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.

The cause of cardiomegaly is not well understood and many cases of cardiomegaly are idiopathic (having no known cause). Prevention of cardiomegaly starts with detection. If a person has a family history of cardiomegaly, one should let one's doctor know so that treatments can be implemented to help prevent worsening of the condition. In addition, prevention includes avoiding certain lifestyle risk factors such as tobacco use and controlling one's high cholesterol, high blood pressure, and diabetes. Non-lifestyle risk factors include family history of cardiomegaly, coronary artery disease (CAD), congenital heart failure, Atherosclerotic disease, valvular heart disease, exposure to cardiac toxins, sleep disordered breathing (such as sleep apnea), sustained cardiac arrhythmias, abnormal electrocardiograms, and cardiomegaly on chest X-ray. Lifestyle factors which can help prevent cardiomegaly include eating a healthy diet, controlling blood pressure, exercise, medications, and not abusing alcohol and cocaine. Current research and the evidence of previous cases link the following (below) as possible causes of cardiomegaly.

The most common causes of Cardiomegaly are congenital (patients are born with the condition based on a genetic inheritance), high blood pressure which can enlarge the left ventricle causing the heart muscle to weaken over time, and coronary artery disease that creates blockages in the heart's blood supply, which can bring on a cardiac infarction (heart attack) leading to tissue death which causes other areas of the heart to work harder, increasing the heart size.

Other possible causes include:

- Heart Valve Disease

- Cardiomyopathy (disease to the heart muscle)

- Pulmonary Hypertension

- Pericardial Effusion (fluid around the heart)

- Thyroid Disorders

- Hemochromatosis (excessive iron in the blood)

- Other rare diseases like Amyloidosis

- Viral infection of the heart

- Pregnancy, with enlarged heart developing around the time of delivery (peripartum cardiomyopathy)

- Kidney disease requiring dialysis

- Alcohol or cocaine abuse

- HIV infection

- Diabetes

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.

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".

Elevated prevalence of cardiac fibrosis and related valvopathies was found to be associated with use of a number of unrelated drugs following long-term statistical analysis once the drugs had been on the market for some time. The cause of this was unknown at the time, but eventually it was realised that all the implicated drugs acted as agonists at 5-HT receptors in the heart in addition to their intended sites of action elsewhere in the body.

The precise mechanisms involved remain elusive however, as while the cardiotoxicity shows some dose-response relationship, it does not always develop, and consistent daily use over an extended period tends to be most strongly predictive of development of valvopathy.

The drugs most classically associated with the condition are weight loss drugs such as fenfluramine and chlorphentermine, and antiparkinson drugs such as pergolide and cabergoline, which are prescribed to be taken several times a day, often for months or years at a time.

Drugs which act as 5-HT agonists tend to be less likely to cause heart problems when used sparingly.

The heart valve changes seen with moderate and intermittent use can result in permanent damage and life-threatening heart problems if use of the causative drug is increased or continued, however longitudinal studies of former patients suggest that the damage will heal over time to some extent at least.

Some appetite suppressant drugs such as fenfluramine (which in combination with phentermine was marketed as "Pondimin" and commonly referred to as fen-phen), chlorphentermine, and aminorex (along with its analogue 4-Methylaminorex which has seen sporadic use as a recreational drug) induce a similar pattern of cardiac fibrosis (and pulmonary hypertension), apparently by over-stimulating 5HT receptors on the cardiac fibroblast cells.

These drugs consequently tend to cause increased risk of heart valve damage and subsequent heart failure, which eventually led to them being withdrawn from the market.

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.

Treatments for cardiomegaly include a combination of medication treatment and medical/surgical procedures. Below are some of the treatment options for individuals with cardiomegaly:

Medications

- Diuretics: to lower the amount of sodium and water in the body, which can help lower the pressure in the arteries and heart.

- Angiotensin-converting enzyme (ACE) inhibitors: to lower the blood pressure and improve the heart's pumping ability.

- Angiotensin receptor blockers (ARBs): to provide the benefits of ACE inhibitors for those who can't take ACE inhibitors.

- Beta blockers: to lower blood pressure and improve heart function.

- Digoxin: to help improve the pumping function of the heart and lessen the need for hospitalization for heart failure.

- Anticoagulants: to reduce the risk of blood clots that could cause a heart attack or stroke.

- Anti-arrhythmics: to keep the heart beating with a normal rhythm.

Medical devices to regulate the heartbeat

- Pacemaker: Coordinates the contractions between the left and right ventricle. In people who may be at risk of serious arrhythmias, drug therapy or an implantable cardioverter-defibrillator (ICD) may be used.

- ICDs: Small devices implanted in the chest to constantly monitor the heart rhythm and deliver electrical shocks when needed to control abnormal, rapid heartbeats. The devices can also work as pacemakers.

Surgical procedures

- Heart valve surgery: If an enlarged heart is caused by a problem with one of the heart valves, one may have surgery to remove the valve and replace it with either an artificial valve or a tissue valve from a pig, cow or deceased human donor. If blood leaks backward through a valve (valve regurgitation), the leaky valve may be surgically repaired or replaced.

- Coronary bypass surgery: If an enlarged heart is related to coronary artery disease, one may opt to have coronary artery bypass surgery.

- Left ventricular assist device: (LVAD): This implantable mechanical pump helps a weak heart pump. LVADs are often implanted while a patient waits for a heart transplant or, if the patient is not a heart transplant candidate, as a long-term treatment for heart failure.

- Heart transplant: If medications can't control the symptoms, a heart transplant is often a final option.

Cardiomegaly can progress and certain complications are common:

- Heart failure: One of the most serious types of enlarged heart, an enlarged left ventricle, increases the risk of heart failure. In heart failure, the heart muscle weakens, and the ventricles stretch (dilate) to the point that the heart can't pump blood efficiently throughout the body.

- Blood clots: Having an enlarged heart may make one more susceptible to forming blood clots in the lining of the heart. If clots enter the bloodstream, they can block blood flow to vital organs, even causing a heart attack or stroke. Clots that develop on the right side of the heart may travel to the lungs, a dangerous condition called a pulmonary embolism.

- Heart murmur: For people who have an enlarged heart, two of the heart's four valves — the mitral and tricuspid valves — may not close properly because they become dilated, leading to a backflow of blood. This flow creates sounds called heart murmurs.

- NOTE* The exact mortality rate for people with cardiomegaly is unknown. However, many people live for a very long time with an enlarged heart and if detected early, treatment can help improve the condition and prolong the lives of these people.

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 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.

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.

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.

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.

Valvular heart disease is any disease process involving one or more of the four valves of the heart (the aortic and mitral valves on the left and the pulmonary and tricuspid valves on the right). These conditions occur largely as a consequence of aging, but may also be the result of congenital (inborn) abnormalities or specific disease or physiologic processes including rheumatic heart disease and pregnancy.

Anatomically, the valves are part of the dense connective tissue of the heart known as the cardiac skeleton and are responsible for the regulation of blood flow through the heart and great vessels. Valve failure or dysfunction can result in diminished heart functionality, though the particular consequences are dependent on the type and severity of valvular disease. Treatment of damaged valves may involve medication alone, but often involves surgical valve repair (valvuloplasty) or replacement (insertion of an artificial heart valve).

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 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.

In terms of treatment for tricuspid insufficiency prosthetic valve substitutes can be used, though artificial prostheses may cause thrombo‐embolic phenomena(bioprostheses may have a degeneration problem). Some evidence suggests that there are no significant differences between a mechanical or biological tricuspid valve in a recipient.

Generally, surgical treatment of tricuspid regurgitation is not indicated when it has arisen as a result of right ventricular dilatation. In such instances of secondary tricuspid regurgitation, the mainstay of therapy is medical. When left-sided heart failure is the cause, the individual is instructed to decrease intake of salt. Medications in this case may include diuretics and angiotensin-converting enzyme inhibitors.

In treating pulmonary insufficiency, it should be determined if pulmonary hypertension is causing the problem to therefore begin the most appropriate therapy as soon as possible (primary pulmonary hypertension or secondary pulmonary hypertension due to thromboembolism). Furthermore, pulmonary insufficiency is generally treated by addressing the underlying condition, in certain cases, the pulmonary valve may be surgically replaced.

Due to Syphilitic aortitis (a complication of tertiary syphilis) the aortic valve ring becomes dilated. The free margins of valve cusps no longer approximate leading to aortic valve insufficiency. As blood regurgitates into the left ventricle between each systole, volume overload ensues and the ventricular wall hypertrophies in an attempt to maintain cardiac output and blood pressure. The massive ventricle can lead to a heart weighing over 1000 grams (the weight of a normal heart is about 350 grams), referred to as "Cor Bovinum" [Latin for cow's heart.]

Fluri and Gebbers define cor bovinum as a heart exceeding 500 g in weight. Looking through autopsies on Internal Medicine patients at the Kantonsspital Luzern, they found 415 cases out of 1181 autopsies in the two periods 1978-81 and 1997-2000. Cor bovinum was found in 25.3% of cases in the earlier period, with mean age at death 67.7 years, and in the later period 20.6% with mean age 74.3 years. The male female ratio was 4:1. "In 93% of all patients with CB, we found coronary atherosclerosis as a sign of high blood pressure and in 79% a COPD."

In 84% of cases the cause of death was directly related to the cor bovinum, but in 37% the cause of death was still unclear. They concluded that cor bovinum was a decreasing but still frequent autopsy finding. High blood pressure, COPD and male sex were the main risk factors. The decreasing incidence was ascribed to improved medical management: they mention treatments for high blood pressure and coronary artery disease, which suggests that "COPD" in their abstract refers to the latter.

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.

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.

The Canadian Cardiovascular Society (CCS) recommends surgical intervention for these indications:

- Limited exercise capacity (NYHA III-IV)

- Increasing heart size (cardiothoracic ratio greater than 65%)

- Important cyanosis (resting oxygen saturation less than 90% - level B)

- Severe tricuspid regurgitation with symptoms

- Transient ischemic attack or stroke

The CCS further recommends patients who require operation for Ebstein's anomaly should be operated on by congenital heart surgeons who have substantial specific experience and success with this operation. Every effort should be made to preserve the native tricuspid valve.

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

Ebstein's cardiophysiology typically presents as an (antidromic) AV reentrant tachycardia with associated pre-excitation. In this setting, the preferred medication treatment agent is procainamide. Since AV-blockade may promote conduction over the accessory pathway, drugs such as beta blockers, calcium channel blockers, and digoxin are contraindicated.

If atrial fibrillation with pre-excitation occurs, treatment options include procainamide, flecainide, propafenone, dofetilide, and ibutilide, since these medications slow conduction in the accessory pathway causing the tachycardia and should be administered before considering electrical cardioversion. Intravenous amiodarone may also convert atrial fibrillation and/or slow the ventricular response.

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.