Congenital heart disease

Diseases

Overview

Introduction

Congenital heart disease (CHD) is the most common birth defect, although still relatively rare.Centers for Disease Control and Prevention (CDC): facts about congenital heart defects Screening for fetal CHD includes ultrasonography in the second trimester of pregnancy and postpartum clinical exam; however, detection rates are low.[1] [2] [3] Fetal echocardiography is becoming the definitive test for diagnosis. The American Society of Echocardiography has produced recommendations for when to refer for fetal imaging, although they acknowledge there are local differences in referral indications depending on the population being screened.[4]

Early recognition of CHD is important because clinical presentation and deterioration may be sudden and some treatable defects may even cause death before diagnosis.[1]

The surgical and medical treatment of CHD has markedly improved over the last 50 years. The first successful open heart surgeries for intracardiac defects were carried out in the US in the 1950s.[5] [6] [7] It was the introduction of machines that perfused the vital organs while a surgeon carefully repaired a non-beating heart that revolutionized the field of corrective surgery. Survival well into adulthood is now expected for most babies born with CHD.[8]

Epidemiology

Worldwide, the prevalence of congenital heart disease (CHD) is estimated to be 0.8% to 1.2% of live births.[9] In high-income North America, including the US, the birth prevalence of CHD is estimated to be 12.3 per 1000 (95% CI, 10.9 to 13.8). An estimated 1% or a minimum of 40,000 infants per year are expected to be affected by CHD each year in the US. Around, 25%, or 2.4 per 1000 live births, will undergo invasive treatment in the first year of life. The most common type of congenital heart defect is bicuspid aortic valve, which occurs in 13.7 of every 1000 people.[10]

Chromosomal abnormalities (e.g., DiGeorge syndrome, Down syndrome, or Turner syndrome) are found in 8% to 10% of individuals with CHDs and single-nucleotide or pathogenic copy number variants are found in 5% to 15%.[10]

Recent reports show a significant decrease in mortality among patients with CHDs. In 2020, there were 2817 deaths related to CHD in the US, an 11.9% decrease from 2010, and the age-adjusted death rate was 0.9 deaths per 100,000 people, an 18.2% decrease from 2010.[10] Due to the improved survival, there is now an aging population of adults with CHD who present with complications related to acquired cardiovascular disease (e.g., thromboembolic events and arrhythmias).[8][11] [12] The increased risk of morbidity and mortality from premature atherosclerotic cardiovascular disease (ASCVD) in this group, poses an increasing challenge and highlights the need for long-term monitoring of patients and awareness of their ASCVD risk factors.[8]

Classification

Left-to-right shunts

Lesions that allow blood to shunt from the left side to the right side of the heart. They are associated with varying degrees of increased pulmonary blood flow and are typically acyanotic. In some defects, the site of the shunt may not be within the heart itself.
Cyanosis occurs only if the lesions are large and are not repaired in childhood, and if the patient develops pulmonary vascular obstructive disease (Eisenmenger physiology). Echocardiography is the primary imaging modality, and, in the current era, the role of cardiac catheterization is primarily for intervention.[13]
Examples include:
- Ventricular septal defect (VSD)
- Atrial septal defect (ASD)
- Atrioventricular septal defect (AVSD)
- Patent ductus arteriosus (PDA)
- Partial anomalous pulmonary venous connection (PAPVC).

Right-to-left shunts

Lesions that result in deoxygenated blood reaching the aorta and are associated with an increased or decreased pulmonary blood flow.
Examples include:
- Tetralogy of Fallot (TOF)
- Pulmonary valve atresia with or without a VSD
- d-Transposition of the great arteries (d-TGA)
- Truncus arteriosus
- Ebstein anomaly
- Total anomalous pulmonary venous connection (TAPVC)
- Hypoplastic left heart syndrome (HLHS).

Obstructive valvular and non-valvular lesions

Left ventricular outflow tract (LVOT) obstruction
Coarctation of the aorta
Pulmonary valve stenosis (PS)
Aortic valve stenosis (AS)

Anatomic and anatomic-physiologic classification of congenital heart disease

Congenital heart defects can also be classified using the anatomic/physiologic (AP) classification introduced by the American Heart Association/American College of Cardiology (AHA/ACC) task force in their 2018 guidelines.[14]

In the AP system, a patient is classified with both an "A" class and "P'' class based on the "highest" relevant anatomic or physiologic feature, and patients may move from one AP classification to another over time. If clinical status worsens, the classification will change to a higher severity group, but improvement in status; for example, after an intervention such as valve replacement or control of arrhythmia, can result in change to a lower severity classification.

In the 2020 guidelines for the management of adults with congenital heart defects published by the European Society of Cardiology (ESC), only the anatomic classification is used, without the physiologic component.[15] There are differences in the severity rating across both classification systems; for example, congenital aortic valve stenosis and congenital mitral valve disease are considered mild defects in the ESC guidelines, whereas the AHA/ACC guidelines grade them as moderate.

Ventricular septal defect (VSD)

VSD is the most common form of CHD, accounting for 20% of all cases, excluding bicuspid aortic valve and mitral valve prolapse.[16] Subtypes based on location include: perimembranous (in the area of the membranous septum); outlet (below 1 or both semilunar valves); inlet (inferior to the atrioventricular [AV] valves); and muscular (in the muscular or trabeculated portion of the ventricular septum).[17]Image

Perimembranous defects typically occur as a solitary lesion and can sometimes close spontaneously by apposition of the septal leaflet of the tricuspid valve to the defect. Outlet defects may be large and associated with more complex forms of congenital heart disease such as tetralogy of Fallot. Both perimembranous and outlet VSDs are in close proximity to the right cusp of the aortic valve. Because of the Venturi effect, these defects can cause prolapse of an aortic valve cusp, which results in both a restriction to flow through the VSD and regurgitation of the aortic valve.[18] Inlet defects do not close spontaneously and may be associated with AVSD and AV valve regurgitation. Muscular defects are the most common type of VSDs in newborns and the vast majority close spontaneously before 2 years of age.Image

Children with a small VSD develop normally and are asymptomatic. With larger defects, the excess pulmonary blood flow that ensues after the age of 6-8 weeks when the normal decrease in the pulmonary blood flow occurs may lead to the developments of tachypnea, tachycardia, pallor, poor feeding, and poor weight gain. Pulmonary vascular remodeling and obstructive disease usually do not develop in infants, but can develop by 2 years of age. If left untreated, most moderate to large VSD eventually lead to severe pulmonary hypertension and at some point reversal of the shunt occurs, leading to central cyanosis. This condition, called Eisenmenger syndrome, does not typically occur until later in life. Once a patient develops Eisenmenger physiology, closure of the VSD is contraindicated.[19] [20]

Patients have a low-to-mid frequency holosystolic murmur, a prominent precordial impulse, and, in patients with pulmonary hypertension, a loud and single second heart sound. If the left-to-right shunt is large, patients develop a mid-diastolic flow murmur ("rumble") across the mitral valve.

CXR and ECG can be normal in small VSDs. In larger defects, there is cardiac enlargement and increased pulmonary vascular markings on CXR, and ECG reveals left ventricle hypertrophy; right ventricle hypertrophy can occur with larger defects. Inlet-type VSDs are associated with left axis deviation on ECG. Echocardiography provides important information regarding the anatomy of the defect, the volume of the shunt, and right ventricular pressure.[21] [22]Image

The goal of treatment is to ensure adequate somatic growth and prevent pulmonary vascular obstructive disease. In the absence of the development of pulmonary hypertension, VSDs typically lead to left ventricular (LV) enlargement, which serves as an indication for closure. Small VSDs with restrictive flow may be left untreated with need for continuous surveillance for the development of LV enlargement and endocarditis. Large VSDs and defects associated with aortic regurgitation due to aortic valve cusp prolapse or excess pulmonary blood flow may require diuretics and an increased caloric formula, followed by closure of the defect (either surgical closure or transcatheter device closure). Those with increased pulmonary blood flow and faltering growth are closed surgically between 1 and 4 months of age; most large defects are typically closed by 6-9 months of age. For patients with Eisenmenger syndrome, pulmonary vasodilator therapy is the treatment of choice, and women of childbearing age should be informed that pregnancy is not advised due to high maternal mortality and fetal complications.[19] [20]

For more information see Ventricular septal defects .

Images

Subtypes of ventricular septal defects: (A) outlet; (B) perimembranous; (C) inlet; (D) muscular
Apical 4-chamber echocardiographic image of a muscular VSD (arrow). (RA) right atrium; (LA) left atrium; (RV) right ventricle; (LV) left ventricle
CXR demonstrating pulmonary overcirculation
Subtypes of atrial septal defects: (A) sinus venosus; (B) ostium secundum; (C) ostium primum; (D) unroofed coronary sinus
Apical 4-chamber echocardiographic image of an ostium primum ASD (arrow). (RA) right atrium; (LA) left atrium; (LV) left ventricle
Parasternal short axis echocardiographic image demonstrating right ventricular enlargement in a patient with an ASD. (RV) right ventricle; (LV) left ventricle
Apical 4-chamber echocardiographic image demonstrating right ventricular enlargement in a patient with an ASD. (RA) right atrium; (RV) right ventricle; (LV) left ventricle
Transesophageal echocardiographic image of an ASD occluder device (arrow). (RA) right atrium; (LA) left atrium; (SVC) superior vena cava
Apical 4-chamber echocardiographic image of complete AVSD. Note the ostium primum ASD (*) and the contiguous inlet VSD (arrow). (RA) right atrium; (LA) left atrium; (RV) right ventricle; (LV) left ventricle
12-lead ECG in an infant with complete AVSD; the ECG is significant for left axis deviation
Parasternal long axis echocardiographic image in a patient with tetralogy of Fallot. The aorta (Ao) overrides the VSD (*). (LA) left atrium; (RV) right ventricle; (LV) left ventricle
Subtypes of truncus arteriosus with ventricular septal defect (type A): Type A1: main pulmonary artery is present and bifurcates into the left and right pulmonary arteries Type A2:right and left branch pulmonary arteries arise from a common trunk. Type A3: One branch pulmonary artery arises from the common trunk and the other is absent/arises from a PDA or the aorta. Type A4: Truncus with aortic arch hypoplasia, coarctation or interrupted aortic arch and a large PDA

Citations

Key Articles

Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Apr 2;139(14):e698-800.[Full Text]
Baumgartner H, De Backer J, Babu-Narayan SV, et al. 2020 ESC Guidelines for the management of adult congenital heart disease. Eur Heart J. 2021 Feb 11;42(6):563-645.[Full Text]
American College of Radiology. Appropriateness criteria: congenital or acquired heart disease. 2023 [internet publication].[Full Text]
Toro-Salazar OH, Steinberger J, Thomas W, et al. Long-term follow-up of patients after coarctation of the aorta repair. Am J Cardiol. 2002 Mar 1;89(5):541-7.[Abstract]

Other Online Resources

Centers for Disease Control and Prevention (CDC): facts about congenital heart defects

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