Rate control to a target heart rate of less than 110 beats per minute is recommended in most people. Lower heart rates may be recommended in those with left ventricular hypertrophy or reduced left ventricular function. Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, decreasing the number of impulses that conduct into the ventricles. This can be done with:

- Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, bisoprolol, or nebivolol)

- Non-dihydropyridine calcium channel blockers (e.g., diltiazem or verapamil)

- Cardiac glycosides (e.g., digoxin) – have less use, apart from in older people who are sedentary. They are not as effective as either beta blockers or calcium channel blockers.

In those with chronic disease either beta blockers or calcium channel blockers are recommended.

In addition to these agents, amiodarone has some AV node blocking effects (in particular when administered intravenously), and can be used in individuals when other agents are contraindicated or ineffective (particularly due to hypotension).

The main goals of treatment are to prevent circulatory instability and stroke. Rate or rhythm control are used to achieve the former, whereas anticoagulation is used to decrease the risk of the latter. If cardiovascularly unstable due to uncontrolled tachycardia, immediate cardioversion is indicated. Regular, moderate-intensity exercise is beneficial for people with AF.

In general, atrial flutter should be managed the same as atrial fibrillation. Because both rhythms can lead to the formation of a blood clot in the atrium, individuals with atrial flutter usually require some form of anticoagulation or antiplatelet agent. Both rhythms can be associated with dangerously fast heart rates and thus require medication to control the heart rate (such as beta blockers or calcium channel blockers) and/or rhythm control with class III antiarrhythmics (such as ibutilide or dofetilide). However, atrial flutter is more resistant to correction with such medications than atrial fibrillation. For example, although the class III antiarrhythmic agent ibutilide is an effective treatment for atrial flutter, rates of recurrence after treatment are quite high (70-90%). Additionally, there are some specific considerations particular to treatment of atrial flutter.

Atrial flutter is considerably more sensitive to electrical direct current cardioversion than atrial fibrillation, with a shock of only (20 to 50) J commonly being enough to cause a return to a normal heart rhythm (sinus rhythm). Exact placement of the pads does not appear important.

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.

First-line therapy for people with heart failure due to reduced systolic function should include angiotensin-converting enzyme (ACE) inhibitors (ACE-I) or angiotensin receptor blockers (ARBs) if the person develops a long term cough as a side effect of the ACE-I. Use of medicines from this class is associated with improved survival and quality of life in people with heart failure.

Beta-adrenergic blocking agents (beta blockers) also form part of the first line of treatment, adding to the improvement in symptoms and mortality provided by ACE-I/ARB. The mortality benefits of beta blockers in people with systolic dysfunction who also have atrial fibrillation (AF) is more limited than in those who do not have AF. If the ejection fraction is not diminished (HFpEF), the benefits of beta blockers are more modest; a decrease in mortality has been observed but reduction in hospital admission for uncontrolled symptoms has not been observed.

In people who are intolerant of ACE-I and ARBs or who have significant kidney dysfunction, the use of combined hydralazine and a long-acting nitrate, such as isosorbide dinitrate, is an effective alternate strategy. This regimen has been shown to reduce mortality in people with moderate heart failure. It is especially beneficial in African-Americans (AA). In AAs who are symptomatic, hydralazine and isosorbide dinitrate (H+I) can be added to ACE-I or ARBs.

In people with markedly reduced ejection fraction, the use of an aldosterone antagonist, in addition to beta blockers and ACE-I, can improve symptoms and reduce mortality.

Second-line medications for CHF do not confer a mortality benefit. Digoxin is one such medication. Its narrow therapeutic window, a high degree of toxicity, and the failure of multiple trials to show a mortality benefit have reduced its role in clinical practice. It is now used in only a small number of people with refractory symptoms, who are in atrial fibrillation and/or who have chronic low blood pressure.

Diuretics have been a mainstay of treatment for treatment of fluid accumulation, and include diuretics classes such as loop diuretics, thiazide-like diuretic, and potassium-sparing diuretic. Although widely used, evidence on their efficacy and safety is limited, with the exception of mineralocorticoid antagonists such as spironolactone. Mineralocorticoid antagonists in those under 75 years old appear to decrease the risk of death. A recent Cochrane review found that in small studies, the use of diuretics appeared to have improved mortality in individuals with heart failure. However, the extent to which these results can be extrapolated to a general population is unclear due to the small number of participants in the cited studies.

Anemia is an independent factor in mortality in people with chronic heart failure. The treatment of anemia significantly improves quality of life for those with heart failure, often with a reduction in severity of the NYHA classification, and also improves mortality rates. The latest European guidelines (2012) recommend screening for iron-deficient anemia and treating with parenteral iron if anemia is found.

The decision to anticoagulate people with HF, typically with left ventricular ejection fractions <35% is debated, but generally, people with coexisting atrial fibrillation, a prior embolic event, or conditions which increase the risk of an embolic event such as amyloidosis, left ventricular noncompaction, familial dilated cardiomyopathy, or a thromboembolic event in a first-degree relative.

People with the most severe heart failure may be candidates for ventricular assist devices (VAD). VADs have commonly been used as a bridge to heart transplantation, but have been used more recently as a destination treatment for advanced heart failure.

In select cases, heart transplantation can be considered. While this may resolve the problems associated with heart failure, the person must generally remain on an immunosuppressive regimen to prevent rejection, which has its own significant downsides. A major limitation of this treatment option is the scarcity of hearts available for transplantation.

Treatment is not necessary in asymptomatic patients.

The treatment options for mitral stenosis include medical management, mitral valve replacement by surgery, and percutaneous mitral valvuloplasty by balloon catheter.

The indication for invasive treatment with either a mitral valve replacement or valvuloplasty is NYHA functional class III or IV symptoms.

Another option is balloon dilatation. To determine which patients would benefit from percutaneous balloon mitral valvuloplasty, a scoring system has been developed. Scoring is based on 4 echocardiographic criteria: leaflet mobility, leaflet thickening, subvalvar thickening, and calcification. Individuals with a score of ≥ 8 tended to have suboptimal results. Superb results with valvotomy are seen in individuals with a crisp opening snap, score < 8, and no calcium in the commissures.

Treatment also focuses on concomitant conditions often seen in mitral stenosis:

- Any angina is treated with short-acting nitrovasodilators, beta-blockers and/or calcium blockers

- Any hypertension is treated aggressively, but caution must be taken in administering beta-blockers

- Any heart failure is treated with digoxin, diuretics, nitrovasodilators and, if not contraindicated, cautious inpatient administration of ACE inhibitors

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.

Mitral valvuloplasty is a minimally invasive therapeutic procedure to correct an uncomplicated mitral stenosis by dilating the valve using a balloon.

Under local anaesthetic, a catheter with a special balloon is passed from the right femoral vein, up the inferior vena cava and into the right atrium. The interatrial septum is punctured and the catheter passed into the left atrium using a "trans-septal technique." The balloon is sub-divided into 3 segments and is dilated in 3 stages. First, the distal portion (lying in the left ventricle) is inflated and pulled against the valve cusps. Second, the proximal portion is dilated, in order to fix the centre segment at the valve orifice. Finally, the central section is inflated, this should take no longer than 30 seconds, since full inflation obstructs the valve and causes congestion, leading to circulatory arrest and flash pulmonary edema.

With careful patient pre-selection, percutaneous balloon mitral valvuloplasty (PBMV) is associated with good success rates and a low rate of complications. By far the most serious adverse event is the occurrence of acute severe mitral regurgitation. Severe mitral regurgitation usually results from a tear in one of the valve leaflets or the subvalvular apparatus. It can lead to pulmonary edema and hemodynamic compromise, necessitating urgent surgical mitral valve replacement.

Other serious complications with PBMV usually relate to the technique of trans-septal puncture (TSP). The ideal site for TSP is the region of the fossa ovalis in the inter-atrial septum. Occasionally, however, the sharp needle used for TSP may inadvertently traumatize other cardiac structures, leading to cardiac tamponade or serious blood loss.

Although the immediate results of PBMV are often quite gratifying, the procedure does not provide permanent relief from mitral stenosis. Regular follow-up is mandatory, to detect restenosis. Long-term follow-up data from patients undergoing PBMV indicates that up to 70-75% individuals can be free of restenosis 10 years following the procedure. The number falls to about 40% 15 years post-PBMV.

Left atrial enlargement can be mild, moderate or severe depending on the extent of the underlying condition. Although other factors may contribute, left atrium size has been found to be a predictor of mortality due to both cardiovascular issues as well as all-cause mortality. Current research suggests that left atrium size as measured by an echo-cardiograph may have prognostic implications for preclinical cardiovascular disease. However, studies that have found LAE to be a predictor for mortality recognize the need for more standardized left atrium measurements than those found in an echo-cardiogram.

In the general population, obesity appears to be the most important risk factor for LAE. LAE has been found to be correlated to body size, independent of obesity, meaning that LAE is more common in people with a naturally large body size. Also, a study found that LAE can occur as a consequence of atrial fibrillation (AF), although another study found that AF by itself does not cause LAE. The latter study also showed that the persistent type of AF was associated with LAE, but the number of years that a subject had AF was not.

Obstructive sleep apnea (OSA) may be a cause of LAE in some cases. When an OSA event occurs, an attempt is made to breathe with an obstructed airway and the pressure inside the chest is suddenly lowered. The negative intrathoracic pressure may cause the left atrium to expand and stretch its walls during each OSA event. Over time, the repetitive stretching of the left atrium may result in a persistent left atrial enlargement.

Preventive measures that can be taken to avoid sustaining a silent stroke are the same as for stroke. Smoking cessation is the most immediate step that can be taken, with the effective management of hypertension the major medically treatable factor.

An embolism is the lodging of an embolus, a blockage-causing piece of material, inside a blood vessel. The embolus may be a blood clot (thrombus), a fat globule (fat embolism), a bubble of air or other gas (gas embolism), or foreign material. An embolism can cause partial or total blockage of blood flow in the affected vessel. Such a blockage (a vascular occlusion) may affect a part of the body distant from where the embolus originated. An embolism in which the embolus is a piece of thrombus is called a thromboembolism. Thrombosis, the process of thrombus formation, often leads to thromboembolism.

An embolism is usually a pathological event, i.e., accompanying illness or injury. Sometimes it is created intentionally for a therapeutic reason, such as to stop bleeding or to kill a cancerous tumor by stopping its blood supply. Such therapy is called embolization.

Arterial embolism can cause occlusion in any part of the body. It is a major cause of infarction, tissue death due to the blockage of blood supply.

An embolus lodging in the brain from either the heart or a carotid artery will most likely be the cause of a stroke due to ischemia.

An arterial embolus might originate in the heart (from a thrombus in the left atrium, following atrial fibrillation or be a septic embolus resulting from endocarditis). Emboli of cardiac origin are frequently encountered in clinical practice. Thrombus formation within the atrium occurs mainly in patients with mitral valve disease, and especially in those with mitral valve stenosis (narrowing), with atrial fibrillation (AF). In the absence of AF, pure mitral regurgitation has a low incidence of thromboembolism.

The risk of emboli forming in AF depends on other risk factors such as age, hypertension, diabetes, recent heart failure, or previous stroke.

Thrombus formation can also take place within the ventricles, and it occurs in approximately 30% of anterior-wall myocardial infarctions, compared with only 5% of inferior ones. Some other risk factors are poor ejection fraction (<35%), size of infarct, and the presence of AF. In the first three months after infarction, left-ventricle aneurysms have a 10% risk of emboli forming.

Patients with prosthetic valves also carry a significant increase in risk of thromboembolism. Risk varies, based on the valve type (bioprosthetic or mechanical); the position (mitral or aortic); and the presence of other factors such as AF, left-ventricular dysfunction, and previous emboli.

Emboli often have more serious consequences when they occur in the so-called "end circulation": areas of the body that have no redundant blood supply, such as the brain and heart.

Transfusion therapy lowers the risk for a new silent stroke in children who have both abnormal cerebral artery blood flow velocity, as detected by transcranial Doppler, and previous silent infarct, even when the initial MRI showed no abnormality. A finding of elevated TCD ultrasonographic velocity warrants MRI of the brain, as those with both abnormalities who are not provided transfusion therapy are at higher risk for developing a new silent infarct or stroke than are those whose initial MRI showed no abnormality.

Treatment should be sought immediately in order to avoid hospitalization. If not treated, hospitalization for an extended period of time (usually two weeks) is likely. During hospitalization, the patient is tested for signs of system degradation, especially of the skeletal structure and the digestive tract. By this time open sores will develop on the upper torso. Some will be the size of dimes, others will be large enough to stick a couple fingers into. They will crust up, causing cohesion to any fabric the sores touch, which is extremely painful to remove. It is recommended to sleep on one's sides until the cystic condition subsides, in order to avoid any uncomfortable situations. Debridement and steroid therapy is preferred over antibiotics. Recurrent AF is extremely rare. Bone lesions typically resolve with treatment, but residual radiographic changes, such as sclerosis and hyperostosis, may remain. Scarring and fibrosis may result from this acute inflammatory process.

The disease activates at the height of puberty, usually at around 13 years of age. Acne fulminans predominantly affects young males aged 13 to 22 years with a history of acne.

Management of AIS is currently limited to symptomatic management; no method is currently available to correct the malfunctioning androgen receptor proteins produced by "AR" gene mutations. Areas of management include sex assignment, genitoplasty, gonadectomy in relation to tumor risk, hormone replacement therapy, genetic counseling, and psychological counseling.

Acne fulminans (also known as "acute febrile ulcerative acne") is a severe form of the skin disease, acne, which can occur after unsuccessful treatment for another form of acne, acne conglobata. The condition is thought to be an immunologically induced disease in which elevated level of testosterone causes a rise in sebum and population of "Propionibacterium acnes" bacteria. The increase in the amount of "P acnes" or related antigens may trigger the immunologic reaction in some individuals and lead to an occurrence of acne fulminans. In addition to testosterone, isotretinoin may also precipitate acne fulminans, possibly related to highly increased levels of "P acnes antigens" in the patient's immune system. Acne fulminans is a rare disease. Over the past several years, fewer cases of this disease have occurred, possibly because of earlier and better treatment of acne. Approximately 100 patients with acne fulminans have been described.

Androgen insensitivity syndrome (AIS) is an intersex condition in which there is a partial or complete inability of many cells in the affected genetic male to respond to androgenic hormones. This can prevent or impair the masculinization of male genitalia in the developing genetic male (chromosomal XY) fetus, as well as the development of male secondary sexual characteristics at puberty. Clinical phenotypes range from a normal male habitus with mild spermatogenic defect or reduced secondary terminal hair; to a full female habitus despite the presence of a Y-chromosome. Women (chromosomal XX) who are heterozygous for the AR gene have normal primary and secondary sexual characteristics; this female carrier will pass the affected AR gene to any child she has with 50% likelihood. AIS is the largest single entity that leads to 46,XY undermasculinized genitalia.

The androgen receptor (AR), which is defective due to a mutation in most of these syndromes, is a type of nuclear receptor that is activated by binding to either of the androgenic hormones (testosterone or dihydrotestosterone) in the cytoplasm, and then translocates into the nucleus where it binds to DNA, provided androgen response elements and coactivators are present. This combination functions as a transcription complex to turn on androgen gene expression. Thus the AR activates these genes to mediate the effects of androgens in the human body, including the development and maintenance of the male sexual phenotype and generalized anabolic effects. Over 400 AR mutations have been reported.

AIS is divided into three categories that are differentiated by the degree of genital masculinization: complete androgen insensitivity syndrome (CAIS) is indicated when the external genitalia are that of a normal female; mild androgen insensitivity syndrome (MAIS) is indicated when the external genitalia are that of a normal male, and partial androgen insensitivity syndrome (PAIS) is indicated when the external genitalia are partially, but not fully, masculinized.

Management of AIS is currently limited to symptomatic management; no method is currently available to correct the malfunctioning androgen receptor proteins produced by "AR" gene mutations. Areas of management include sex assignment, genitoplasty, gonadectomy in relation to tumor risk, hormone replacement therapy, genetic counseling, and psychological counseling.

When someone is suffering from RA, their memory cannot be recovered from simply being told personal experiences and their identity. This is called reminder effect or reminder treatment. The reminder effect consists of re-exposing the patient to past personal information, which cannot reverse RA. Thus, reminding the patient details of their life has no scientific bearings on recovering memory. Fortunately, memory can be and usually is recovered due to spontaneous recovery and plasticity.

Clinically induced RA has been achieved using different forms of electrical induction.

- Electroconvulsive therapy (ECT), used as a depression therapy, can cause impairments in memory. Tests show that information of days and weeks before the ECT can be permanently lost. The results of this study also show that severity of RA is more extreme in cases of bilateral ECT rather than unilateral ECT. Impairments can also be more intense if ECT is administered repetitively (sine wave simulation) as opposed to a single pulse (brief-pulse stimulation).

- Electroconvulsive shock (ECS): The research in this field has been advanced by using animals as subjects. Researchers induce RA in rats, for example, by giving daily ECS treatments. This is done to further understand RA.