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.

Due to non-compaction cardiomyopathy being a relatively new disease, its impact on human life expectancy is not very well understood. In a 2005 study that documented the long-term follow-up of 34 patients with NCC, 35% had died at the age of 42 +/- 40 months, with a further 12% having to undergo a heart transplant due to heart failure. However, this study was based upon symptomatic patients referred to a tertiary-care center, and so were suffering from more severe forms of NCC than might be found typically in the population. Sedaghat-Hamedani et al. also showed the clinical course of symptomatic LVNC can be severe. In this study cardiovascular events were significantly more frequent in LVNC patients compared with an age-matched group of patients with non-ischaemic dilated cardiomyopathy (DCM). As NCC is a genetic disease, immediate family members are being tested as a precaution, which is turning up more supposedly healthy people with NCC who are asymptomatic. The long-term prognosis for these people is currently unknown.

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.

Therapies that support reverse remodeling have been investigated, and this may suggests a new approach to the prognosis of cardiomyopathies (see ventricular remodeling).

One paper

has listed the various types of management of care that have been used for various types of NCC. These are similar to management programs for other types of cardiomyopathies which include the use of ACE inhibitors, beta blockers and aspirin therapy to relieve the pressure on the heart, surgical options such as the installation of pacemaker is also an option for those thought to be at a high risk of arrhythmia problems.

In severe cases, where NCC has led to heart failure, with resulting surgical treatment including a heart valve operation, or a heart transplant.

Drug therapy can slow down progression and in some cases even improve the heart condition. Standard therapy may include salt restriction, ACE inhibitors, diuretics, and beta blockers. Anticoagulants may also be used for antithrombotic therapy. There is some evidence for the benefits of coenzyme Q10 in treating heart failure.

Treatment of restrictive cardiomyopathy should focus on management of causative conditions (for example, using corticosteroids if the cause is sarcoidosis), and slowing the progression of cardiomyopathy. Salt-restriction, diuretics, angiotensin-converting enzyme inhibitors, and anticoagulation may be indicated for managing restrictive cardiomyopathy.

Calcium channel blockers are generally contraindicated due to their negative inotropic effect, particularly in cardiomyopathy caused by amyloidosis. Digoxin, calcium channel blocking drugs and beta-adrenergic blocking agents provide little benefit, except in the subgroup of restrictive cardiomyopathy with atrial fibrillation. Vasodilators are also typically ineffective because systolic function is usually preserved in cases of RCM.

Heart failure resulting from restrictive cardiomyopathy will usually eventually have to be treated by cardiac transplantation or left ventricular assist device.

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

Current treatment options for Boxer cardiomyopathy are largely restricted to the use of oral anti-arrhythmic medications. The aim of therapy is to minimize ventricular ectopy, eliminate syncopal episodes, and prevent sudden cardiac death. A number of medications have been used for this purpose, including atenolol, procainamide, sotalol, mexiletine, and amiodarone. Combinations can also be used. Sotalol is probably the most commonly used antiarrhythmic at this time. It has been demonstrated that sotalol alone, or a combination of mexiletine and atenolol, results in a reduction in the frequency and complexity of ventricular ectopy. It is likely that these medications also reduce syncopal episodes, and it is hoped this extends to a reduced risk of sudden death. Consequently, antiarrhythmic therapy is typically recommended by veterinary cardiologists for Boxer dogs with ARVC. Although relatively rare, oral antiarrhythmic medications may be proarrhythmic in some dogs; consequently, appropriate monitoring and follow-up is recommended.

The ideal therapy for Boxer cardiomyopathy would be implantation of an implantable cardioverter-defibrillator (ICD). This has been attempted in a limited number of dogs. Unfortunately, ICDs are programmed for humans and the algorithms used are not appropriate for dogs, increasing the risk of inappropriate shocks. In the future, reprogramming of ICDs may allow them to emerge as a viable option in the treatment for Boxer cardiomyopathy.

Endomyocardial fibrosis is generally limited to the tropics and sub-saharan Africa. The highest incidence of death caused by cardiac sarcoidosis is found in Japan.

Treatment may include suggestion of lifestyle changes to better manage the condition. Treatment depends on the type of cardiomyopathy and condition of disease, but may include medication (conservative treatment) or iatrogenic/implanted pacemakers for slow heart rates, defibrillators for those prone to fatal heart rhythms, ventricular assist devices (VADs) for severe heart failure, or ablation for recurring dysrhythmias that cannot be eliminated by medication or mechanical cardioversion. The goal of treatment is often symptom relief, and some patients may eventually require a heart transplant.

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.

An ICD is the most effective prevention against sudden cardiac death. Due to the prohibitive cost of ICDs, they are not routinely placed in all individuals with ARVD.

Indications for ICD placement in the setting of ARVD include:

- Cardiac arrest due to VT or VF

- Symptomatic VT that is not inducible during programmed stimulation

- Failed programmed stimulation-guided drug therapy

- Severe RV involvement with poor tolerance of VT

- Sudden death of immediate family member

Since ICDs are typically placed via a transvenous approach into the right ventricle, there are complications associated with ICD placement and follow-up.

Due to the extreme thinning of the RV free wall, it is possible to perforate the RV during implantation, potentially causing pericardial tamponade. Because of this, every attempt is made at placing the defibrillator lead on the ventricular septum.

After a successful implantation, the progressive nature of the disease may lead to fibro-fatty replacement of the myocardium at the site of lead placement. This may lead to undersensing of the individual's electrical activity (potentially causing inability to sense VT or VF), and inability to pace the ventricle.

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.

Cardiomyopathy is a group of diseases that affect the heart muscle. Early on there may be few or no symptoms. Some people may have shortness of breath, feel tired, or have swelling of the legs due to heart failure. An irregular heart beat may occur as well as fainting. Those affected are at an increased risk of sudden cardiac death.

Types of cardiomyopathy include hypertrophic cardiomyopathy, dilated cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right ventricular dysplasia, and takotsubo cardiomyopathy (broken heart syndrome). In hypertrophic cardiomyopathy the heart muscle enlarges and thickens. In dilated cardiomyopathy the ventricles enlarge and weaken. In restrictive cardiomyopathy the ventricle stiffens.

The cause is frequently unknown. Hypertrophic cardiomyopathy is often, and dilated cardiomyopathy in a third of cases is inherited from a person's parents. Dilated cardiomyopathy may also result from alcohol, heavy metals, coronary heart disease, cocaine use, and viral infections. Restrictive cardiomyopathy may be caused by amyloidosis, hemochromatosis, and some cancer treatments. Broken heart syndrome is caused by extreme emotional or physical stress.

Treatment depends on the type of cardiomyopathy and the degree of symptoms. Treatments may include lifestyle changes, medications, or surgery. In 2015 cardiomyopathy and myocarditis affected 2.5 million people. Hypertrophic cardiomyopathy affects about 1 in 500 people while dilated cardiomyopathy affects 1 in 2,500. They resulted in 354,000 deaths up from 294,000 in 1990. Arrhythmogenic right ventricular dysplasia is more common in young people.

Boxer cardiomyopathy is a genetic disease inherited in an autosomal dominant pattern. The presentation in affected offspring is quite variable, suggesting incomplete penetrance. In 2009, a group led by Dr. Kathryn Meurs at Washington State University announced that they had identified one genetic anomaly associated with Boxer cardiomyopathy but as of 2012 there is still debate over the significance of the discovery.

Treatment for alcoholic cardiomyopathy involves lifestyle changes, including complete abstinence from alcohol use, a low sodium diet, and fluid restriction, as well as medications. Medications may include ACE inhibitors, beta blockers, and diuretics which are commonly used in other forms of cardiomyopathy to reduce the strain on the heart. Persons with congestive heart failure may be considered for surgical insertion of an ICD or a pacemaker which can improve heart function. In cases where the heart failure is irreversible and worsening, heart transplant may be considered.

Treatment will possibly prevent the heart from further deterioration, and the cardiomyopathy is largely reversible if complete abstinence from alcohol is maintained.

For patients in acute heart failure, ACE inhibitors, angiotensin receptor blockers, and beta blockers, are considered mainstays of heart failure treatment. But use of beta blockers specifically for takotsubo cardiomyopathy is controversial, because they may confer no benefit.

Treatment of TIC involves treating both the tachyarrhythmia and the heart failure with the goal of adequate rate control or restoration of the normal heart rhythm (aka. normal sinus rhythm) to reverse the cardiomyopathy. The treatment of the tachyarrhythmia depends on the specific arrhythmia, but possible treatment modalities include rate control, rhythm control with antiarrhythmic agents and cardioversion, radiofrequency (RF) catheter ablation, or AV node ablation with permanent pacemaker implantation.

For TIC due to atrial fibrillation, rate control, rhythm control, and RF catheter ablation can be effective to control the tachyarrhythmia and improve left ventricular systolic function. For TIC due to atrial flutter, rate control is often difficult to achieve, and RF catheter ablation has a relatively high success rate with a low risk of complications. In patients with TIC due to other types of SVT, RF catheter ablation is recommended as a first-line treatment. In patients with TIC due to VT or PVCs, both antiarrhythmics and RF catheter ablation can be used. However, the options for antiarrhythmic agents are limited because certain agents can be proarrhythmic in the setting of myocardial dysfunction in TIC. Therefore, RF catheter ablation is often a safe and effective choice for treatment VT and PVCs causing TIC. In cases where other treatment strategies fail, AV node ablation with permanent pacemaker implantation can also be used to treat the tachyarrhythmia.

The treatment of heart failure commonly involves neurohormonal blockade with beta-blockers and angiotensin convertase inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) along with symptomatic management with diuretics. Beta-blockers and ACE inhibitors can inhibit and potentially reverse the negative cardiac remodeling, which refers to structural changes in the heart, that occurs in TIC. However, the need to continue these agents after treatment of the tacharrhythmia and resolution of left ventricular systolic dysfunction remains controversial.

The treatment of takotsubo cardiomyopathy is generally supportive in nature, for it is considered a transient disorder. Treatment is dependent on whether patients experience heart failure or acute hypotension and shock. In many individuals, left ventricular function normalizes within two months. Aspirin and other heart drugs also appear to help in the treatment of this disease, even in extreme cases. After the patient has been diagnosed, and myocardial infarction (heart attack) ruled out, the aspirin regimen may be discontinued, and treatment becomes that of supporting the patient.

While medical treatments are important to address the acute symptoms of Takotsubo cardiomyopathy, further treatment includes lifestyle changes. It is important that the individual stay physically healthy while learning and maintaining methods to manage stress, and to cope with future difficult situations.

Although the symptoms of Takotsubo cardiomyopathy usually go away on their own and the condition completely resolves itself within a few weeks, some serious complications can happen that must be treated. These most commonly include congestive heart failure and very low blood pressure, and less commonly include blood clotting in the apex of the left ventricle, irregular heart beat, and tearing of the heart wall.

The prognosis for TIC after treatment of the underlying tachyarrhythmia is generally good. Studies show that left ventricular function often improves within 1 month of treatment of the tachyarrhythmia, and normalization of the left ventricular ejection fraction occurs in the majority of patients by 3 to 4 months. In some patients however, recovery of this function can take greater than 1 year or be incomplete. In addition, despite improvement in the left ventricular ejection fraction, studies have demonstrated that patients with prior TIC continue to demonstrate signs of negative cardiac remodeling including increased left ventricular end-systolic dimension, end-systolic volume, and end-diastolic volume. Additionally, recurrence of the tachyarrhythmia in patients with a history of TIC has been associated with a rapid decline in left ventricular ejection fraction and more severe cardiomyopathy that their prior presentation, which may be a result of the negative cardiac remodeling. There have also been cases of sudden death in patients with a history of TIC, which may be associated with worse baseline left ventricular dysfunction. Given these risks, routine monitoring with clinic visits, ECG, and echocardiography is recommended.

Ventricular hypertrophy (VH) is thickening of the walls of a ventricle (lower chamber) of the heart. Although left ventricular hypertrophy (LVH) is more common, right ventricular hypertrophy (RVH), as well as concurrent hypertrophy of both ventricles can also occur.

Ventricular hypertrophy can result from a variety of conditions, both adaptive and maladaptive. For example, it occurs in what is regarded as a physiologic, adaptive process in pregnancy in response to increased blood volume; but can also occur as a consequence of ventricular remodeling following a heart attack. Importantly, pathologic and physiologic remodeling engage different cellular pathways in the heart and result in different gross cardiac phenotypes.

Mortality in HIV-infected patients with cardiomyopathy is increased independently of CD4 count, age, sex, and HIV risk group.

The therapy is similar to therapy for non-ischemic cardiomyopathy: after medical therapy is begun, serial echocardiographic studies should be performed at 4-months intervals. If function continues to worsen or the clinical course deteriorates, a biopsy should be considered.

HAART has reduced the incidence of myocarditis thus reducing the prevalence of HIV-associated cardiomyopathy by about 30% in developed countries. However, the prevalence in developing countries is 32% and increasing as HAART is scarce – not to mention the effects of other risk factors such as high cholesterol and lipid diet. IVIGs can also help patients with HIV-associated myocarditis as mentioned earlier.

Isolated PVCs with benign characteristics require no treatment.

In healthy individuals, PVCs can often be resolved by restoring the balance of magnesium, calcium and potassium within the body. In one randomized controlled trial with 60 people those with 260 mg magnesium daily supplementation (in magnesium pidolate) had an average reduction of PVC by 77%. In another trial with 232 persons with frequent ventricular arrhythmias (> 720 PVC/24 h) those with 6 mmol of magnesium (146 mg Mg)/12 mmol of potassium-DL-hydrogenaspartate daily supplementation had median reduction of PVCs by 17%.

The most effective treatment is the elimination of triggers (particularly stopping the use of substances such as caffeine and certain drugs, like tobacco).

- Medications

- Antiarrhythmics: these agents alter the electrophysiologic mechanisms responsible for PVCs. In CAST study of survivors of myocardial infarction encainide and flecainide, although could suppress PVC, they increased death risk; moricizine increased death rate when used with diuretics and decreased it when used alone.

- Beta blockers

- Calcium channel blockers

- Electrolytes replacement

- Magnesium supplements (e.g. magnesium citrate, orotate, Maalox, etc.)

- Potassium supplements (e.g. chloride potassium with citrate ion)

- Radiofrequency catheter ablation treatment. It is advised for people with ventricular dysfunction and frequent arrhythmias or very frequent PVC (>20% in 24 h) and normal ventricular function. This procedure is a way to destroy the area of the heart tissue that is causing the irregular contractions characteristic of PVCs using radio frequency energy.

- Implantable cardioverter-defibrillator

- Lifestyle modification

- Frequently stressed individuals should consider therapy, or joining a support group.

- Heart attacks can increase the likelihood of having PVCs.

In the setting of existing heart disease, however, PVCs must be watched carefully, as they may cause a form of ventricular tachycardia (rapid heartbeat).

The American College of Cardiology and the American Heart Association recommend evaluation for coronary artery disease (CAD) in patients who have frequent PVCs and cardiac risk factors, such as hypertension and smoking (SOR C). Evaluation for CAD may include stress testing, echocardiography, and ambulatory rhythm monitoring.

HIV is a major cause of cardiomyopathy – in particular dilated cardiomyopathy. Dilated cardiomyopathy can be due to pericardial effusion or infective endocarditis, especially in intravenous drug users which are common in the HIV population. However, the most researched causes of cardiomyopathy are myocardial inflammation and infection caused by HIV-1. Toxoplasma gondii is the most common opportunistic infectious agent associated with myocarditis in AIDS. Coinfection with viruses (usually, coxsackievirus B3 and cytomegalovirus) seems to have an important affect in myocarditis. HIV-1 infection produces additional virus and cytokines such as TNF-α. This induces cardiomyocyte apoptosis. TNF-α causes a negative inotropic effect by interfering with the intracellular calcium ion concentrations. The intensity of the stains for TNF-α and iNOS of the myocardium was greater in patients with HIV associated cardiomyopathy, myocardial viral infection and was inversely correlated with CD4 count with antiretroviral therapy having no effect. Cardiac autoimmunity affects the pathogenesis of HIV-related heart disease as HIV-infected patients with dilated cardiomyopathy are more likely to have cardiac-specific autoantibodies than HIV-infected patients with healthy hearts and HIV-negative controls. Many patients with HIV have nutritional deficiencies which have been linked to left ventricular dysfunction. HIV-infected patients with encephalopathy are more likely to die of congestive heart failure than are those without encephalopathy. HAART has reduced the incidence of myocarditis thus reducing the prevalence of HIV-associated cardiomyopathy. Intravenous immunoglobulins (IVIGs) can also help patients with HIV-associated myocarditis.