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.

Individuals with mitral valve prolapse, particularly those without symptoms, often require no treatment. Those with mitral valve prolapse and symptoms of dysautonomia (palpitations, chest pain) may benefit from beta-blockers (e.g., propranolol). Patients with prior stroke and/or atrial fibrillation may require blood thinners, such as aspirin or warfarin. In rare instances when mitral valve prolapse is associated with severe mitral regurgitation, mitral valve repair or surgical replacement may be necessary. Mitral valve repair is generally considered preferable to replacement. Current ACC/AHA guidelines promote repair of mitral valve in patients before symptoms of heart failure develop. Symptomatic patients, those with evidence of diminished left ventricular function, or those with left ventricular dilatation need urgent attention.

Aortic insufficiency or aortic regurgitation can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction. Surgical treatment in asymptomatic patients has been recommended if the ejection fraction falls to 50% or below, in the face of progressive and severe left ventricular dilatation, or with symptoms or abnormal response to exercise testing. For both groups of patients, surgery before the development of worsening ejection fraction/LV dilatation is expected to reduce the risk of sudden death, and is associated with lower peri-operative mortality. Also, surgery is optimally performed immediately in acute cases.

The effect of statins on the progression of AS is unclear. The latest trials do not show any benefit in slowing AS progression, but did demonstrate a decrease in ischemic cardiovascular events.

In general, medical therapy has relatively poor efficacy in treating aortic stenosis. However, it may be useful to manage commonly coexisting conditions that correlate with aortic stenosis:

- Any angina is generally treated with beta-blockers and/or calcium blockers. Nitrates are contraindicated due to their potential to cause profound hypotension in aortic stenosis.

- Any hypertension is treated aggressively, but caution must be taken in administering beta-blockers.

- Any heart failure is generally treated with digoxin and diuretics, and, if not contraindicated, cautious administration of ACE inhibitors.

While observational studies demonstrated an association between lowered cholesterol with statins and decreased progression, a randomized clinical trial published in 2005 failed to find any effect on calcific aortic stenosis. A 2007 study did demonstrate a slowing of aortic stenosis with the statin rosuvastatin.

Treatment is generally not necessary in people without symptoms. In moderate cases, echocardiography is performed every 1–2 years to monitor the progression, possibly complemented with a cardiac stress test. In severe cases, echocardiography is performed every 3–6 months. In both moderate and mild cases, the person should immediately make a revisit or be admitted for inpatient care if any new related symptoms appear. There are no therapeutic options currently available to treat people with aortic valve stenosis; however, studies have indicated that the disease occurs as a result of active cellular processes, suggesting that targeting these processes may lead to viable therapeutic approaches.

Medical therapy of chronic aortic insufficiency that is stable and asymptomatic involves the use of vasodilators. Trials have shown a short term benefit in the use of ACE inhibitors or angiotensin II receptor antagonists, nifedipine, and hydralazine in improving left ventricular wall stress, ejection fraction, and mass. The goal in using these pharmacologic agents is to decrease the afterload so that the left ventricle is somewhat spared. The regurgitant fraction may not change significantly, since the gradient between the aortic and left ventricular pressures is usually fairly low at the initiation of treatment. Other rather conservative medical treatments for stable and asymptomatic cases include low sodium diet, diuretics, digoxin, calcium blockers and avoiding very strenuous activity.

As of 2007, the American Heart Association no longer recommends antibiotics for endocarditis prophylaxis before certain procedures in patients with aortic insufficiency. Antibiotic prophylaxis to prevent endocarditis before gastrointestinal or genitourinary procedures is no longer recommended for any patient with valvular disease. Cardiac stress test is useful in identifying individuals that may be best suited for surgical intervention. Radionuclide angiography is recommended and useful when the systolic wall stress is calculated and combined to the results.

The treatment of mitral insufficiency depends on the acuteness of the disease and whether there are associated signs of hemodynamic compromise.

In acute MI secondary to a mechanical defect in the heart (i.e., rupture of a papillary muscle or chordae tendineae), the treatment of choice is mitral valve surgery. If the patient is hypotensive prior to the surgical procedure, an intra-aortic balloon pump may be placed in order to improve perfusion of the organs and to decrease the degree of MI.

If the individual with acute MI is normotensive, vasodilators may be of use to decrease the afterload seen by the left ventricle and thereby decrease the regurgitant fraction. The vasodilator most commonly used is nitroprusside.

Individuals with chronic MI can be treated with vasodilators as well to decrease afterload. In the chronic state, the most commonly used agents are ACE inhibitors and hydralazine. Studies have shown that the use of ACE inhibitors and hydralazine can delay surgical treatment of mitral insufficiency. The current guidelines for treatment of MI limit the use of vasodilators to individuals with hypertension, however. Any hypertension is treated aggressively, e.g. by diuretics and a low-sodium diet. In both hypertensive and normotensive cases, digoxin and antiarrhythmics are also indicated. Also, chronic anticoagulation is given where there is concomitant mitral valve prolapse or atrial fibrillation. In general, medical therapy is non-curative and is used for mild-to-moderate regurgitation or in patients unable to tolerate surgery.

Surgery is curative of mitral valve regurgitation. There are two surgical options for the treatment of MI: mitral valve replacement and mitral valve repair. Mitral valve repair is preferred to mitral valve replacement where a repair is feasible as bioprosthetic replacement valves have a limited lifespan of 10 to 15 years, whereas synthetic replacement valves require ongoing use of blood thinners to reduce the risk of stroke. There are two general categories of approaches to mitral valve repair: Resection of the prolapsed valvular segment (sometimes referred to as the 'Carpentier' approach), and installation of artificial chordae to "anchor" the prolapsed segment to the papillary muscle (sometimes referred to as the 'David' approach). With the resection approach, any prolapsing tissue is resected, in effect removing the hole through which the blood is leaking. In the artificial chordae approach, ePTFE (expanded polytetrafluoroethylene, or Gore-Tex) sutures are used to replace the broken or stretched chordae tendonae, bringing the natural tissue back into the physiological position, thus restoring the natural anatomy of the valve. With both techniques, an annuloplasty ring is typically secured to the annulus, or opening of the mitral valve, to provide additional structural support. In some cases, the "double orifice" (or 'Alfieri') technique for mitral valve repair, the opening of the mitral valve is sewn closed in the middle, leaving the two ends still able to open. This ensures that the mitral valve closes when the left ventricle pumps blood, yet allows the mitral valve to open at the two ends to fill the left ventricle with blood before it pumps. In general, mitral valve surgery requires "open-heart" surgery in which the heart is arrested and the patient is placed on a heart-lung machine (cardiopulmonary bypass). This allows the complex surgery to proceed in a still environment.

Due to the physiological stress associated with open-heart surgery, elderly and very sick patients may be subject to increased risk, and may not be candidates for this type of surgery. As a consequence, there are attempts to identify means of correcting MI on a beating heart. The Alfieri technique for instance, has been replicated using a percutaneous catheter technique, which installs a "MitraClip" device to hold the middle of the mitral valve closed.

Treatment is not necessary in asymptomatic patients.

The treatment options for mitral stenosis include medical management, mitral valve replacement by surgery, and percutaneous mitral valvuloplasty by balloon catheter.

The indication for invasive treatment with either a mitral valve replacement or valvuloplasty is NYHA functional class III or IV symptoms.

Another option is balloon dilatation. To determine which patients would benefit from percutaneous balloon mitral valvuloplasty, a scoring system has been developed. Scoring is based on 4 echocardiographic criteria: leaflet mobility, leaflet thickening, subvalvar thickening, and calcification. Individuals with a score of ≥ 8 tended to have suboptimal results. Superb results with valvotomy are seen in individuals with a crisp opening snap, score < 8, and no calcium in the commissures.

Treatment also focuses on concomitant conditions often seen in mitral stenosis:

- Any angina is treated with short-acting nitrovasodilators, beta-blockers and/or calcium blockers

- Any hypertension is treated aggressively, but caution must be taken in administering beta-blockers

- Any heart failure is treated with digoxin, diuretics, nitrovasodilators and, if not contraindicated, cautious inpatient administration of ACE inhibitors

Indications for surgery for chronic MI include signs of left ventricular dysfunction with ejection fraction less than 60%, severe pulmonary hypertension with pulmonary artery systolic pressure greater than 50 mmHg at rest or 60 mmHg during activity, and new onset atrial fibrillation.

Tricuspid valve stenosis itself usually doesn't require treatment. If stenosis is mild, monitoring the condition closely suffices. However, severe stenosis, or damage to other valves in the heart, may require surgical repair or replacement.

The treatment is usually by surgery (tricuspid valve replacement) or percutaneous balloon valvuloplasty. The resultant tricuspid regurgitation from percutaneous treatment is better tolerated than the insufficiency occurring during mitral valvuloplasty.

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.

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.

The natural history of mitral stenosis secondary to rheumatic fever (the most common cause) is an asymptomatic latent phase following the initial episode of rheumatic fever. This latent period lasts an average of 16.3 ± 5.2 years. Once symptoms of mitral stenosis begin to develop, progression to severe disability takes 9.2 ± 4.3 years.

In individuals having been offered mitral valve surgery but refused, "survival" with medical therapy alone was 44 ± 6% at 5 years, and 32 ± 8% at 10 years after they were offered correction.

Bicuspid aortic valve (BAV) is an inherited form of heart disease in which two of the leaflets of the aortic valve fuse during development in the womb resulting in a two-leaflet valve (bicuspid valve) instead of the normal three-leaflet valve (tricuspid). BAV is the most common cause of heart disease present at birth and affects approximately 1.3% of adults. Normally, the mitral valve is the only bicuspid valve and this is situated between the heart's left atrium and left ventricle. Heart valves play a crucial role in ensuring the unidirectional flow of blood from the atrium to the ventricles, or from the ventricle to the aorta or pulmonary trunk.

A significant number of people with hypertrophic cardiomyopathy do not have any symptoms and will have normal life expectancies, although they should avoid particularly strenuous activities or competitive athletics, and should be screened for risk factors for sudden cardiac death. In people with resting or inducible outflow obstructions, situations that will cause dehydration or vasodilation (such as the use of vasodilatory or diuretic blood pressure medications) should be avoided. Septal reduction therapy is not recommended in asymptomatic people.

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.

Tricuspid Valve Stenosis is a valvular heart disease that narrows the opening of the heart's tricuspid valve. It is a relatively rare condition that causes stenosis-increased restriction of blood flow through the valve.

To treat Lutembacher's syndrome, the underlying causes of the disorder must first be treated: mitral stenosis and atrial septal defect. Lutembacher's syndrome is usually treated surgically with treatments such as:

- percutaneous transcatheter therapy for MS

- Device closure of ASD

Percutaneous transcatheter treatment for the MS can include transcatheter therapies of such as balloon valuloplasty.

Until recently, it was generally assumed that the prognosis for individuals with diastolic dysfunction and associated intermittent pulmonary edema was better than those with systolic dysfunction. In fact, in two studies appearing in the New England Journal of Medicine in 2006, evidence was presented to suggest that the prognosis in diastolic dysfunction is the same as that in systolic dysfunction.

Prior to correction of an ASD, an evaluation is made of the severity of the individual's pulmonary hypertension (if present at all) and whether it is reversible (closure of an ASD may be recommended for prevention purposes, to avoid such a complication in the first place. Pulmonary hypertension is not always present in adults who are diagnosed with an ASD in adulthood).

If pulmonary hypertension is present, the evaluation may include a right heart catheterization. This involves placing a catheter in the venous system of the heart and measuring pressures and oxygen saturations in the superior vena cava, inferior vena cava, right atrium, right ventricle, and pulmonary artery, and in the wedge position. Individuals with a pulmonary vascular resistance (PVR) less than 7 wood units show regression of symptoms (including NYHA functional class). However, individuals with a PVR greater than 15 wood units have increased mortality associated with closure of the ASD.

If the pulmonary arterial pressure is more than two-thirds of the systemic systolic pressure, a net left-to-right shunt should occur at least 1.5:1 or evidence of reversibility of the shunt when given pulmonary artery vasodilators prior to surgery. (If Eisenmenger's physiology has set in, the right-to-left shunt must be shown to be reversible with pulmonary artery vasodilators prior to surgery.)

Surgical mortality due to closure of an ASD is lowest when the procedure is performed prior to the development of significant pulmonary hypertension. The lowest mortality rates are achieved in individuals with a pulmonary artery systolic pressure less than 40 mmHg. If Eisenmenger's syndrome has occurred, a significant risk of mortality exists regardless of the method of closure of the ASD. In individuals who have developed Eisenmenger's syndrome, the pressure in the right ventricle has raised high enough to reverse the shunt in the atria. If the ASD is then closed, the afterload that the right ventricle has to act against has suddenly increased. This may cause immediate right ventricular failure, since it may not be able to pump the blood against the pulmonary hypertension.

Due to the communication between the atria that occurs in ASDs, disease entities or complications from the condition are possible. Patients with an uncorrected atrial septal defect may be at increased risk for developing a cardiac arrhythmia, as well as more frequent respiratory infections.

To treat ASD a device closure can be used. In fact an ASD closure is often recommended for certain cases such as with a patient who has significant left-to-right shunt with a pulmonary and/or systemic flow fraction of Qp/Qs >1.5. It is best to perform this procedure/surgery between the ages of 2–4 years. The closure is done by two methods: interventionally or surgically.

Heart valve dysplasia is a congenital heart defect which affects the aortic, pulmonary, mitral, and tricuspid heart valves. Dysplasia of the mitral and tricuspid valves can cause leakage of blood or stenosis.

Dysplasia of the mitral and tricuspid valves - also known as the atrioventricular (AV) valves - can appear as thickened, shortened, or notched valves. The chordae tendinae can be fused or thickened. The papillary muscles can be enlarged or atrophied. The cause is unknown, but genetics play a large role. Dogs and cats with tricuspid valve dysplasia often also have an open foramen ovale, an atrial septal defect, or inflammation of the right atrial epicardium. In dogs, tricuspid valve dysplasia can be similar to Ebstein's anomaly in humans.

Mitral valve stenosis is one of the most common congenital heart defects in cats. In dogs, it is most commonly found in Great Danes, German Shepherd Dogs, Bull Terriers, Golden Retrievers, Newfoundlands, and Mastiffs. Tricuspid valve dysplasia is most common in the Old English Sheepdog, German Shepherd Dog, Weimaraner, Labrador Retriever, Great Pyrenees, and sometimes the Papillon. It is inherited in the Labrador Retriever.

The disease and symptoms are similar to progression of acquired valve disease in older dogs. Valve leakage leads to heart enlargement, arrhythmias, and congestive heart failure. Heart valve dysplasia can be tolerated for years or progress to heart failure in the first year of life. Diagnosis is with an echocardiogram. The prognosis is poor with significant heart enlargement.

In adults and children found to have coarctation, treatment is conservative if asymptomatic, but may require surgical resection of the narrow segment if there is arterial hypertension. The first operations to treat coarctation were carried out by Clarence Crafoord in Sweden in 1944. In some cases angioplasty can be performed to dilate the narrowed artery, with or without the placement of a stent graft.

For fetuses at high risk for developing coarctation, a novel experimental treatment approach is being investigated, wherein the mother inhales 45% oxygen three times a day (3 x 3–4 hours) beyond 34 weeks of gestation. The oxygen is transferred via the placenta to the fetus and results in dilatation of the fetal lung vessels. As a consequence, the flow of blood through the fetal circulatory system increases, including that through the underdeveloped arch. In suitable fetuses, marked increases in aortic arch dimensions have been observed over treatment periods of about two to three weeks.

The long term outcome is very good. Some patients may, however, develop narrowing (stenosis) or dilatation at the previous coarctation site. All patients with unrepaired or repaired aortic coarctation require follow up in specialized Congenital Heart Disease centers.

The primary goal of medications is to relieve symptoms such as chest pain, shortness of breath, and palpitations. Beta blockers are considered first-line agents, as they can slow down the heart rate and decrease the likelihood of ectopic beats. For people who cannot tolerate beta blockers, nondihydropyridine calcium channel blockers such as verapamil can be used, but are potentially harmful in people who also have low blood pressure or severe shortness of breath at rest. These medications also decrease the heart rate, though their use in people with severe outflow obstruction, elevated pulmonary artery wedge pressure, and low blood pressures should be done with caution. Dihydropyridine calcium channel blockers should be avoided in people with evidence of obstruction. For people whose symptoms are not relieved by the above treatments, disopyramide can be considered for further symptom relief. Diuretics can be considered for people with evidence of fluid overload, though cautiously used in those with evidence of obstruction. People who continue to have symptoms despite drug therapy can consider more invasive therapies. Intravenous phenylephrine (or another pure vasoconstricting agent) can be used in the acute setting of low blood pressure in those with obstructive hypertrophic cardiomyopathy who do not respond to fluid administration.