Marine-derived omega-3 polyunsaturated fatty acids (PUFAs) has been promoted for the prevention of sudden cardiac death due to its postulated ability to lower triglyceride levels, prevent arrhythmias, decrease platelet aggregation, and lower blood pressure. However, according to a recent systematic review, omega-3 PUFA supplementation are not being associated with a lower risk of sudden cardiac death.

An implantable cardioverter defibrillator (ICD) is a battery powered device that monitors electrical activity in the heart and when an arrhythmia or asystole is detected is able to deliver an electrical shock to terminate the abnormal rhythm. ICDs are used to prevent sudden cardiac death (SCD) in those that have survived a prior episode of sudden cardiac arrest (SCA) due to ventricular fibrillation or ventricular tachycardia (secondary prevention). ICDs are also used prophylactically to prevent sudden cardiac death in certain high risk patient populations (primary prevention).

Numerous studies have been conducted on the use of ICDs for the secondary prevention of SCD. These studies have shown improved survival with ICDs compared to the use of anti-arrhythmic drugs. ICD therapy is associated with a 50% relative risk reduction in death caused by an arrhythmia and a 25% relative risk reduction in all cause mortality.

Primary prevention of SCD with ICD therapy for high risk patient populations has similarly shown improved survival rates in a number of large studies. The high risk patient populations in these studies were defined as those with severe ischemic cardiomyopathy (determined by a reduced left ventricular ejection fraction (LVEF)). The LVEF criteria used in these trials ranged from less than or equal to 30% in MADIT-II to less than or equal to 40% in MUSTT.

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

Many factors influence the time course and extent of remodeling, including the severity of the injury, secondary events (recurrent ischemia or infarction), neurohormonal activation, genetic factors and gene expression, and treatment. Medications may attenuate remodeling. Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease remodeling in animal models or transmural infarction and chronic pressure overload. Clinical trials have shown that ACE inhibitor therapy after myocardial infarction leads to improved myocardial performance, improved ejection fraction, and decreased mortality compared to patients treated with placebo. Likewise, inhibition of aldosterone, either directly or indirectly, leads to improvement in remodeling. Carvedilol, a 3rd generation beta blocker, may actually reverse the remodeling process by reducing left ventricular volumes and improving systolic function. Early correction of congenital heart defects, if appropriate, may prevent remodeling, as will treatment of chronic hypertension or valvular heart disease. Often, reverse remodeling, or improvement in left ventricular function, will also be seen.

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.

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.

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.

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.

Certain antimigraine drugs which are targeted at serotonin receptors as vasoconstrictive agents, have long been known to be associated with pulmonary hypertension and Raynaud's phenomenon (both vasoconstrictive effects), as well as retroperitoneal fibrosis (a fibrotic cell/fibrocyte proliferation effect, thought to be similar to cardiac valve fibrosis).

These drugs include ergotamine and methysergide and both drugs can also cause cardiac fibrosis.

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.

In cardiology, ventricular remodeling (or cardiac remodeling) refers to changes in the size, shape, structure, and function of the heart. This can happen as a result of exercise (physiological remodeling) or after injury to the heart muscle (pathological remodeling). The injury is typically due to acute myocardial infarction (usually transmural or ST segment elevation infarction), but may be from a number of causes that result in increased pressure or volume, causing pressure overload or volume overload (forms of strain) on the heart. Chronic hypertension, congenital heart disease with intracardiac shunting, and valvular heart disease may also lead to remodeling. After the insult occurs, a series of histopathological and structural changes occur in the left ventricular myocardium that lead to progressive decline in left ventricular performance. Ultimately, ventricular remodeling may result in diminished contractile (systolic) function and reduced stroke volume.

Physiological remodeling is reversible while pathological remodeling is mostly irreversible. Remodeling of the ventricles under left/right pressure demand make mismatches inevitable. Pathologic pressure mismatches between the pulmonary and systemic circulation guide compensatory remodeling of the left and right ventricles. The term "reverse remodeling" in cardiology implies an improvement in ventricular mechanics and function following a remote injury or pathological process.

Ventricular remodeling may include ventricular hypertrophy, ventricular dilation, cardiomegaly, and other changes. It is an aspect of cardiomyopathy, of which there are many types. Concentric hypertrophy is due to pressure overload, while eccentric hypertrophy is due to volume overload.

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.

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.

Cardiac resuscitation guidelines (ACLS/BCLS) advise that Cardiopulmonary resuscitation should be initiated promptly to maintain cardiac output until the PEA can be corrected. The approach in treatment of PEA is to treat the underlying cause, if known (e.g. relieving a tension pneumothorax). Where an underlying cause for PEA cannot be determined and/or reversed, the treatment of pulseless electrical activity is similar to that for asystole. There is no evidence that external cardiac compression can increase cardiac output in any of the many scenarios of PEA, such as hemorrhage, in which impairment of cardiac filling is the underlying mechanism producing loss of a detectable pulse.

An intravenous or intraosseous line should be started to provide medications through. The mainstay of drug therapy for PEA is epinephrine (adrenaline) 1 mg every 3–5 minutes. Although previously the use of atropine was recommended in the treatment of PEA/asystole, this recommendation was withdrawn in 2010 by the American Heart Association due to lack of evidence for therapeutic benefit. Epinephrine too has a limited evidence base, and it is recommended on the basis of its mechanism of action.

Sodium bicarbonate 1meq per kilogram may be considered in this rhythm as well, although there is little evidence to support this practice. Its routine use is not recommended for patients in this context, except in special situations (e.g. preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose).

All of these drugs should be administered along with appropriate CPR techniques. Defibrillators cannot be used to correct this rhythm, as the problem lies in the response of the myocardial tissue to electrical impulses.

Therapy may be directed either at terminating an episode of the abnormal heart rhythm or at reducing the risk of another VT episode. The treatment for stable VT is tailored to the specific person, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. Individuals suffering from pulseless VT or unstable VT are hemodynamically compromised and require immediate electric cardioversion to shock them out of the VT rhythm.

For those who are stable with a monomorphic waveform the medications procainamide or sotalol may be used and are better than lidocaine. Evidence does not show that amiodarone is better than procainamide.

As a low magnesium level in the blood is a common cause of VT, magnesium sulfate can be given for torsades de pointes or if a low blood magnesium level is found/suspected.

Long-term anti-arrhythmic therapy may be indicated to prevent recurrence of VT. Beta-blockers and a number of class III anti-arrhythmics are commonly used, such as the beta-blockers carvedilol, metoprolol, and bisoprolol, and the Potassium-Channel-Blockers amiodarone, dronedarone,bretylium, sotalol, ibutilide, and dofetilide. Angiotensin-converting-eynsyme (ACE) inhibitors and aldostrone antatagonists are also sometimes used in this setting.

Artificial pacemakers have been used in the treatment of sick sinus syndrome.

Bradyarrhythmias are well controlled with pacemakers, while tachyarrhythmias respond well to medical therapy.

However, because both bradyarrhythmias and tachyarrhythmias may be present, drugs to control tachyarrhythmia may exacerbate bradyarrhythmia. Therefore, a pacemaker is implanted before drug therapy is begun for the tachyarrhythmia.

It can result in many abnormal heart rhythms (arrhythmias), including sinus arrest, sinus node exit block, sinus bradycardia, and other types of bradycardia (slow heart rate).

Sick sinus syndrome may also be associated with tachycardias (fast heart rate) such as atrial tachycardia (PAT) and atrial fibrillation. Tachycardias that occur with sick sinus syndrome are characterized by a long pause after the tachycardia. Sick sinus syndrome is also associated with azygos continuation of interrupted inferior vena cava.

Pulseless electrical activity (PEA), also known as electromechanical dissociation, refers to cardiac arrest in which the electrocardiogram shows a heart rhythm that should produce a pulse, but does not. Pulseless electrical activity is found initially in about 55% of people in cardiac arrest.

Under normal circumstances, electrical activation of muscle cells precedes mechanical contraction of the heart (known as "electromechanical coupling"). In PEA, there is electrical activity, but the heart either does not contract or there are other reasons this results in an insufficient cardiac output to generate a pulse and supply blood to the organs. While PEA is classified as a form of cardiac arrest, significant cardiac output may still be present which may be determined and best visualized by bedside ultrasound.

Cardiopulmonary resuscitation (CPR) is the first treatment for PEA, while potential underlying causes are identified and treated. The medication epinephrine may be administered. Survival is about 20%.

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".

Treatment in emergency situations ultimately involves electrical pacing. Pharmacological management of suspected beta-blocker overdose might be treated with glucagon, calcium channel blocker overdose treated with calcium chloride and digitalis toxicity treated with the digoxin immune Fab.

Third-degree AV block can be treated by use of a dual-chamber artificial pacemaker. This type of device typically listens for a pulse from the SA node via lead in the right atrium and sends a pulse via a lead to the right ventricle at an appropriate delay, driving both the right and left ventricles. Pacemakers in this role are usually programmed to enforce a minimum heart rate and to record instances of atrial flutter and atrial fibrillation, two common secondary conditions that can accompany third-degree AV block. Since pacemaker correction of third-degree block requires full-time pacing of the ventricles, a potential side effect is pacemaker syndrome, and may necessitate use of a biventricular pacemaker, which has an additional 3rd lead placed in a vein in the left ventricle, providing a more coordinated pacing of both ventricles.

The 2005 Joint European Resuscitation and Resuscitation Council (UK) guidelines state that atropine is the first line treatment especially if there were any adverse signs, namely: 1) heart rate 3 seconds. Mobitz Type 2 AV block is another indication for pacing.

As with other forms of heart block, secondary prevention may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce risk factors associated with heart attack and stroke.

The prognosis of patients with complete heart block is generally poor without therapy. Patients with 1st and 2nd degree heart block are usually asymptomatic.

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.

Literature survey on epidemiology and pathology of cardiac fibroma:

During this study, researchers searched through the literature databases on cardiac fibroma to find factors that predict poor outcomes that lead to death. Researchers found that patients who did not survive were significantly younger than those who did survive. These results suggest that younger individuals diagnosed with cardiac fibroma are associated with a poorer outcome. They found no significant difference between the maximum diameter of the tumor between age groups. Even though younger individuals have smaller hearts, the high ratio of tumor-to-heart sizes may generate low cardiac output, which leads to a poor outcome. Literature revealed that 18 of 178 patients with cardiac fibroma were diagnosed during prenatal and neonatal periods, resulting in the tumor having a certain size regardless of the child's age. These findings suggest that cardiac fibromas may be a congenital disorder.

Successful Surgical Excision of a Large Cardiac Fibroma in an Asymptomatic Child:

A 3-year-old girl, who was asymptomatic, underwent a successful surgical excision of a large cardiac fibroma. She had frequent coughs, which led to a chest radiograph. A cardiac mass was found on the echocardiography and later was confirmed by magnetic resonance imaging (MRI). After 24 hours of being monitored, it showed sinus rhythms of normal variability. The mass dimensions were 38 X 28 mm in the apical area of the left ventricle. A surgical procedure was recommended due to the risk of ventricular arrhythmias and sudden cardiac death. The surgery was a success and they were able to remove the entire tumor without any complications. Follow-up evaluations at six-months and a year showed the patient was in good health and no signs of tumor recurrence. Asymptomatic patients with cardiac fibroma becomes controversial because these tumors have the tendency to grow. Situations like this, a surgical removal will be the top recommendation for patients.

Primary cardiac tumors in children: a center's experience:

The Department of Cardiac Surgery Children's Hospital in China conducted a study to analyze different characteristics and outcomes of pediatric patients who have primary cardiac tumors treated in their center. They had sixteen patients with primary cardiac tumors between the ages of 1–13 years. All patients were diagnosed by echocardiography, MRI, and computed tomography (CT). As a result, they were able to successfully remove the mass from 15 patients with cardiopulmonary bypass, whereas partial resection was done in one patient. Unfortunately, one patient died during surgery due to low cardiac output syndrome at 5 days after operation. The pathological examination of the cardiac masses showed that rhabdomyoma is the most frequent tumor in children, followed by myxoma, fibromas, etc. Morbidity of rhabdomyomas and fibromas were reported higher in infancy, while myxomas are more frequent in older children.