardiography (ECG) was conducted in 82.61% of the children, while Chest X-ray was used in 76.09% of cases. Cardiac catheterization was performed in a limited number of patients (8.70%).
Table 4. Distribution of study patients by type and size of VSD (n = 46).

Type

Number

Percentage (%)

Perimembranous

31

67.39

Muscular

8

17.39

Inlet

4

8.70

Outlet

3

6.52

Size

Small (<5 mm)

27

58.70

Moderate (5-10 mm)

15

32.61

Large (>10 mm)

4

8.70
Table 4 shows the distribution of study participants by types of ventricular septal defect (VSD). The majority of participants had perimembranous VSD (67.39%), followed by muscular VSD (17.39%), inlet VSD (8.70%), and outlet VSD (6.52%). The majority of lesions were of small size (<5 mm), accounting for 58.70% of cases. Moderate-sized (5-10 mm) lesions were observed in 32.61% of participants, while large lesions (>10 mm) were present in 8.70% of cases.
Figure 2. Associated complications in VSD patients.
The bar chart illustrates that pulmonary hypertension was the most common complication, observed in 58.70% of participants. Other complications included aortic cusp prolapse (23.91%), aortic regurgitation (17.39%), right ventricular outflow tract obstruction (10.87%), left ventricular outflow tract obstruction (8.70%), and infective endocarditis (4.35%).
4. Discussion
Ventricular septal defect (VSD) is the most common congenital cardiac malformation, accounting for approximately 25% of all congenital heart diseases.
[8, 25]
It results from deficient growth or failure in the alignment or fusion of the components of the ventricular septum. The natural history of VSD spans a wide clinical spectrum from spontaneous closure to severe complications such as congestive heart failure and early infant mortality.
[26]
One study analyzing the natural and modified history of isolated VSD reported that VSD constituted 25.5% of all congenital heart defects. In cases of moderate to large VSD, delayed physical growth, decreased exercise tolerance, recurrent pulmonary infections, and congestive heart failure are relatively frequent during infancy.
[27]
VSD can be anatomically classified into perimembranous, outlet, inlet, and muscular types.
[28]
In the current study, perimembranous VSD was the most frequent subtype, observed in 67.39% of participants, followed by muscular (17.39%), inlet (8.70%), and outlet (6.52%) types. These findings are consistent with earlier studies. For instance, Chaudhry et al. (2011) reported that among 1,276 patients, 79.3% had perimembranous VSD, 9.8% had muscular VSD, 6.7% had doubly committed subarterial (DCSA) VSD, and 4.2% had inlet VSD.
[23]
Similarly, Kazmi et al. (2009) found that the most common type was perimembranous, followed by muscular (11.7%) and DCSA (2.9%) VSDs.
[8]
These findings align with Western literature, where perimembranous VSDs are also the most common, followed by muscular and DCSA types.
[13]
There are limited local studies on the distribution of VSD types. In a study conducted at the National Institute of Cardiovascular Diseases (NICVD) in Karachi, Aziz et al. (2000) found that 92% of VSDs were perimembranous, 7% were DCSA, and only 1.7% were muscular.
[29]
Sadiq et al. (2002) reported a 32% incidence of VSD among all congenital heart diseases in a tertiary care pediatric cardiology unit.
[7]
Contrastingly, studies in Southeast Asian children suggest a higher prevalence of DCSA, reaching up to 29–30% of all VSDs.
[8]
A Sri Lankan study also reported VSDs accounting for 27.5% of all congenital heart diseases.
[10]
The clinical presentation of VSD primarily depends on the size of the defect. Large VSDs may remain asymptomatic in the neonatal period, while smaller defects often produce loud murmurs and are thus detected early in infancy.
[28]
In the present study, the majority of lesions were of small size (58.70%), followed by moderate-sized (32.61%) lesions, and large lesions (>10 mm) were present in 8.70% of cases. In a study conducted by Layangoo et al. (2008), the distribution of small, moderate, and large defects was 62.5%, 15.9%, and 21.6%, respectively.
[30]
Management of VSD depends on the defect size and associated complications. Small VSDs often do not require intervention, whereas moderate defects may behave similarly to large ones and may necessitate surgical or catheter-based procedures.
[28]
Device closure is recommended for selected muscular VSDs.
[31]
In this study, echocardiography was the definitive diagnostic tool and was performed in all cases. Other investigations included ECG (82.61%), chest X-ray (76.09%), and cardiac catheterization (8.70%). Kazmi et al. (2009) performed echocardiography as the primary diagnostic tool for detecting ventricular septal defects. All of their patients underwent transthoracic echocardiography, utilizing 2D imaging, continuous wave Doppler, and color Doppler techniques.
[8]
A study by Chaudhry et al. (2011) reported that the diagnosis was primarily made using echocardiography. The size, number, and exact location of the defect, as well as the magnitude of the shunt, were identified using two-dimensional and Doppler echocardiography.
[23]
Regarding complications, pulmonary hypertension was the most frequently observed, affecting 58.70% of participants. Other notable complications included aortic cusp prolapse (23.91%) and aortic regurgitation (17.39%). These findings are consistent with those reported by Kazmi et al. (2009), who observed 76 cases of right coronary cusp (RCC) prolapse among 729 patients with perimembranous VSDs (10.4%).
[8]
Lue et al. (1981) reported aortic valve prolapse and regurgitation in 11.9% of their VSD patients
[20]
, while Brauner et al. (1995) noted aortic valve prolapse in over 5% of affected children.
[32]
Ando et al. (1986) found RCC prolapse in 16% of VSD cases
[33]
, and Chiu et al. (2005) observed that the prolapsed cusp in DCSA was always the RCC. In perimembranous outlet VSDs, the non-coronary cusp (NCC) was involved in 16.5% of cases.
[22]
Somanath et al. (1990) identified RCC prolapse in 48% of their patients with perimembranous VSD, NCC in 41%, and both cusps in 11%.
[34]
Detection of RCC prolapse is critical in patients with outlet VSD, as it can lead to permanent aortic regurgitation.
[35]
Surgical intervention is warranted in patients with clinically significant aortic regurgitation or right ventricular outflow tract (RVOT) obstruction
[36]
, and early repair may prevent progression of aortic insufficiency.
[37]
Glen et al. (2004) reported infundibular stenosis in 5.8% and aortic valve prolapse in 3.6% of their VSD patients.
[38]
These findings highlight the diverse clinical presentations and potential severity of VSD, underscoring the importance of early detection, precise classification, and timely intervention to prevent complications.
5. Conclusion and Recommendations
The study findings highlight that VSD often presents with significant clinical symptoms, including respiratory distress, feeding difficulties, and poor weight gain, although a notable proportion of cases remain asymptomatic. Early diagnosis, based on clinical signs and use of simple investigation tools like X-ray and echocardiography (ECHO), may reduce the life-threatening complications and mortality. Pulmonary hypertension emerged as the most frequent complication, affecting more than half of the participants. Other notable complications included aortic cusp prolapse, aortic regurgitation, right & left ventricular outflow tract obstructions, and infective endocarditis.
Further study with a prospective and longitudinal study design, including a larger sample size, needs to be done to validate the findings of this study.
Abbreviations

CHD

Congenital Heart Disease

VSD

Ventricular Septal Defect

ECHO

Echocardiography

ECG

Electrocardiogram
Author Contributions
Mohammad Moniruzzaman is the sole author. The author read and approved the final manuscript.
Ethical Approval
This study was ethically approved.
Funding
No funding sources.
Conflicts of Interest
The author declares no conflicts of interest.
References
[1] Tantchou Tchoumi JC, Butera G, Giamberti A, Ambassa JC, Sadeu JC. Occurrence and pattern of congenital heart diseases in a rural area of sub-Saharan Africa. Cardiovasc J Afr. 2011; 22(2): 63-6.

https://doi.org/10.5830/CVJA-2010-046

[2] Van Der Linde D, Konings EEM, Slager MA, Witsenburg M, Helbing WA, Takkenberg JJ, Roos-Hesselink JW. Birth prevalence of congenital heart disease worldwide: A systematic review and meta-analysis. J Am Coll Cardiol. 2011; 58(21): 2241-7.

https://doi.org/10.1016/j.jacc.2011.08.025

[3] Penny DJ, Vick GW III. Ventricular septal defect. Lancet. 2011; 377(9771): 1103-12.
[4] Shafer K, Brickner ME. Ventricular septal defect. In: Braunwald’s heart disease: Essential echocardiography: a companion. Elsevier; 2018. p. 435-9.
[5] Sarwar S, Shabana, Ehsan F, Tahir A, Jamil M, Shahid SU, Hasnain S, Khan A, Hyder SN. Hematological and demographic profile of Pakistani children with isolated ventricular septal defects (VSDs). Egypt J Med Hum Genet. 2020; 21: 1-8.
[6] Rhodes LA, Keane JF, Keane JP, Fellows KE, Jonas RA, Castaneda AR. Long follow-up (43 years) of ventricular septal defect with audible aortic regurgitation. Am J Cardiol. 1990; 66: 340-5.
[7] Sadiq M, Roshan B, Latif F, Bashir I, Sheikh SA, Khan A. Pattern of paediatric heart disease in Pakistan. J Coll Physicians Surg Pak. 2002; 12: 149-53.
[8] Kazmi U, Sadiq M, Hyder SN. Pattern of ventricular septal defects and associated complications. J Coll Physicians Surg Pak. 2009 Jun; 19(6): 342-5.
[9] Soto B, Becker AE, Moulaert AJ, Lie JT, Anderson RH. Classification of ventricular septal defects. Br Heart J. 1980; 43: 332-43.
[10] Wickramasinghe P, Lamabadusuriya SP, Narenthiran S. Prospective study of congenital heart disease in children. Ceylon Med J. 2001; 46: 96-8.
[11] Wu MH, Wu JM, Chang CI, et al. Implication of aneurysmal transformation in isolated perimembranous ventricular septal defect. Am J Cardiol. 1993; 72: 596-601.
[12] Hrahshah AS, Hijazi IS. Natural and modified history of ventricular septal defect in infants. Pak J Med Sci. 2006; 22: 136-40.
[13] McDaniel NL, Gutgesell HP. Ventricular septal defect. In: Allen HD, Driscoll DJ, Sheddy RE, Feltes TF, editors. Moss and Adams’ Heart Disease in Infants, Children, and Adolescents. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2008. p. 667-82.
[14] Rao PS. Diagnosis and Management of Ventricular Septal Defects. Reviews in Cardiovascular Medicine. 2024 Nov 20; 25(11): 411.
[15] Syamasundar Rao P. Diagnosis and management of acyanotic heart disease: part II– left-to-right shunt lesions. Indian Journal of Pediatrics. 2005; 72: 503–512.
[16] Rao PS, Harris AD. Recent advances in managing septal defects: ventricular septal defects and atrioventricular septal defects. F1000Research. 2018; 7: F1000 Faculty Rev-498.
[17] Rao PS. Congenital heart defects– A review. In: Rao PS, editor. Congenital Heart Disease: Selected Aspects. Rijeka (Croatia): InTech; 2011. p. 3–44.
[18] Rees AH, Rao PS, Rigby JJ, Miller MD. Echocardiographic estimation of a left-to-right shunt in isolated ventricular septal defects. European Journal of Cardiology. 1978; 7: 25–33.
[19] Rao PS. Other acyanotic heart defects presenting in the neonate. In: Rao PS, Vidyasagar D, editors. A Multidisciplinary Approach to Perinatal Cardiology. Vol. 2. New Castle upon Tyne (UK): Cambridge Scholars Publishing; 2021. p. 615–654.
[20] Lue HC, Sung TC, Hou SH, Wu MH, Cheng SJ, Chu SH, et al. Ventricular septal defect in Chinese with aortic valve prolapse and aortic regurgitation. Heart Vessels. 1981; 2: 111-6.
[21] Kobayashi J, Koike K, Senzaki H, Kobayashi T, Trunemoto M, Ishizawa A, et al. Correlation of anatomic and hemodynamic features with aortic valve leaflet deformity in doubly committed subarterial ventricular septal defect. Heart Vessels. 1999; 14: 240-5.
[22] Chiu SN, Wang JK, Lin MT, Wu ET, Lu FL, Chang CI, et al. Aortic valve prolapse associated with outlet-type ventricular septal defect. Ann Thorac Surg. 2005; 79: 1366-71.
[23] Chaudhry TA, Younas M, Baig A. Ventricular septal defect and associated complications. JPMA. 2011; 61(10): 1001-4.
[24] Zielinsky P, Rossi M, Haertel JC. Subaortic fibrous ridge and ventricular septal defect: role of septal malalignment. Circulation. 1987; 75: 1124-9.
[25] Kliegman RM, Jenson HB, Stanton NF. The cardiovascular system. In: Behrman RE, editor. Nelson Textbook of Pediatrics. 20th ed. Philadelphia: Saunders; 2016. p. 2194-7.
[26] Fauci SA, Kasper DL, Longo DL, Braunwald E, Hauser SL, Jameson JL, et al. Disorders of cardiovascular system. In: Elliott M, Antman MD, editors. Harrison’s Principles of Medicine. 19th ed. USA: McGraw-Hill Companies; 2016. p. 1556-8.
[27] Frontera-Izquierdo P, Cabezuelo-Huerta G, Cabezuelo-Huerta G. Natural and modified history of isolated ventricular septal defect: A 17-year study. Arch Dis Child. 1999 Nov; 81(5): 413-6.
[28] Meryl S, Lopez L. Ventricular septal defect. In: Hugh D, Robert, Daniel J, Timothy F, Frank C, Howard PG, editors. Moss and Adams Heart Disease in Infants, Children, and Adolescents. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2016. p. 1450-60.
[29] Aziz K. Ventricular septal defects. In: Heart Disease in Children. 2nd ed. Karachi: The Authors; 2000. p. 254-77.
[30] Layangool T, Kirawittaya T, Sangtawesin C, Kojaranjit V, Makarapong P, Pechdamrongsakul A, Intasorn Y, Noisang P. Natural aortic valve complications of ventricular septal defect: A prospective cohort study. J Med Assoc Thai. 2008; 91: 53-9.
[31] Rafiq I, Freeman L, Orzalkiewicz M, et al. Natural history of repaired and unrepaired VSD. Heart. 2015; 101: A82-A83.
[32] Brauner R, Birk E, Blieden L, Sahar G, Vidne BA. Surgical management of ventricular septal defect with aortic valve prolapse: Clinical considerations and results. Eur J Cardiothorac Surg. 1995; 9: 315-9.
[33] Ando M, Takao A. Pathological anatomy of ventricular septal defect associated with aortic valve prolapse and regurgitation. Heart Vessels. 1986; 2: 117-26.
[34] Somanath HS, Gupta SK, Reddy KN, Murthy JS, Rao AS, Abraham KA. Ventricular septal defect with aortic regurgitation: A hemodynamic and angiographic profile in Indian subjects. Indian Heart J. 1990; 42: 113-6.
[35] Hori Y, Yoshimura N, Kimura M. Right coronary cusp prolapse, evaluation by MRI. RSNA presentation Dec 2004 Hall D, Lakeside Centre.
[36] Webb GD. Challenges in the care of adult patients with congenital heart defects. Heart. 2003; 89: 465-9.
[37] Yetkin G, Refile B. An unusual case of chrysomonas luteala in infective endocarditis in a patient with ventricular septal defect. Indus Universatisi Tip Facultesi Dergisi. 2005; 12: 193-5.
[38] Glen S, Burns J, Bloomfield P. Prevalence and development of additional cardiac abnormalities in 1448 patients with congenital ventricular septal defects. Heart. 2004; 90: 1321-5.
Cite This Article
Plain Text BibTeX RIS

  • APA Style

    Moniruzzaman, M. (2025). Epidemiological Profile, Diagnostic Approach and Associated Complications of Ventricular Septal Defect in a Pediatric Population. American Journal of Pediatrics, 11(3), 166-172. https://doi.org/10.11648/j.ajp.20251103.18

    Copy | Download

    ACS Style

    Moniruzzaman, M. Epidemiological Profile, Diagnostic Approach and Associated Complications of Ventricular Septal Defect in a Pediatric Population. Am. J. Pediatr. 2025, 11(3), 166-172. doi: 10.11648/j.ajp.20251103.18

    Copy | Download

    AMA Style

    Moniruzzaman M. Epidemiological Profile, Diagnostic Approach and Associated Complications of Ventricular Septal Defect in a Pediatric Population. Am J Pediatr. 2025;11(3):166-172. doi: 10.11648/j.ajp.20251103.18

    Copy | Download 

  • @article{10.11648/j.ajp.20251103.18,
  author = {Mohammad Moniruzzaman},
  title = {Epidemiological Profile, Diagnostic Approach and Associated Complications of Ventricular Septal Defect in a Pediatric Population
},
  journal = {American Journal of Pediatrics},
  volume = {11},
  number = {3},
  pages = {166-172},
  doi = {10.11648/j.ajp.20251103.18},
  url = {https://doi.org/10.11648/j.ajp.20251103.18},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajp.20251103.18},
  abstract = {Ventricular septal defect (VSD) is the most common congenital heart defect in children, associated with important considerations for disease epidemiology, diagnosis, and long-term outcomes. VSD results from a deficiency in growth or the failure of alignment or fusion of the components of the ventricular septum. This study aimed to describe the epidemiological profile, diagnostic approach, and associated complications of VSD in a pediatric population. This cross-sectional study was conducted in the Department of Pediatric Cardiology, Combined Military Hospital, Dhaka, Bangladesh, from January 2018 to December 2018. This study included 46 pediatric patients less than 12 years old with isolated VSD. The mean age of the participants was 2.78 ± 3.44 years, with a slight male predominance (male-to-female ratio of 1.09:1). Most patients (60.87%) were under one year of age. A family history of congenital heart disease was reported in 13.04% of cases. Common presenting symptoms included feeding difficulty (69.57%), cough (60.87%), poor weight gain (54.35%), and head sweating (50%). Respiratory distress was the most frequently observed clinical sign (71.74%), followed by tachycardia (47.83%) and failure to thrive (41.30%). Echocardiography was the definitive diagnostic tool, performed in all cases. Other investigations included ECG (82.61%), chest X-ray (76.09%), and cardiac catheterization (8.70%). Perimembranous VSD was the most prevalent type (67.39%), and the majority of defects were small in size (58.70%). Pulmonary hypertension was the most common complication, noted in 58.70% of patients, followed by aortic cusp prolapse (23.91%) and aortic regurgitation (17.39%). Ventricular septal defect remains a significant pediatric cardiac condition, predominantly affecting infants. Early diagnosis, with the help of a clinical picture and widely and easily accessible diagnostic tools like echocardiography (ECHO), will help initiate timely treatment and decrease mortality. Pulmonary hypertension was the most frequent complication, followed by aortic cusp prolapse and aortic regurgitation.},
 year = {2025}
}

    Copy | Download 

  • TY  - JOUR
T1  - Epidemiological Profile, Diagnostic Approach and Associated Complications of Ventricular Septal Defect in a Pediatric Population

AU  - Mohammad Moniruzzaman
Y1  - 2025/07/28
PY  - 2025
N1  - https://doi.org/10.11648/j.ajp.20251103.18
DO  - 10.11648/j.ajp.20251103.18
T2  - American Journal of Pediatrics
JF  - American Journal of Pediatrics
JO  - American Journal of Pediatrics
SP  - 166
EP  - 172
PB  - Science Publishing Group
SN  - 2472-0909
UR  - https://doi.org/10.11648/j.ajp.20251103.18
AB  - Ventricular septal defect (VSD) is the most common congenital heart defect in children, associated with important considerations for disease epidemiology, diagnosis, and long-term outcomes. VSD results from a deficiency in growth or the failure of alignment or fusion of the components of the ventricular septum. This study aimed to describe the epidemiological profile, diagnostic approach, and associated complications of VSD in a pediatric population. This cross-sectional study was conducted in the Department of Pediatric Cardiology, Combined Military Hospital, Dhaka, Bangladesh, from January 2018 to December 2018. This study included 46 pediatric patients less than 12 years old with isolated VSD. The mean age of the participants was 2.78 ± 3.44 years, with a slight male predominance (male-to-female ratio of 1.09:1). Most patients (60.87%) were under one year of age. A family history of congenital heart disease was reported in 13.04% of cases. Common presenting symptoms included feeding difficulty (69.57%), cough (60.87%), poor weight gain (54.35%), and head sweating (50%). Respiratory distress was the most frequently observed clinical sign (71.74%), followed by tachycardia (47.83%) and failure to thrive (41.30%). Echocardiography was the definitive diagnostic tool, performed in all cases. Other investigations included ECG (82.61%), chest X-ray (76.09%), and cardiac catheterization (8.70%). Perimembranous VSD was the most prevalent type (67.39%), and the majority of defects were small in size (58.70%). Pulmonary hypertension was the most common complication, noted in 58.70% of patients, followed by aortic cusp prolapse (23.91%) and aortic regurgitation (17.39%). Ventricular septal defect remains a significant pediatric cardiac condition, predominantly affecting infants. Early diagnosis, with the help of a clinical picture and widely and easily accessible diagnostic tools like echocardiography (ECHO), will help initiate timely treatment and decrease mortality. Pulmonary hypertension was the most frequent complication, followed by aortic cusp prolapse and aortic regurgitation.
VL  - 11
IS  - 3
ER  -

    Copy | Download

Author Information
Download PDF
Submit an Article

About Us

Science Publishing Group (SciencePG) is an Open Access publisher, with more than 300 online, peer-reviewed journals covering a wide range of academic disciplines.

Learn More About SciencePG

Products

Information

Important Link

Copyright © 2012 -- 2025 Science Publishing Group – All rights reserved.