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.

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.

The goal of management of ARVD is to decrease the incidence of sudden cardiac death. This raises a clinical dilemma: How to prophylactically treat the asymptomatic patient who was diagnosed during family screening.

A certain subgroup of individuals with ARVD are considered at high risk for sudden cardiac death. Associated characteristics include:

- Young age

- Competitive sports activity

- Malignant familial history

- Extensive RV disease with decreased right ventricular ejection fraction.

- Left ventricular involvement

- Syncope

- Episode of ventricular arrhythmia

Management options include pharmacological, surgical, catheter ablation, and placement of an implantable cardioverter-defibrillator.

Prior to the decision of the treatment option, programmed electrical stimulation in the electrophysiology laboratory may be performed for additional prognostic information. Goals of programmed stimulation include:

- Assessment of the disease's arrhythmogenic potential

- Evaluate the hemodynamic consequences of sustained VT

- Determine whether the VT can be interrupted via antitachycardia pacing.

Regardless of the management option chosen, the individual is typically advised to undergo lifestyle modification, including avoidance of strenuous exercise, cardiac stimulants (i.e.: caffeine, nicotine, pseudoephedrine) and alcohol. If the individual wishes to begin an exercise regimen, an exercise stress test may have added benefit.

Pharmacologic management of ARVD involves arrhythmia suppression and prevention of thrombus formation.

Sotalol, a beta blocker and a class III antiarrhythmic agent, is the most effective antiarrhythmic agent in ARVD. Other antiarrhythmic agents used include amiodarone and conventional beta blockers (i.e.: metoprolol). If antiarrhythmic agents are used, their efficacy should be guided by series ambulatory holter monitoring, to show a reduction in arrhythmic events.

While angiotensin converting enzyme inhibitors (ACE Inhibitors) are well known for slowing progression in other cardiomyopathies, they have not been proven to be helpful in ARVD.

Individuals with decreased RV ejection fraction with dyskinetic portions of the right ventricle may benefit from long term anticoagulation with warfarin to prevent thrombus formation and subsequent pulmonary embolism.

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.

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

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

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.

The underlying condition may be treated by medications to control hypertension or diabetes, if they are the primary underlying cause. If coronary arteries are blocked, an invasive coronary angioplasty may relieve the impending RBBB.

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.

The S4 heart sound itself does not require treatment; rather plans should be laid to stop the progression of whatever causes the underlying ventricular dysfunction. The S4 heart sound is a secondary manifestation of a primary disease process and treatment should be focused on treating the underlying, primary disease.

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.

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.

Treatment is surgical and involves closure of the atrial and ventricular septal defects and restoration of a competent left AV valve as far as is possible. Open surgical procedures require a heart-lung machine and are done with a median sternotomy. Surgical mortality for uncomplicated ostium primum defects in experienced centers is 2%; for uncomplicated cases of complete atrioventricular canal, 4% or less. Certain complications such as tetralogy of Fallot or highly unbalanced flow across the common AV valve can increase risk significantly.

Infants born with AVSD are generally in sufficient health to not require immediate corrective surgery. If surgery is not required immediately after birth, the newborn will be closely monitored for the next several months, and the operation held-off until the first signs of lung distress or heart failure. This gives the infant time to grow, increasing the size of, and thereby the ease of operation on, the heart, as well as the ease of recovery. Infants will generally require surgery within three to six months, however, they may be able to go up to two years before the operation becomes necessary, depending on the severity of the defect.

If an affected individual begins to experience severe TDBBB, then medical intervention is often advised. Suggested therapy for the treatment of TDBBB can include the prescription of certain medications or the implantation of a pacemaker device. Advised medications would possess anti-coagulant mechanisms to reduce the risk of blood clot formation ensuring that no further restriction of arteries would deprive the heart of oxygen and further damage the bundle branches. The use of a pacemaker would ensure that the heart receives a constant rhythmic electrical input that never changes in frequency. While this would effectively eliminate the occurrence of TDBBB, the pacemaker would restrict the patient's heart to a permanent rhythm, eliminating the ability of patients to perform physical activity. Future pacemakers that adaptively respond to physiological requirements are being developed in order to negate the limitations observed with their current use.

Generally, diastolic dysfunction is a chronic process. When this chronic condition is well tolerated by an individual, no specific treatment may be indicated. Rather, therapy should be directed at the root cause of the stiff left ventricle, with potential causes and aggravating factors like high blood pressure and diabetes treated appropriately. Conversely (as noted above), diastolic dysfunction tends to be better tolerated if the atrium is able to pump blood into the ventricles in a coordinated fashion. This does not occur in atrial fibrillation (AF), where there is no coordinated atrial activity and the left ventricle loses around 20% of its output. However, in chronic AF and in geriatric patients, AF is better tolerated and the cardiologist must choose between a stable AF at a lower rate and the risk of having an intermittent AF if he pretends to treat AF aggressively with all the thrombo-embolic risk it implies. In the same light, and also as noted above, if the atrial fibrillation persists and is resulting in a rapid heart rate, treatment must be given to slow down that rate. Usually digoxin maintains a stable rhythm. The use of a self-expanding device that attaches to the external surface of the left ventricle has been suggested, yet still awaits FDA approval. When the heart muscle squeezes, energy is loaded into the device, which absorbs the energy and releases it to the left ventricle in the diastolic phase. This helps retain muscle elasticity.

The role of specific treatments for diastolic dysfunction "per se" is as yet unclear. Diuretics can be useful, if these patients develop significant congestion, but patients must be monitored because they frequently develop hypotension.

Beta-blockers are the first-line therapy as they induce bradycardia and give time for ventricles to fill. There is some evidence that calcium channel blocker drugs may be of benefit in reducing ventricular stiffness in some cases (verapamil has the benefit lowering the heart rate). Likewise, treatment with angiotensin converting enzyme inhibitors, such as enalapril, ramipril, and many others, may be of benefit due to their effect on preventing ventricular remodeling but under control to avoid hypotension.

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.

The enlargement is not permanent in all cases, and in some cases the growth can regress with the reduction of blood pressure.

LVH may be a factor in determining treatment or diagnosis for other conditions. For example, LVH causes a patient to have an irregular ECG. Patients with LVH may have to participate in more complicated and precise diagnostic procedures, such as imaging, in situations in which a physician could otherwise give advice based on an ECG.

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.

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.

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.

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.

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.

Most cases do not need treatment and heal at the first years of life. Treatment is either conservative or surgical. Smaller congenital VSDs often close on their own, as the heart grows, and in such cases may be treated conservatively.

Some cases may necessitate surgical intervention, i.e. with the following indications:

1. Failure of congestive cardiac failure to respond to medications

2. VSD with pulmonic stenosis

3. Large VSD with pulmonary hypertension

4. VSD with aortic regurgitation

For the surgical procedure, a heart-lung machine is required and a median sternotomy is performed. Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only suitable for certain patients. Repair of most VSDs is complicated by the fact that the conducting system of the heart is in the immediate vicinity.

Ventricular septum defect in infants is initially treated medically with cardiac glycosides (e.g., digoxin 10-20 µg/kg per day), loop diuretics (e.g., furosemide 1–3 mg/kg per day) and ACE inhibitors (e.g., captopril 0.5–2 mg/kg per day).

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.