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CONGENITAL HEART DEFECTS IN CHILDREN (LITERATURE REVIEW)
Odilova Shakhzoda Rustamovna
1st-year master's resident of the Department of Pediatrics and Neonatology, Samarkand
State Medical University, Samarkand, Uzbekistan.
Tilavova Aziza Komilovna
1st-year master's resident of the Department of Pediatrics and Neonatology, Samarkand
State Medical University, Samarkand, Uzbekistan.
Congenital heart defects (CHDs) represent one of the most significant challenges in pediatric
cardiology and cardiovascular surgery worldwide [1]. According to the World Health
Organization (WHO), the incidence of CHDs ranges from 8 to 12 per 1,000 live births [2].
In the structure of childhood mortality, cardiovascular pathology remains one of the leading
causes, with CHDs accounting for 30–45% of all mortality associated with congenital
developmental anomalies [3].
The formation of the heart in the fetus occurs during the earliest stages of embryogenesis,
when the basic structures of future organs and systems are being laid down [5]. External and
internal factors, such as genetic mutations, infectious agents, toxic exposures, and metabolic
disorders in the mother, can influence the process of heart and major vessel formation,
leading to various developmental defects [6]. Additionally, several studies highlight the
significant role of chromosomal abnormalities and syndromes in which the incidence of
CHDs is significantly higher than in the general population (e.g., Down syndrome or
DiGeorge syndrome) [7].
Modern methods of prenatal diagnosis, particularly fetal echocardiography, allow for the
detection of some defects as early as 18–20 weeks of gestation [8]. However, not all changes
in the cardiovascular system can be visualized prenatally, especially in cases of minor
defects or defects with mixed hemodynamics [9]. Timely diagnosis is critical for
determining the management strategy for the newborn (e.g., the need for emergency surgical
intervention or transfer to a specialized hospital) and reducing the risk of adverse outcomes
[10].
According to leading Russian clinics, there has been a relative decrease in severe forms of
CHDs in recent years due to the wider use of early ultrasound screening during pregnancy
[4]. However, some authors emphasize that in many regions, the level of specialized care for
expectant mothers remains insufficient, access to high-precision diagnostic equipment is
limited, and extended screening for chromosomal and genetic abnormalities is not routinely
performed [11]. As a result, children with CHDs do not always receive timely and accurate
diagnosis and treatment, which negatively affects survival rates and quality of life [12].
Significant interest lies in research on the structural classification of congenital heart defects,
which reflects the complexity and variability of defects in both morphological and
hemodynamic terms [13]. The most common forms include ventricular septal defects (VSD),
patent ductus arteriosus (PDA), atrial septal defects (ASD), tetralogy of Fallot, transposition
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of the great arteries (TGA), coarctation of the aorta, and others [14]. Critical CHDs requiring
urgent surgical intervention in the neonatal period (e.g., hypoplastic left heart syndrome) are
less common but have extremely high mortality rates in the absence of timely surgery [15].
According to several Russian authors, risk factors for CHDs include an unfavorable obstetric
and gynecological history (infections during pregnancy, use of teratogenic medications),
maternal age (over 35 years), environmental factors (air pollution, radiation), and hereditary
predisposition [16]. The polyetiological nature of CHDs is emphasized: often, multiple
causal factors may contribute to the formation of a single defect [17].
In pediatric practice, clinical symptoms play a crucial role, directly depending on the type
and severity of the defect and the degree of hemodynamic impairment [18]. In some children,
the defect may manifest immediately after birth (cyanosis, dyspnea, heart failure), while in
others, symptoms may appear later in childhood (episodes of weakness, fatigue, delayed
physical development) [19]. Diagnosis of CHDs, in addition to standard methods (physical
examination, electrocardiography, chest X-ray), includes echocardiography, Doppler
ultrasound, and often cardiac catheterization and angiocardiography [20]. Modern treatment
approaches are based on interventional cardiology and cardiac surgery, with the timing and
method of intervention depending on the morphology of the defect and the child's overall
condition [21].
One of the most pressing issues remains the determination of prognostic factors for
outcomes, particularly long-term survival, quality of life, and physical and psychomotor
development in children with CHDs [22]. Several large multicenter studies show that with
timely and adequate surgical treatment, many children can achieve satisfactory or even
normal health levels [23]. However, the presence of severe associated developmental defects
(including those outside the cardiovascular system), genetic syndromes, and other
complicating factors can significantly worsen the prognosis [24].
Thus, the analysis of scientific literature indicates the high prevalence of congenital heart
defects and their significant impact on childhood morbidity and mortality rates. Despite
advances in modern diagnosis and treatment, challenges remain in early detection,
preoperative preparation, and rehabilitation of children with CHDs, as well as in prevention
and genetic counseling [25]. This article provides a literature review aimed at systematizing
current knowledge on congenital heart defects in children, from epidemiology and
classification to diagnostic and therapeutic approaches.
**Brief Overview of Epidemiology and Etiology of CHDs**
Congenital heart defects account for a significant proportion of all congenital anomalies:
according to various authors, up to 30% of children with any congenital anomalies have
cardiovascular system pathologies [1]. Overall, the global prevalence of CHDs is estimated
at 0.8% to 1.2% per 1,000 live births, although these rates may vary in different regions
[2,3].
Risk factors for CHDs can be divided into genetic, intrauterine (antenatal), and external
(environmental, socio-domestic) factors. The genetic nature of CHDs is supported by the
presence of chromosomal abnormalities (e.g., trisomy 21, 13, 18) and microdeletions
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(22q11.2—DiGeorge syndrome), which significantly increase the risk of heart defects [7].
There are also several monogenic mutations that affect the process of cardiogenesis [6].
Intrauterine factors may include maternal infections during pregnancy (rubella,
cytomegalovirus, toxoplasmosis), maternal diabetes, hormonal dysfunctions, toxic exposures
(alcohol, smoking, drugs), and the use of certain pharmacological agents with teratogenic
potential [16]. The literature also highlights the role of chronic stress and adverse
environmental factors (air pollution, high doses of radiation) [11]. Maternal age over 35
years, especially with a family history of CHDs, is also an important predisposing factor
[7,17].
**Classification of Congenital Heart Defects**
Various classification systems for CHDs are proposed in domestic and foreign literature, but
the most common approach is to categorize defects based on hemodynamic characteristics,
such as defects with increased pulmonary blood flow, decreased pulmonary blood flow,
combined defects, and "cyanotic" and "acyanotic" defects (based on the presence or absence
of cyanosis) [18].
Defects with increased pulmonary blood flow include, for example, ventricular septal
defects (VSD), atrial septal defects (ASD), patent ductus arteriosus (PDA), and other
anomalies associated with left-to-right shunting [26]. "Cyanotic" defects (e.g., tetralogy of
Fallot, transposition of the great arteries) are characterized by cyanosis due to the shunting
of venous blood into the systemic circulation [15]. There are also complex combined defects
involving multiple components (e.g., triads or pentads of Fallot).
Some authors distinguish critical CHDs, where surgical intervention or emergency palliative
measures are necessary for the child's survival (e.g., hypoplastic left heart syndrome, total
anomalous pulmonary venous connection) [21]. This classification has practical significance,
as it determines the urgency of surgical treatment and the need for specialized resuscitation
measures in the delivery room or during the first days of life [27].
**Clinical Manifestations**
The clinical manifestations of congenital heart defects in children vary depending on the
type of defect, the severity of hemodynamic disturbances, and the degree of compensation
[19]. The most severe forms typically manifest immediately after birth or in the first weeks
of life (severe cyanosis, respiratory failure, circulatory disturbances), while milder defects
(e.g., small VSD) may remain asymptomatic for a long time [9,18].
Key symptoms that may suggest CHDs in neonates include:
- Severe dyspnea or cyanotic episodes;
- Cyanosis of the nasolabial triangle, mucous membranes, or skin (especially during crying
or feeding);
- Tachycardia or, conversely, bradycardia;
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- Signs of heart failure (hepatomegaly, edema, poor weight gain);
- Characteristic auscultatory findings (murmurs, accentuated second heart sound over the
pulmonary artery, etc.) [19,20].
In older children, if the defect is non-critical and did not manifest in the neonatal period,
symptoms may include fatigue, dyspnea during physical activity, frequent respiratory
infections, and delayed physical development [8,22].
**Modern Diagnostic Methods**
Standard diagnostic methods for CHDs in pediatric practice include:
1. Clinical examination: history taking (including family history), physical examination,
auscultation, and assessment of skin and mucous membrane color [19].
2. Electrocardiography (ECG): allows for the evaluation of rhythm, conduction, and cardiac
chamber hypertrophy [20].
3. Chest X-ray: provides information on heart size and pulmonary vascular markings [5].
4. Echocardiography with Doppler: the primary method for visualizing cardiac anatomy and
major vessels, detecting septal defects, abnormal blood flows, valve regurgitation, etc. [8,28].
5. Fetal echocardiography: performed prenatally (from 18–20 weeks of gestation) to detect
major CHDs and assess fetal blood flow [10].
6. Cardiac catheterization and angiocardiography: invasive methods used in complex
diagnostic cases and for clarifying hemodynamic parameters before surgical intervention
[20].
7. Genetic testing: indicated in cases of suspected chromosomal abnormalities or hereditary
syndromes associated with CHDs [29].
In recent years, advanced imaging techniques such as cardiac magnetic resonance imaging
(MRI) and multislice computed tomography (CT) with three-dimensional reconstruction
have gained wider use [30]. These methods provide detailed visualization of the defect's
structure and aid in planning surgical interventions.
**Medical Therapy and Palliative Measures**
In most cases, congenital heart defects with significant hemodynamic disturbances require
surgical correction. However, medical therapy is often used in preparation for surgery and to
maintain compensation [31]. Medications of choice include diuretics (furosemide,
spironolactone), inotropic agents (cardiac glycosides), vasodilators (ACE inhibitors), beta-
blockers, and others [32]. In some defects (e.g., PDA) in preterm infants, ibuprofen or
indomethacin may be used to close the ductus arteriosus [33].
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Surgical Treatment
The primary method for radical correction or repair of CHDs is surgical intervention.
Depending on the type of defect, the child's age, and condition, surgeries may be performed
on an emergency, early, or delayed basis [14,21]. The main types of interventions include:
- Radical: completely correcting the anatomical defect (e.g., VSD closure, ASD repair, PDA
ligation).
- Palliative: improving hemodynamics without fully correcting the defect (e.g.,
aortopulmonary anastomosis, shunt creation).
- Single-stage and multi-stage (staged correction): particularly relevant for complex
combined defects (tetralogy of Fallot, transposition of the great arteries, hypoplastic left
heart syndrome) [27].
One of the achievements of modern cardiac surgery is the widespread use of endovascular
(catheter-based) interventions: occluder placement for ASD and VSD, endovascular closure
of PDA, and stenting of narrowed segments (e.g., in coarctation of the aorta) [34]. These
methods are less invasive, reduce hospitalization time, and are highly effective for certain
indications.
Rehabilitation and Long-Term Outcomes
Rehabilitation of children who have undergone surgical treatment for CHDs includes a range
of measures: medical support, hemodynamic monitoring, nutritional and physical activity
adjustments, and psychological and educational assistance [35]. Regular follow-up with a
cardiologist and pediatrician allows for the timely detection of potential complications
(restenosis, arrhythmias, heart failure) and adjustment of therapy [36].
The prognosis for children with CHDs has significantly improved compared to 20–30 years
ago. According to some data, with timely radical surgery, children with the most common
defects (VSD, ASD, PDA) can achieve nearly normal life expectancy [23]. However, for
critical CHDs requiring multi-stage interventions, the risk of complications and mortality
remains high [15,27].
Prevention of Congenital Heart Defects
Prevention of CHDs aims to reduce the risk of defects during the intrauterine period and to
ensure early detection and timely treatment [17,25]. Prenatal counseling for expectant
parents, considering genetic factors, and maintaining a healthy lifestyle during pregnancy
(avoiding alcohol and other teratogenic substances, managing chronic conditions) play a
crucial role [7,16].
In cases of a family history of CHDs or suspected genetic disorders, genetic screening and
high-precision prenatal diagnosis (non-invasive prenatal testing, amniocentesis if necessary)
are recommended [29]. Folic acid supplementation during pregnancy planning is also
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advised, as it not only reduces the risk of neural tube defects but may also positively impact
overall fetal development [37].
Timely ultrasound screening during the first and second trimesters of pregnancy (including
fetal echocardiography) allows for the detection of most severe forms of CHDs and
determines the management strategy for delivery (e.g., delivery in a specialized perinatal
center with the capability for neonatal surgery within the first hours of life) [10,38].
Discussion
The analysis of modern scientific literature highlights the significant impact of congenital
heart defects as one of the leading causes of childhood mortality and disability [3,4].
Advances in medical science and technological progress in perinatal diagnosis and cardiac
surgery have led to substantial improvements: survival rates for severe CHDs have increased,
and early mortality rates have decreased [15,23].
However, according to some authors, challenges remain in the uneven availability of high-
tech care across regions and insufficient prenatal screening coverage [11,25]. Additionally,
organizational issues related to the creation of multidisciplinary teams (obstetricians,
cardiologists, neonatologists, cardiac surgeons) working in close collaboration for timely
diagnosis and treatment of CHDs are crucial [39].
Further research is needed to clarify the genetic mechanisms underlying CHDs, which could
lead to the development of primary prevention methods. Currently, molecular genetic
research aimed at identifying specific genes responsible for cardiogenesis and mutations that
increase the risk of CHDs is actively progressing [6,7].
Long-term follow-up of children with CHDs, including postoperative outcomes, will
provide a better understanding of factors influencing quality and length of life in these
patients. Research on psychosocial aspects is also important, as children with severe defects
may experience psychological difficulties and physical limitations, affecting their
socialization [35,40].
Conclusion
1. Congenital heart defects in children remain a pressing issue in pediatrics and pediatric
cardiac surgery, contributing significantly to childhood mortality and disability.
2. The main risk factors include genetic and chromosomal abnormalities, adverse pregnancy
conditions, teratogenic exposures, and environmental factors.
3. Modern diagnostic methods (prenatal echocardiography, echocardiography with color
Doppler, CT, and MRI of the heart) enable early detection of CHDs and planning of timely
surgical or interventional interventions.
4. Surgical and endovascular interventions allow for the radical correction of many forms of
CHDs; however, long-term rehabilitation and follow-up are necessary.
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5. Prevention of congenital heart defects involves a range of measures—from pregnancy
planning and proper prenatal care to promoting healthy lifestyles and genetic counseling.
The development of a multidisciplinary approach, further advancements in diagnostic and
surgical technologies, and research into the genetic basis of CHDs offer opportunities for
reducing the incidence of CHDs and improving the quality of life for affected children.
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