Tetralogy of Fallot occurs approximately 400 times per million live births and accounts for 7 to 10% of all congenital heart abnormalities.

Some recent research has suggested that a proportion of cases of migraine may be caused by PFO. While the exact mechanism remains unclear, closure of a PFO can reduce symptoms in certain cases. This remains controversial; 20% of the general population has a PFO, which for the most part, is asymptomatic. About 20% of the female population has migraines, and the placebo effect in migraine typically averages around 40%. The high frequency of these facts finding statistically significant relationships between PFO and migraine difficult (i.e., the relationship may just be chance or coincidence). In a large randomized controlled trial, the higher prevalence of PFO in migraine patients was confirmed, but migraine headache cessation was not more prevalent in the group of migraine patients who underwent closure of their PFOs.

Presence of a cystic hygroma increases the risk of HLHS in a fetus.

Genetic loci associated with HLHS include GJA1 (connexin 43), HAND1, NKX2.5, 10q22, and 6q23. There is a slight risk of recurrence in future pregnancies, estimated to be 2-4%, which increases to 25% in families with two affected children. This is thought to be mediated by genetic mutations with incomplete penetrance.

HLHS is also associated with several genetic syndromes, including trisomy 13 (Patau syndrome), trisomy 18 (Edwards syndrome), partial trisomy 9, Turner's syndrome (XO), Jacobsen syndrome (11q deletion syndrome), Holt-Oram syndrome, and Smith-Lemli-Opitz syndrome.

Untreated, tetralogy of Fallot rapidly results in progressive right ventricular hypertrophy due to the increased resistance caused by narrowing of the pulmonary trunk. This progresses to heart failure which begins in the right ventricle and often leads to left heart failure and dilated cardiomyopathy. Mortality rate depends on the severity of the tetralogy of Fallot. If left untreated, TOF carries a 35% mortality rate in the first year of life, and a 50% mortality rate in the first three years of life. Untreated TOF also causes delayed growth and development, including delayed puberty.

Patients who have undergone total surgical repair of tetralogy of Fallot have improved hemodynamics and often have good to excellent cardiac function after the operation with some to no exercise intolerance (New York Heart Association Class I-II). Surgical success and long-term outcome greatly depend on the particular anatomy of the patient and the surgeon's skill and experience with this type of repair.

Ninety percent of people with total repair as babies develop a progressively leaky pulmonary valve later in life. It is recommended that they follow up at a specialized adult congenital heart disease center.

Down syndrome is often associated with AVCD. Other risk factors include: having a parent with a congenital heart defect, alcohol use while pregnant, uncontrolled diabetes treatment during pregnancy and some medications during pregnancy.

This type of congenital heart defect is associated with patients with Down syndrome (trisomy 21) or heterotaxy syndromes. 45% of children with Down syndrome have congenital heart disease. Of these, 35–40% have AV septal defects. Similarly, one-third of all children born with AVSDs also have Down syndrome.

A study also showed that there is also an increased risk of atrioventricular canal in patients who suffer from Noonan syndrome. The pattern seen in those patients with Noonan syndrome differ from those patients who have Down syndrome in that "partial" AVCD is more prevalent in those who suffer from NS, where as those who suffer from down syndrome show a prevalence of the "complete" form of AVCD.

Known environmental factors include certain infections during pregnancy such as Rubella, drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus).

Being overweight or obese increases the risk of congenital heart disease. Additionally, as maternal obesity increases, the risk of heart defects also increases. A distinct physiological mechanism has not been identified to explain the link between maternal obesity and CHD, but both prepregnancy folate deficiency and diabetes have been implicated in some studies.

Persistent truncus arteriosus is a rare cardiac abnormality that has a prevalence of less than 1%.

As a group, atrial septal defects are detected in one child per 1500 live births. PFOs are quite common (appearing in 10–20% of adults), but asymptomatic, so undiagnosed. ASDs make up 30 to 40% of all congenital heart diseases that are seen in adults.

The ostium secundum atrial septal defect accounts for 7% of all congenital heart lesions. This lesion shows a male:female ratio of 1:2.

VSDs are the most common congenital cardiac abnormalities. They are found in 30-60% of all newborns with a congenital heart defect, or about 2-6 per 1000 births. During heart formation, when the heart begins life as a hollow tube, it begins to partition, forming septa. If this does not occur properly it can lead to an opening being left within the ventricular septum. It is debatable whether all those defects are true heart defects, or if some of them are normal phenomena, since most of the trabecular VSDs close spontaneously. Prospective studies give a prevalence of 2-5 per 100 births of trabecular VSDs that close shortly after birth in 80-90% of the cases.

A PDA is sometimes idiopathic. Known risk factors include:

- Preterm birth

- Congenital rubella syndrome

- Chromosomal abnormalities (e.g., Down syndrome)

- Genetic conditions such as Loeys-Dietz syndrome (would also present with other heart defects), Wiedemann-Steiner syndrome, and CHAR syndrome.

Complete vascular rings represent about 0.5-1% of all congenital cardiovascular malformations. The majority of these are double aortic arches.

There is no known gender preference, i.e. males and females are about equally affected. There is also no known ethnic or geographic disposition.

Associated cardiovascular anomalies are found in 10-15% of patients. These include:

- Atrial septal defect (ASD)

- Ventricular septal defect (VSD)

- Patent ductus arteriosus (PDA)

- Tetralogy of Fallot (ToF)

- Transposition of the great arteries (D-TGA)

In terms of the cause of pulmonary atresia, there is uncertainty as to what instigates this congenital heart defect. Potential risk factors that can cause this congenital heart defect are those the pregnant mother may come in contact with, such as:

- Certain medications

- Diet

- Smoking

Hypoplastic right heart syndrome is less common than hypoplastic left heart syndrome which occurs in 4 out of every 10,000 births. [3].

This rare anomaly requires prenatal diagnosis since it needs immediate and emergency treatment. Pregnant women whose pregnancy is complicated with this anomaly should be referred to a level 3 hospital with pediatric cardiology and pediatric cardiothoracic surgical team.[3]

It can be associated with aortic stenosis.

The cause of congenital heart disease may be genetic, environmental, or a combination of both.

When there are holes in the septum that divide the four chambers of the heart the oxygen-rich blood and oxygen-poor blood mix this creates more stress on the heart to pump blood to where oxygen is needed. As a result, you get enlargement of the heart, heart failure (being unable to adequately supply body with needed oxygen, pulmonary hypertension, and pneumonia.

The development of pulmonary hypertension is very serious. And this because the left ventricle is weakened due to its overuse. When this happens, the pressure backs up into the pulmonary veins and the lungs. This type of damage is irreversible which is why immediate treatment is recommended after diagnosis.

The prognosis of tricuspid insufficiency is less favorable for males than females. Furthermore, increased tricuspid insufficiency (regurgitation) severity is an indication of a poorer prognosis according to Nath, et al. It is also important to note that since tricuspid insufficiency most often arises from left heart failure or pulmonary hypertension, the person's prognosis is usually dictated by the prognosis of the latter conditions and not by the tricuspid insufficiency "per se".

Since PDA is usually identified in infants, it is less common in adults, but it can have serious consequences, and is usually corrected surgically upon diagnosis.

Good peer to peer support is available on Facebook. For new and existing parents The group, Transposition of the Great Arteries

For ADULT survivors of D-TGA the Facebook group Mustard or Senning Survivors, gathers several hundred global survivors in their 20s to 50s into a single community. Supporting ADULTS born with TGA that have had a Mustard, Senning, Rastelli or Nikaidoh Heart Procedure *This group is not recommended for Parents of Arterial Switch children.

The prognosis for pulmonary atresia varies for every child, if the condition is left uncorrected it may be fatal, but the prognosis has greatly improved over the years for those with pulmonary atresia. Some factors that affect how well the child does include how well the heart is beating, and the condition of the blood vessels that supply the heart. Most cases of pulmonary atresia can be helped with surgery, if the patient's right ventricle is exceptionally small, many surgeries will be needed in order to help stimulate normal circulation of blood to the heart.If uncorrected, babies with this type of congenital heart disease may only survive for the first few days of life. Many children with pulmonary atresia will go on to lead normal lives, though complications such as endocarditis, stroke and seizures are possible.

Aortopulmonary septal defect is a rare congenital heart disorder accounting for only 0.1-0.3% of congenital heart defects worldwide. It is characterized by a communication between the aortic and pulmonary arteries, with preservation of two normal semilunar valves. It is the result of an incomplete separation of the aorticopulmonary trunk that normally occurs in early fetal development with formation of the spiral septum. Aortopulmonary septal defects occur in isolation in about half of cases, the remainder are associated with more complex heart abnormalities.

Little is known regarding the exact causes of aortic arch anomalies. However, the association with chromosome 22q11 deletion (CATCH 22) implies that a genetic component is likely in certain cases. Esophageal atresia also occurs in some patients with double aortic arch.

The epidemiology of pulmonary valve stenosis can be summed up by the congenital aspect which is the majority of cases, in broad terms PVS is rare in the general population.

Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome.

A VSD can also form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.

The causes of congenital VSD (ventricular septal defect) include the

incomplete looping of the heart during days 24-28 of development. Faults with NKX2.5 gene are usually associated with isolated (non syndromic) ASD in humans when one copy is missing.

As Lutembacher's syndrome is known for ASD and MS, most of the symptoms experienced will be associated with ASD and MS. For most people, they will remain asymptomatic (experience no symptoms) but when symptoms are shown, they are due mainly to ASD and will vary depending on the size of the hole in the atria. If the patient has a large ASD, pulmonary congestion (blood or fluid buildup in the lungs) will happen later but if the patient has a small ASD, symptoms will appear early in the disorder. In general, unless the ASD and mitral stenosis causing Lutembacher's syndrome is severe, symptoms may not appear until the second and third decade of the patient's life. As many of the symptoms are asymptomic and may not appear until later in life, the duration or frequency of the symptoms varies. For symptoms such as palipitations, ventricular overload, heart failure, and pulmonary congenstion, these symptoms may be sudden and not that frequent as they are very severe symptoms. For symptoms such as loud mitral S1, pulmonary S2, mid-diastolic murmur, fatigue, reduced exercise tolerance, weight gain, ankle edema, and right upper quadrant pain, and ascities, these symptoms may be less frequent and severe; their duration may be only a few seconds, minutes, or even months.