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.

Individuals with MVP are at higher risk of bacterial infection of the heart, called infective endocarditis. This risk is approximately three- to eightfold the risk of infective endocarditis in the general population. Until 2007, the American Heart Association recommended prescribing antibiotics before invasive procedures, including those in dental surgery. Thereafter, they concluded that "prophylaxis for dental procedures should be recommended only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis."

Many organisms responsible for endocarditis are slow-growing and may not be easily identified on routine blood cultures (these fastidious organisms require special culture media to grow). These include the HACEK organisms, which are part of the normal oropharyngeal flora and are responsible for perhaps 5 to 10% of infective endocarditis affecting native valves. It is important when considering endocarditis to keep these organisms in mind.

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".

Bicuspid aortic valves are the most common cardiac valvular anomaly, occurring in 1–2% of the general population. It is twice as common in males as in females.

Bicuspid aortic valve is a heritable condition, with a demonstrated association with mutations in the NOTCH1 gene. Its heritability (formula_1) is as high as 89%. Both familial clustering and isolated valve defects have been documented. The incidence of bicuspid aortic valve can be as high as 10% in families affected with the valve problem..Recent studies suggest that BAV is an autosomal dominant condition with incomplete penetrance. Other congenital heart defects are associated with bicuspid aortic valve at various frequencies, including coarctation of the aorta.

Quadricuspid aortic valves are very rare cardiac valvular anomalies with a prevalence of 0.013% to 0.043% of cardiac cases and a prevalence of 1 in 6000 patients that undertake aortic valve surgery. There is a slight male predominance in all of the cases, and the mean age is 50.7.

A patent foramen ovale (PFO) is a small channel that has some hemodynamic consequence; it is a remnant of the fetal foramen ovale, which normally closes at birth. In medical use, the term "patent" means open or unobstructed. In about 25% of people, the foramen ovale fails to close properly, leaving them with a PFO or at least with what some physicians classify as a "pro-PFO", which is a PFO that is normally closed, but can open under increased blood pressure. On echocardiography, shunting of blood may not be noted except when the patient coughs.

Clinically, PFO is linked to stroke, sleep apnea, migraine with aura, and decompression sickness. No cause is established for a foramen ovale to remain open instead of closing naturally, but heredity and genetics may play a role.

The mechanism by which a PFO may play a role in stroke is called paradoxical embolism. In the case of PFO, a blood clot from the venous circulatory system is able to pass from the right atrium directly into the left atrium via the PFO, rather than being filtered by the lungs, and thereupon into systemic circulation toward the brain. PFO is common in patients with atrial septal aneurysms (ASA) which are also linked to cryptogenic (i.e. of unknown cause) strokes.

PFO is more prevalent in patients with cryptogenic stroke than in patients with a stroke of known cause. While PFO is present in only 25% in the general population, the probability of someone having a PFO increases to about 40 to 50% in patients who have had a cryptogenic stroke. Statistically speaking, this is particularly true for patients who have a stroke before the age of 55.

PFO is not treated in the absence of other symptoms, and no consensus exists on treatment of PFO even in the presence of transient ischemic attack or stroke. Moreover, no "gold standard" treatment option is known. However, treatments for PFO include surgical closure and percutaneous device closure, as well as medical therapies such as anticoagulant therapy, and antiplatelet agents.

Research studies of the efficacy of surgical closure treatments versus medical therapies of PFOs in preventing the recurrence of strokes have been conducted; the results are mixed, although “as-treated” and “per-protocol” analyses were positive for closure devices.

PFO closure devices may be implanted via catheter-based procedures, and using a variety of closure devices.

Debate exists within the neurology and cardiology communities about the role of a PFO in cryptogenic neurologic events such as strokes and transient ischemia attacks without any other potential cause. Some data suggest that PFOs may be involved in the pathogenesis of some migraine headaches. Several clinical trials are currently underway to investigate the role of PFO in these clinical situations.

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.

In a retrospective analysis of over 1,300 newborns (born between 1996 and 2006) from 24 children’s hospitals in the United States, researchers at Cincinnati Children’s Hospital in Ohio found that babies with HLHS were more likely to be born in summer months, suggesting that seasonality and environmental factors may play a significant role in causation.

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

The following table includes the main types of valvular stenosis and regurgitation. Major types of valvular heart disease not included in the table include mitral valve prolapse, rheumatic heart disease and endocarditis.

Prior to the strict criteria for the diagnosis of mitral valve prolapse, as described above, the incidence of mitral valve prolapse in the general population varied greatly. Some studies estimated the incidence of mitral valve prolapse at 5 to 15 percent or even higher. One study suggested MVP in up to 35% of healthy teenagers.

Recent elucidation of mitral valve anatomy and the development of three-dimensional echocardiography have resulted in improved diagnostic criteria, and the true prevalence of MVP based on these criteria is estimated at 2-3%. As part of the Framingham Heart Study, for example, the prevalence of mitral valve prolapse in Framingham, MA was estimated at 2.4%. There was a near-even split between classic and nonclassic MVP, with no significant age or sex discrimination. MVP is observed in 7% of autopsies in the United States.

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

Inflammation of the heart valves due to any cause is called valvular endocarditis; this is usually due to bacterial infection but may also be due to cancer (marantic endocarditis), certain autoimmune conditions (Libman-Sacks endocarditis, seen in systemic lupus erythematosus) and hypereosinophilic syndrome (Loeffler endocarditis). Certain medications have been associated with valvular heart disease, most prominently ergotamine derivatives pergolide and cabergoline.

Valvular heart disease resulting from rheumatic fever is referred to as "rheumatic heart disease". Damage to the heart valves follows infection with beta-hemolytic bacteria, such as typically of the respiratory tract. Pathogenesis is dependent on cross reaction of M proteins produced by bacteria with the myocardium. This results in generalized inflammation in the heart, this manifests in the mitral valve as vegetations, and thickening or fusion of the leaflets, leading to a severely compromised buttonhole valve.

Rheumatic heart disease typically only involves the mitral valve (70% of cases), though in some cases the aortic and mitral valves are both involved (25%). Involvement of other heart valves without damage to the mitral are exceedingly rare.

While developed countries once had a significant burden of rheumatic fever and rheumatic heart disease, medical advances and improved social conditions have dramatically reduced their incidence. Many developing countries, as well as indigenous populations within developed countries, still carry a significant burden of rheumatic fever and rheumatic heart disease and there has been a resurgence in efforts to eradicate the diseases in these populations.

There is no exact mechanism for Lutembacher's syndrome but instead a combination of disorders as the result of Atrial septal defect (ASD) and/or Mitral valve stenosis.

Bicuspid aortic valve abnormality is seen in 1 to 2 percent of all live births. It is associated with a number of mutations affecting Notch signalling pathway.

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.

The risk of death in individuals with aortic insufficiency, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2 percent per year. Risk increases if the ejection fraction decreases or if the individual develops symptoms.

Individuals with chronic (severe) aortic regurgitation follow a course that once symptoms appear, surgical intervention is needed. AI is fatal in 10 to 20% of individuals who do not undergo surgery for this condition. Left ventricle dysfunction determines to an extent the outlook for severity of aortic regurgitation cases.

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.

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.

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.

In Heyde's syndrome, aortic stenosis is associated with gastrointestinal bleeding due to angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenotic valve.

If untreated, severe symptomatic aortic stenosis carries a poor prognosis with a 2-year mortality rate of 50-60% and a 3-year survival rate of less than 30%. Prognosis after aortic valve replacement for people who are younger than 65 is about five years less than that of the general population; for people older than 65 it is about the same.

Significant mitral valve regurgitation has a prevalence of approximately 2% of the population, affecting males and females equally. It is one of the two most common valvular heart diseases in the elderly.

Almost all cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Uncommon causes of mitral stenosis are calcification of the mitral valve leaflets, and as a form of congenital heart disease. However, there are primary causes of mitral stenosis that emanate from a cleft mitral valve. It is the most common valvular heart disease in pregnancy.

Other causes include infective endocarditis where the vegetations may favor increase risk of stenosis. Other rare causes include mitral annular calcification, endomyocardial fibroelastosis, malignant carcinoid syndrome, systemic lupus erythematosus, whipple disease, fabry disease, and rheumatoid arthritis. hurler' disease, hunter's disease, amyloidosis.

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.