Although not based on a human clinical trial, the only currently accepted disease-modifying therapeutic strategy available for familial amyloid cardiomyopathy is a combined liver and heart transplant. Treatments aimed at symptom relief are available, and include diuretics, pacemakers, and arrhythmia management. Thus, Senile systemic amyloidosis and familial amyloid polyneuropathy are often treatable diseases that are misdiagnosed.

In 2013, the European Medicines Agency approved the drug tafamidis (Vyndaqel) to slow the progression of familial amyloid polyneuropathy, a related disease caused by TTR aggregation that first presents as an autonomic and/or peripheral neuropathy (later progressing to a cardiomyopathy).

No drug has been shown to be able to arrest or slow down the process of this condition. There is promise that two drugs, tafamidis and diflunisal, may improve the outlook, since they were demonstrated in randomized clinical trials to benefit patient affected by the related condition FAP-1 otherwise known as transthyretin-related hereditary amyloidosis. Permanent pacing can be employed in cases of symptomatic slow heart rate (bradycardia). Heart failure medications can be used to treat symptoms of difficulty breathing and congestion.

The drug tafamidis has completed a phase II/III 18-month-long placebo controlled clinical trial

and these results in combination with an 18-month follow-on study demonstrated that Tafamidis or Vyndaqel slowed progression of FAP, particularly when administered to patients early in the course of FAP. This drug is now approved by the European Medicines Agency.

The US Food and Drug Administration's Peripheral and Central Nervous System Drugs Advisory Committee rejected the drug in June 2012, in a 13-4 vote. The committee stated that there was not enough evidence supporting efficacy of the drug, and requested additional clinical trials.

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

Initial treatment can be medical, involving the use of drugs like isoprenaline (Isuprel) and epinephrine (adrenaline). Definitive treatment is surgical, involving the insertion of a pacemaker – most likely one with sequential pacing such as a DDI mode as opposed to the older VVI mechanisms, and the doctor may arrange the patient to undergo electrocardiography to confirm this type of treatment.

As there is no known cure, Loeys–Dietz syndrome is a lifelong condition. Due to the high risk of death from aortic aneurysm rupture, patients should be followed closely to monitor aneurysm formation, which can then be corrected with interventional radiology or vascular surgery.

Previous research in laboratory mice has suggested that the angiotensin II receptor antagonist losartan, which appears to block TGF-beta activity, can slow or halt the formation of aortic aneurysms in Marfan syndrome. A large clinical trial sponsored by the National Institutes of Health is currently underway to explore the use of losartan to prevent aneurysms in Marfan syndrome patients. Both Marfan syndrome and Loeys–Dietz syndrome are associated with increased TGF-beta signaling in the vessel wall. Therefore, losartan also holds promise for the treatment of Loeys–Dietz syndrome. In those patients in which losartan is not halting the growth of the aorta, irbesartan has been shown to work and is currently also being studied and prescribed for some patients with this condition.

If an increased heart rate is present, atenolol is sometimes prescribed to reduce the heart rate to prevent any extra pressure on the tissue of the aorta. Likewise, strenuous physical activity is discouraged in patients, especially weight lifting and contact sports.

In the absence of a liver transplant, FAP is invariably fatal, usually within a decade. The disadvantage of liver transplantation is that approximately 10% of the subjects die from the procedure or complications resulting from the procedure, which is a form of gene therapy wherein the liver expressing wild type and mutant TTR is replaced by a liver only expressing wild type TTR. Moreover, transplanted patients must take immune suppressants (drugs) for the remainder of their life, which can lead to additional complications. In late 2011, the European Medicines Agency approved the transthyretin kinetic stabilizer Tafamidis or Vyndaqel discovered by Jeffery W. Kelly and developed by FoldRx pharmaceuticals (acquired by Pfizer in 2010) for the treatment of FAP based on clinical trial data. Tafamidis (20 mg once daily) slowed the progression of FAP over a 36-month period and importantly reversed the weight loss and muscle wasting associated with disease progression.

There is currently no cure for FD and death occurs in 50% of the affected individuals by age 30. There are only two treatment centers, one at New York University Hospital and one at the Sheba Medical Center in Israel. One is being planned for the San Francisco area.

The survival rate and quality of life have increased since the mid-1980s mostly due to a greater understanding of the most dangerous symptoms. At present, FD patients can be expected to function independently if treatment is begun early and major disabilities avoided.

A major issue has been aspiration pneumonia, where food or regurgitated stomach content would be aspirated into the lungs causing infections. Fundoplications (by preventing regurgitation) and gastrostomy tubes (to provide nonoral nutrition) have reduced the frequency of hospitalization.

Other issues which can be treated include FD crises, scoliosis, and various eye conditions due to limited or no tears.

An FD crisis is the body's loss of control of various autonomic nervous system functions including blood pressure, heart rate, and body temperature. Both short-term and chronic periodic high or low blood pressure have consequences and medication is used to stabilize blood pressure.

If undiagnosed (or untreated), Stokes–Adams attacks have a 50% mortality within a year of the first episode. The prognosis following treatment is very good.

The cause of sudden death in Brugada syndrome is ventricular fibrillation (VF). The average age of death is 41. According to clinical reports, sudden death in people with Brugada syndrome most often happens during sleep. The episodes of syncope (fainting) and sudden death (aborted or not) are caused by fast polymorphic ventricular tachycardias or ventricular fibrillation. These arrhythmias appear with no warning. While there is no exact treatment modality that reliably and totally prevents ventricular fibrillation from occurring in this syndrome, treatment lies in termination of this lethal arrhythmia before it causes death. This is done via insertion of an implantable cardioverter-defibrillator (ICD), which continuously monitors the heart rhythm and will shock the wearer if ventricular fibrillation is sensed.

Studies have evaluated the role of quinidine, a Class Ia antiarrhythmic drug, for decreasing VF episodes occurring in this syndrome. Quinidine has been found to both decrease the number of VF episodes and correct spontaneous ECG changes, possibly via inhibiting I channels.

Some drugs have been reported to induce the type-1 ECG and/or (fatal) arrhythmias in Brugada syndrome patients. Patients with Brugada syndrome can prevent arrhythmias by avoiding these drugs or using them only in controlled conditions. Those with risk factors for coronary artery disease may require an angiogram before ICD implantation.

Familial Amyloid Cardiomyopathy (FAC), or Transthyretin Amyloid Cardiomyopathy (ATTR-CM) results from the aggregation and deposition of mutant and wild-type transthyretin (TTR) protein in the heart. TTR amyloid fibrils infiltrate the myocardium, leading to diastolic dysfunction from restrictive cardiomyopathy, and eventual heart failure. Both mutant and wild-type transthyretin comprise the aggregates because the TTR blood protein is a tetramer composed of mutant and wild-type TTR subunits in heterozygotes. Several mutations in TTR are associated with FAC, including V122I, V20I, P24S, A45T, Gly47Val, Glu51Gly, I68L, Gln92Lys, and L111M. One common mutation (V122I), which is a substitution of isoleucine for valine at position 122, occurs with high frequency in African-Americans, with a prevalence of approximately 3.5%. FAC is clinically similar to senile systemic amyloidosis, in which cardiomyopathy results from the aggregation of wild-type transthyretin exclusively.

Wild-type transthyretin amyloid (WTTA), also known as senile systemic amyloidosis (SSA) and abbreviated as ATTR, is a disease that typically affects the heart and tendons of elderly people. It is caused by accumulation of a wild-type (that is to say a normal) protein called transthyretin. This is in contrast to a related condition called transthyretin-related hereditary amyloidosis where a genetically mutated transthyretin protein tends to deposit at a much earlier age than in WTTA, due to abnormal conformation and bioprocessing.

It belongs to a group of diseases called amyloidosis, chronic progressive conditions linked to abnormal deposition of normal or abnormal proteins, because these proteins are misshapen and cannot be properly degraded and eliminated by the cell metabolism.

Currently there is no curative treatment for KSS. Because it is a rare condition, there are only case reports of treatments with very little data to support their effectiveness. Several promising discoveries have been reported which may support the discovery of new treatments with further research. Satellite cells are responsible for muscle fiber regeneration. It has been noted that mutant mtDNA is rare or undetectable in satellite cells cultured from patients with KSS. Shoubridge et al. (1997) asked the question whether wildtype mtDNA could be restored to muscle tissue by encouraging muscle regeneration. In the forementioned study, regenerating muscle fibers were sampled at the original biopsy site, and it was found that they were essentially homoplasmic for wildtype mtDNA. Perhaps with future techniques of promoting muscle cell regeneration and satellite cell proliferation, functional status in KSS patients could be greatly improved.

One study described a patient with KSS who had reduced serum levels of coenzyme Q10. Administration of 60–120 mg of Coenzyme Q10 for 3 months resulted in normalization of lactate and pyruvate levels, improvement of previously diagnosed first degree AV block, and improvement of ocular movements.

A screening ECG is recommended in all patients presenting with CPEO. In KSS, implantation of pacemaker is advised following the development of significant conduction disease, even in asymptomatic patients.

Screening for endocrinologic disorders should be performed, including measuring serum glucose levels, thyroid function tests, calcium and magnesium levels, and serum electrolyte levels. Hyperaldosteronism is seen in 3% of KSS patients.

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People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.

In itself, NSML is not a life-threatening diagnosis, most people diagnosed with the condition live normal lives. Obstructive cardiomyopathy and other pathologic findings involving the cardiovascular system may be a cause of death in those whose cardiac deformities are profound.

Although the FD-causing gene has been identified and it seems to have tissue specific expression, there is no definitive treatment at present.

Treatment of FD remains preventative, symptomatic and supportive. FD does not express itself in a consistent manner. The type and severity of symptoms displayed vary among patients and even at different ages on the same patients. So patients should have specialized individual treatment plans. Medications are used to control vomiting, eye dryness, and blood pressure. There are some commonly needed treatments including:

1. Artificial tears: using eye drops containing artificial tear solutions (methylcellulose)

2. Feeding: Maintenance of adequate nutrition, avoidance of aspiration; thickened formula and different shaped nipples are used for baby.

3. Daily chest physiotherapy (nebulization, bronchodilators, and postural drainage): for Chronic lung disease from recurrent aspiration pneumonia

4. Special drug management of autonomic manifestations such as vomiting: intravenous or rectal diazepam (0.2 mg/kg q3h) and rectal chloral hydrate (30 mg/kg q6h)

5. Protecting the child from injury (coping with decreased taste, temperature and pain perception)

6. Combating orthostatic hypotension: hydration, leg exercise, frequent small meals, a high-salt diet, and drugs such as fludrocortisone.

7. Treatment of orthopedic problems (tibial torsion and spinal curvature)

8. Compensating for labile blood pressures

There is no cure for Familial Dysautonomia.

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.

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.

If untreated, this abnormal heart rhythm can lead to dizziness, chest pain, a sensation of fluttering or pounding in the chest (palpitations), shortness of breath, or fainting (syncope). Atrial fibrillation also increases the risk of stroke. Complications of familial atrial fibrillation can occur at any age, although some people with this heart condition never experience any health problems associated with the disorder.

Atrial fibrillation is the most common type of sustained abnormal heart rhythm (arrhythmia), affecting more than 3 million people in the United States. The risk of developing this irregular heart rhythm increases with age. The incidence of the familial form of atrial fibrillation is unknown; however, recent studies suggest that up to 30 percent of all people with atrial fibrillation may have a history of the condition in their family.

In patients with advanced disease who are refractory to medical therapy, heart transplantation may be considered. For these people 1-year survival approaches 90% and over 50% survive greater than 20 years.

The number of people affected by Brugada ECG is higher in Asia than in the United States and Europe. Specifically, Brugada Type 1 ECG appears more frequently in Asia (0%–0.36% of the population) and Europe (0%–0.25%) than in the United States (0.03%). Type 2 and Type 3 ECG is more prevalent in Asia (0.12%–2.23%) than in Europe (0.0%–0.6%) or the United States (0.02%).

It is the most common cause of sudden death in young men without known underlying cardiac disease in Thailand and Laos.

The treatment for diffuse distal conduction system disease is insertion of a pacemaker. If the PR prolongation is due to AV nodal disease, a case may be made for observation, as it may never progress to complete heart block with life threateningly low heart rates.

Regardless of where in the conduction system the block is, if the block is believed to be the cause of syncope in an individual, a pacemaker is an appropriate treatment.

Fucosidosis is an extremely rare disorder first described in 1962 in two Italian siblings who showed progressive intellectual disability and neurological deterioration. The disease itself is extremely rare (less than 100 documented cases) only affecting 1:2,000,000, with most cases being occurring in Italy, Cuba, and the southwest U.S. The disease has three different types. Type 1 and 2 are considered severe, and Type 3 being a mild disease. Symptoms are highly variable with mild cases being able to live to within the third or fourth decade. Type 1 and 2 are both linked with mental retardation. Severe cases can develop life-threatening complications early in childhood.

Because the major accumulating glycoconjugate in fucosidosis patients is the blood group H-antigen, it is intriguing to speculate, but the evidence is not clear at this time, that blood type may affect the course of the disease.

Although a myxoma is not cancer, complications are common. Untreated, a myxoma can lead to an embolism (tumor cells breaking off and traveling with the bloodstream), which can block blood flow. Myxoma fragments can move to the brain, eye, or limbs.

If the tumor grows inside the heart, it can block blood flow through the mitral valve and cause symptoms of mitral stenosis or mitral regurgitation. This may require emergency surgery to prevent sudden death.

Treatment: There is no treatment or way to reverse the disease. Treatment will focus on the symptoms an individual has, such as seizure medication.

- It is possible that if an individual receives a bone marrow transplant, they could receive healthy bone marrow cells which would produce normal amounts of fucosidase. But there not is enough research to prove this is an effective treatment.