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.

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.

A surgical treatment for AI is aortic valve replacement; this is currently an open-heart procedure. In the case of severe "acute" aortic insufficiency, all individuals should undergo surgery, if there are no absolute contraindications (for surgery). Individuals with bacteremia with aortic valve endocarditis should not wait for treatment with antibiotics to take effect, given the high mortality associated with the acute AI. Replacement with an aortic valve homograft should be performed if feasible.

Aortic valve repair or aortic valve reconstruction describes the reconstruction of both form and function of the native and dysfunctioning aortic valve. Most frequently it is applied for the treatment of aortic regurgitation. It can also become necessary for the treatment of an aortic aneurysm, less frequently for congenital aortic stenosis.

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

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.

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.

Surgical treatment involves resection of the stenosed segment and re-anastomsis. Two complications specific to this surgery are Left recurrent nerve palsy and chylothorax, as the recurrent laryngeal nerve and thoracic duct are in the vicinity. Chylothorax is a troublesome complication and is usually managed conservatively by adjusting the diet to eliminate long chain fatty acids and supplementing medium chain triglycerides. When conservative management fails surgical intervention is required. Fluorescein dye can aid in the localisation of chyle leak.

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.

Medical therapy of aneurysm of the aortic sinus includes blood pressure control through the use of drugs, such as beta blockers.

Another approach is surgical repair. The determination to perform surgery is usually based upon the diameter of the aortic root (with 5 centimeters being a rule of thumb - a normal size is 2-3 centimeters) and the rate of increase in its size (as determined through repeated echocardiography).

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.

Aortic dissection generally presents as a hypertensive emergency, and the prime consideration of medical management is strict blood pressure control. The target blood pressure should be a mean arterial pressure (MAP) of 60 to 75 mmHg, or the lowest blood pressure tolerated. Initial decreases should be by about 20%.

Another factor is to reduce the shear-force dP/dt (force of ejection of blood from the left ventricle). Long-term management of physical, emotional, and psychological stresses are important to controlling blood pressure.

Beta blockers are the first-line treatment for patients with acute and chronic aortic dissection. In acute dissection, fast-acting agents which can be given intravenously and have doses that are easier to adjust (such as esmolol, propranolol, or labetalol) are preferred. Vasodilators such as sodium nitroprusside can be considered for people with ongoing high blood pressure, but they should never be used alone, as they often stimulate a reflexive increase in the heart rate.

Calcium channel blockers can be used in the treatment of aortic dissection, particularly if a contraindication to the use of beta blockers exists. The calcium channel blockers typically used are verapamil and diltiazem, because of their combined vasodilator and negative inotropic effects.

If the individual has refractory hypertension (persistent hypertension on the maximum doses of three different classes of antihypertensive agents), an involvement of the renal arteries in the aortic dissection plane should be considered.

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.

The Norwood procedure is a procedure to correct fetal aortic stenosis that occurs after birth. This typically consists of three surgeries creating and removing shunts. The atrial septum is removed, the aortic arch is reconstructed to remove any hypoplasia, and then the main pulmonary artery is connected into this reconstructed arch, resulting in the right ventricle ejecting directly into systemic circulation. In the end, the right ventricle is pumping blood to systemic circulation and to the lungs. However, this procedure carries a very high risk of failure and the patient will likely require a heart transplant.

Another treatment option is to correct the stenosis in utero. In this procedure, fetal positioning is crucial. It is important that the left chest is located anteriorly, and that there are no limbs between the uterine wall and the apex of the left ventricle. The LV apex needs to be within 9 cm of the abdominal wall and the left ventricle outflow track has to be parallel to the intended cannula course in order for the wire to be blindly directed at the aortic valve. A 11.5 cm long, 19-gauge cannula and stylet needle passes through the mother’s abdomen, uterine wall, and fetal chest wall into the left ventricle of the fetus. Then a 0.014 inch guide wire is passed across the stenosis aortic valve, where a balloon is inflated to stretch the aortic annulus.

An alternative to the Norwood procedure is known as the hybrid procedure, was developed in 2008. In the hybrid procedure, bilateral pulmonary artery bands are positioned to limit pulmonary flow while, at the same time, placing a stent in the ductus arteriosus to hold it open. This maintains the connection between the aorta and the systemic circulation. A balloon atrial septostomy is also done. This ensures that there is enough of a connection between the two atria of the heart to provide open blood flow and mixing of oxygen rich and poor blood This procedure spares the baby from undergoing open heart surgery until they are older. They typically come back at 4–6 months of age when they are stronger for the open heart surgery.

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.

Mitral valvuloplasty is a minimally invasive therapeutic procedure to correct an uncomplicated mitral stenosis by dilating the valve using a balloon.

Under local anaesthetic, a catheter with a special balloon is passed from the right femoral vein, up the inferior vena cava and into the right atrium. The interatrial septum is punctured and the catheter passed into the left atrium using a "trans-septal technique." The balloon is sub-divided into 3 segments and is dilated in 3 stages. First, the distal portion (lying in the left ventricle) is inflated and pulled against the valve cusps. Second, the proximal portion is dilated, in order to fix the centre segment at the valve orifice. Finally, the central section is inflated, this should take no longer than 30 seconds, since full inflation obstructs the valve and causes congestion, leading to circulatory arrest and flash pulmonary edema.

With careful patient pre-selection, percutaneous balloon mitral valvuloplasty (PBMV) is associated with good success rates and a low rate of complications. By far the most serious adverse event is the occurrence of acute severe mitral regurgitation. Severe mitral regurgitation usually results from a tear in one of the valve leaflets or the subvalvular apparatus. It can lead to pulmonary edema and hemodynamic compromise, necessitating urgent surgical mitral valve replacement.

Other serious complications with PBMV usually relate to the technique of trans-septal puncture (TSP). The ideal site for TSP is the region of the fossa ovalis in the inter-atrial septum. Occasionally, however, the sharp needle used for TSP may inadvertently traumatize other cardiac structures, leading to cardiac tamponade or serious blood loss.

Although the immediate results of PBMV are often quite gratifying, the procedure does not provide permanent relief from mitral stenosis. Regular follow-up is mandatory, to detect restenosis. Long-term follow-up data from patients undergoing PBMV indicates that up to 70-75% individuals can be free of restenosis 10 years following the procedure. The number falls to about 40% 15 years post-PBMV.

Without life-prolonging interventions, HLHS is fatal, but with intervention, an infant may survive. A cardiothoracic surgeon may perform a series of operations or a full heart transplant. While surgical intervention has emerged as the standard of care in the United States, other national health systems, notably in France, approach diagnosis of HLHS in a more conservative manner, with an emphasis on termination of pregnancy or compassionate care after delivery.

Before surgery, the ductus must be kept open to allow blood-flow using medication containing prostaglandin. Air with less oxygen than normal is used for infants with hypoplastic left heart syndrome. These low oxygen levels increases the pulmonary vascular resistance (PVR) and thus improve blood flow to the rest of the body, due to the greater pressure difference between the lungs and body. Achieving oxygen levels below atmosphere requires the use of inhaled nitrogen. Nitric oxide is a potent pulmonary vasodilator, and thus reduces PVR and improves venous return. Any factor that increases PVR will impede right sided flow.

A device, known as the Amplatzer muscular VSD occluder, may be used to close certain VSDs. It was initially approved in 2009. It appears to work well and be safe. The cost is also lower than having open heart surgery. The device is placed through a small incision in the groin.

The Amplatzer septal occluder was shown to have full closure of the ventricular defect within the 24 hours of placement. It has a low risk of embolism after implantation. Some tricuspid valve regurgitation was shown after the procedure that could possibly be due from the right ventricular disc. There have been some reports that the Amplatzer septal occluder may cause life-threatening erosion of the tissue inside the heart. This occurs in one percent of people implanted with the device and requires immediate open-heart surgery. This erosion occurs due to improper sizing of the device resulting with it being too large for the defect, causing rubbing of the septal tissue and erosion.

Certain antiparkinson drugs, although targeted at dopaminergic receptors, cross-react with serotoninergic 5-HT receptors as well, and have been reported to cause cardiac fibrosis.

These drugs include pergolide and cabergoline.

Surgical operations to assist with hypoplastic left heart are complex and need to be individualized for each patient. A cardiologist must assess all medical and surgical options on a case-by-case basis.

Currently, infants undergo either the staged reconstructive surgery (Norwood or Sano procedure within a few days of birth, Glenn or "Hemi-Fontan procedure" at 3 to 6 months of age, and the Fontan procedure at 1 1/2 to 5 years of age) or cardiac transplantation. Current expectations are that 70% of those with HLHS will reach adulthood. Many studies show that the higher the volume (number of surgeries performed) at a hospital, the lower the mortality (death) rate. Factors that increase an infant's risk include lower birth weight, additional congenital anomalies, a genetic syndrome or those with a highly restrictive atrial septum.) For patients without these additional risk factors, 5 year survival now approaches 80%. Further, studies show that about 50% of those children who survived surgery in the early development of staged reconstruction have developmental delay or need special education; about 25% of these surgical survivors have severe disabilities. There is growing evidence that while the incidence of developmental and behavioral disabilities continues to be higher than that in the general population, children operated upon in the more current era have shown significantly better neurological outcomes. An alternative to the traditional Norwood is the Hybrid procedure.

Some physicians offer "compassionate care", instead of the surgeries, which results in the child's death, usually within 2 weeks of birth. Compassionate care is overseen by a physician, and may be carried out either in the hospital or at home. However, due to the vast improvement of surgical intervention, with many hospitals achieving over 90% survival, there is debate on whether or not "compassionate care" should still be offered to families. A study in 2003 concluded that a selection of physicians who are experts in the care of children with HLHS were evenly split when asked what they would do if their own children were born with HLHS, with 1/3 stating that they would choose surgery, 1/3 stating that they would choose palliative (compassionate) treatment without surgery, and 1/3 stating that they are uncertain which choice they would make.

The three-stage procedure is a palliative procedure (not a cure), as the child's circulation is made to work with only two of the heart's four chambers.

Pergolide was an antiparkinson medications that was in decreasing use since reported in 2003 to be associated with cardiac fibrosis. In March 2007, pergolide was withdrawn from the U.S. market due to serious valvular damage that was shown in two independent studies.

Tet spells may be treated with beta-blockers such as propranolol, but acute episodes require rapid intervention with morphine or intranasal fentanyl to reduce ventilatory drive, a vasopressor such as phenylephrine, or norepinephrine to increase systemic vascular resistance, and IV fluids for volume expansion.

Oxygen (100%) may be effective in treating spells because it is a potent pulmonary vasodilator and systemic vasoconstrictor. This allows more blood flow to the lungs by decreasing shunting of deoxygenated blood from the right to left ventricle through the VSD. There are also simple procedures such as squatting and the knee chest position which increase systemic vascular resistance and decrease right-to-left shunting of deoxygenated blood into the systemic circulation.

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.

Type 1 and Type 2 FAD call for the same treatment: immediate surgery to replace the aorta. Surgery is required due to the high risk of mortality. Type 3 is less severe and requires the maintenance of blood pressure through diet and exercise. Upon diagnosing someone with FAD intravenous antihypertensive treatment is frequently used. Often intravenous sodium nitroprusside is used for its efficiency in lessening the pulsatile load thus reducing blood pressure. Reducing this force slows the progression of the dissection. Surgical success depends on age, severity of symptoms, postoperative organ dysfunction and stroke. Surgical intervention is always indicated in Type 1 cases. Aortic surgery is palliative, not curative. The goal is to merely to prevent rupture, restore blood flow, and fix any aortic valve dysfunction. Post operative protocols include frequent monitoring of the aorta diameter. Statins and beta blockers are also popular treatments used to reduce future plaque build up and blockage of epinephrine receptors as a way to control heart rate and blood pressure.

Long term treatment should also include regular check ups every 3 to 6 months. A CT scan or MRI is recommended, along with required chest x-rays. Antihypertensive therapy with beta adrenergic antagonists is required regardless of medical versus surgical treatment. Ten to twenty percent of those who choose surgical intervention are re-operated on due to compression, aneurysm development or blood leakage.

The size cut off for aortic aneurysm is crucial to its treatment. A thoracic aorta greater than 4.5 cm is generally defined as aneurysmal, while a size greater than 6 cm is the distinction for treatment, which can be either endovascular or surgical, with the former reserved for pathology at the descending aorta.

Indication for surgery may depend upon the size of the aneurysm. Aneurysms in the ascending aorta may require surgery at a smaller size than aneurysms in the descending aorta.

Treatment may be via open or via endovascular means.