The Askaheartsurgeon AF Page This site provides a comprehensive discussion on AF with ECG (EKG) traces of a typical AF pattern The Askaheartsurgeon Homepage

Atrial fibrillation and flutter are abnormal heart rhythms in which the atria, or upper chambers of the heart, are out of sync with the ventricles, or lower chambers of the heart.
Describing how the heart beats normally helps to explain what happens during an arrhythmia. The heart is a muscular pump divided into four chambers--two atria located on the top and two ventricles located on the bottom.

Normally each heartbeat starts in the right atrium. Here, a specialized group of cells called the sinus node, or natural pacemaker, sends an electrical signal. The signal spreads throughout the atria to the area between the atria called the atrioventricular (AV) node.

The AV node connects to a group of special pathways that conduct the signal to the ventricles below. As the signal travels through the heart, the heart contracts. First the atria contract, pumping blood into the ventricles. A fraction of a second later, the ventricles contract, sending blood throughout the body.

Usually the whole heart contracts between 60 and 100 times per minute. Each contraction equals one heartbeat.

It is not a directly life threatening irregular heart beat. It is however a morbid type of condition because it is a major source of blood clots being released from the heart and into the blood stream. These clots can cause strokes, heart attacks, partial loss of conscienceness (near syncope) and/or damage to organs to which the clot travels. Other indirect causes of morbidity include worsening heart muscle function and size as well as weakening of the normal electrical system of the heart.
Atrial fibrillation (AF) is the most frequent occurring cardiac rhythm disturbance. The prevalence of atrial fibrillation increases with age; this arrhythmia is most often seen in patients older than 65 years.The incidence and frequency increase with age. AF progresses gradually from brief undetected, transient bouts of irregular heart beat to more sustained episodes that spontaneously revert to normal sinus rhythm and can finally enter a chronic stage that seldom returns to normal sinus rhythm.

Please note the chaotic cardio electric activity in the Atria, and that until an electro-chemical pulse reaches the AV-node with enough energy to over come the AV-node threshold, the A/V node will not depolarize.Also note the flattened EKG base line with the fibrillating f-waves, in the EKG strip ABOVE.

Please note in this animated demonstration, the Atrial Fibrillation f-waves, and the chaotic variability of the rate

Please note in this animated demonstration the cyclic Atrial Flutter that causes the abnormal cardio conduction pattern from the Atrium to the A/V Node.

Please note the lack of PR Interval in the wave pattern, and the related "Saw tooth" F- waves in this animation of the EKG strip.

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The condition AF is difficult to detect and can range from being very symptomatic to an incidental finding during a routine physical examination. Patients can have any one of the following symptoms: shortness of breath, loss of exercise ability, chest pain, rapid heart beating (as if one's heart is jumping out of one's chest), inability to lay flat, lightheadedness and/or loss of consciousness. The exam demonstrates a pulse that is irregularly irregular and is usually more rapid than normal. That is, greater than 100 beats per minute.

AF is usually the consequence of heart disease which increases the occurrence of AF by three to five fold. It is most commonly seen in hypertensive, heart artery (coronary) and valvular disease especially in the setting of heart failure (poor heart muscle function). Other heart conditions that predispose one to AF are acute blockages of any heart artery, heart surgery and inflammation of the heart's lining (pericardium).

AF can also be triggered by alcohol intake, certain drugs and medical procedures as well as thyroid organ disease. Occasionally, AF is seen in patients with no discernible cause. This is referred to as "lone" AF. This is possibly due to microscopic changes in the tissue anatomy and function of the atria (the two top chambers of the heart).

Neurohormonal influences (nerves and hormones) also play a large role in the coming and going of AF. These influences can either speed up the heart rate or slow it down. The cause of AF is very broad but is very important to know when treatment is being considered. Recent experiments have suggested that AF causes AF. That is, the more you have AF then the harder it is to revert to normal sinus rhythm.

Diagnosis

The method of diagnosis is at the discretion of the patients symptoms and their physician. In other words, it is patient specific.

Tests for Detecting Arrhythmias
Electrocardiogram (ECG or EKG). A record of the electrical activity of the heart. Disks are placed on the chest and connected by wires to a recording machine. The heart's electrical signals cause a pen to draw lines across a strip of graph paper in the ECG machine. The doctor studies the shapes of these lines to check for any changes in the normal rhythm. The types of ECGs are:

Resting ECG. The diagnosis of AF requires an electrocardiogram (ECG) which can be done in the office or as an outpatient via a portable monitor (holter). The patient lies down for a few minutes while a record is made. In this type of ECG, disks are attached to the patient's arms and legs as well as to the chest. Another method of diagnosis is an event monitor which can be applied when symptoms of irregular heart beat start.

Exercise ECG (stress test). The patient exercises either on a treadmill machine or bicycle while connected to the ECG machine. This test tells whether exercise causes arrhythmias or makes them worse or whether there is evidence of inadequate blood flow to the heart muscle ("ischemia").

24-hour ECG (Holter) monitoring. The patient goes about his or her usual daily activities while wearing a small, portable tape recorder that connects to the disks on the patient's chest. Over time, this test shows changes in rhythm (or "ischemia") that may not be detected during a resting or exercise ECG.

Transtelephonic monitoring. The patient wears the tape recorder and disks over a period of a few days to several weeks. When the patient feels an arrhythmia, he or she telephones a monitoring station where the record is made. If access to a telephone is not possible, the patient has the option of activating the monitor's memory function. Later, when a telephone is accessible, the patient can transmit the recorded information from the memory to the monitoring station. Transtelephonic monitoring can reveal arrhythmias that occur only once every few days or weeks.

Electrophysiologic study (EPS). A test for arrhythmias that involves cardiac catheterization. Very thin, flexible tubes (catheters) are placed in a vein of an arm or leg and advanced to the right atrium and ventricle. This procedure allows doctors to find the site and type of arrhythmia and how it responds to treatment.

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P&S Medical Review: Oct 1994, Vol.2, No.1

Treatment of Cardiac Arrhythmias

Brian F. Hoffman, M.D.

Department of Pharmacology, College of Physicians and Surgeons, New York, NY

ABSTRACT:

The pharmacological treatment of many cardiac arrhythmias is unsatisfactory in terms of both efficacy and safety. Some of the reasons for this are described. Even though the electrophysiological mechanisms for different types of arrhythmias have been adequately described, often it is not possible to assign a particular mechanism to the arrhythmia presented by a patient. Improved means to identify mechanisms in patients clearly are needed. Also, we have a reasonably adequate understanding of the mechanisms of action of available antiarrhythmic agents. With respect to the arrhythmogenic potential of both class I and class III drugs probable mechanisms have been identified. This information indicates that the production of new arrhythmias is an anticipated consequence of the primary mechanism of action of both classes of agents. To improve efficacy of available agents the suggestion is made that, for each arrhythmogenic mechanism, a suitable vulnerable parameter be identified and selection of a particular agent be based on the electrophysiological basis for this parameter. To reduce arrhythmogenic potential a suggestion is made that antiarrhythmic drugs acting by new mechanisms are needed.

For the full text of this article please click on this link

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Anticoagulation/Antiplatelet therapy

Coumadin (Warfarin)

Despite the lack of resolve regarding rhythm treatments, blood thinning therapy has been well tested and accepted in the prevention of strokes in patients with AF. Multiple studies have confirmed the benefit of warfarin (coumadin) therapy over aspirin therapy in specific patients with AF. AF patient populations, over the age of 65 or with one of the following: hypertension, diabetes mellitus, congestive heart failure or previous strokes, clearly benefit from wafarin.

Aspirin AF patients under age 65 and typically with "lone" AF (structurally normal heart) can safely be treated with aspirin (antiplatelet) therapy.

Without treatment with either warfarin or aspirin, patients with AF can suffer strokes at an incidence of ~4% / year. With treatments, the incidence of stroke is less than 1%.

The treatment of atrial fibrillation is extremely variable. It depends on the presentation of the patient as well as the underlying heart disease. Often your physician's practice theories and beliefs play a role in therapy. There are many ongoing investigational trials involving patients with AF and related conditions. The current options include:

ExternalCardioversion

- Conversion of AF to normal sinus rhythm can be accomplished with some of the medicines mentioned above. It can also be performed with an across the chest shock using DC energy. The shock treatment is about 92% effective at acutely converting AF back to normal rhythm. It is performed under deep anesthesia and is very safe. The safety has been increased with the added benefits of anticoagulation described above and the emergence of the mildly invasive procedure called transesophageal echocardiography. Warfarin prevents the formation of clots in the heart and the echocardiogram confirms the absence of any clots.

This procedure takes about 30 minutes and 1-2 hours of recovery. It is not meant to maintain normal rhythm but to regain it immediately. The maintenance of normal rhythm requires one of the drug therapies or procedures described above.

Depending on the clinical circumstances surrounding the initiation of AF, electrical or pharmacologic conversion to normal rhythm may be an emergency. This emergent type of therapy is reserved usually for critically ill patients who may require normal rhythm.

Drugs and their effects
Control of Heart Rate- blocking the junction between the two upper and two lower chambers can be accomplished by a variety of methods that range between medicines to a cautery procedure called ablation. Both are designed to decrease normal conduction of impulses to the ventricles via the atrio ventricular node (AV node). (See below)

Medications used to control the heart rate include classes of drugs such as digitalis, beta - blockers (metoprolol ,atenolol, etc.) and calcium channel blockers (verapamil, diltiazem). Rarely other more potent drugs can be used including amiodarone or sotalol.

Medications: One rhythm controlling treatment is medications that control the electrical pathways of the heart muscle. These medicines are taken daily to in effect maintain a normal heart rate and rhythm and prevent AF. There are five classes of drugs that are used in this endeavor. They include:

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Procainamide increases the effective refractory period of the atria, and to a lesser extent, the bundle of His-Purkinje system and ventricles of the heart. It reduces impulse conduction velocity in the atria, His-Purkinje fibers and ventricular muscle, but has variable effects on the atrioventricular (A-V) node, a direct slowing action and a weaker vagolytic effect which may speed A-V conduction slightly. Myocardial excitability is reduced in the atria, Purkinje fibers, papillary muscles and ventricles by an increase in the threshold for excitation, combined with inhibition of ectopic pacemaker activity by retardation of the slow phase of diastolic depolarization, thus decreasing automaticity especially in ectopic sites.
This exerpt is taken from the introductary paragraph of this excellent link - RxList

Heart and Vascular Education Foundation

Montifiore Einstein heart Center

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TAMBOCOR has local anesthetic activity and belongs to the membrane stabilizing (Class 1) group of antiarrhythmic agents; it has electrophysiologic effects characteristic of the IC class of antiarrhythmics.

Electrophysiology. In man, TAMBOCOR produces a dose-related decrease in intracardiac conduction in all parts of the heart with the greatest effect on the His-Purkinje system (H-V conduction). Effects upon atrioventricular (AV) nodal conduction time and intra-atrial conduction times, although present, are less pronounced than those on ventricular conduction velocity. Significant effects on refractory periods were observed only in the ventricle. Sinus node recovery times (corrected) following pacing and spontaneous cycle lengths are somewhat increased. This latter effect may become significant in patients with sinus node dysfunction. (See Warnings.)

TAMBOCOR causes a dose-related and plasma-level related decrease in single and multiple PVCs and can suppress recurrence of ventricular tachycardia. In limited studies of patients with a history of ventricular tachycardia, TAMBOCOR has been successful 30-40% of the time in fully suppressing the inducibility of arrhythmias by programmed electrical stimulation. Based on PVC suppression, it appears that plasma levels of 0.2 to 1.0 µg/mL may be needed to obtain the maximal therapeutic effect. It is more difficult to assess the dose needed to suppress serious arrhythmias, but trough plasma levels in patients successfully treated for recurrent ventricular tachycardia were between 0.2 and 1.0 µg/mL. Plasma levels above 0.7-1.0 µg/mL are associated with a higher rate of cardiac adverse experiences such as conduction defects or bradycardia. The relation of plasma levels to proarrhythmic events is not established, but dose reduction in clinical trials of patients with ventricular tachycardia appears to have led to a reduced frequency and severity of such events. ............
Extract from:Tambocor - 3M

Occasionally doctors prescribe Lopressor for the treatment of aggressive behavior, prevention of migraine headache, and relief of temporary anxiety.

An extended-release form of this drug, called Toprol-XL, is also available.

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Corgard (nadolol) is a nonselective beta-adrenergic receptor blocking agent.

Corgard blocks the response to beta adrenergic stimulation by specifically competing with adrenergic receptor agonists for available beta-1 and beta-2 receptor sites. At beta-1 adrenergic receptor sites - located chiefly in cardiac muscle - it inhibits the chronotropic and inotropic responses of the heart; in the bronchial and vascular musculature, it occupies beta-2 adrenergic receptor sites, thus inhibiting brochodilation and vasodilation. Corgard has neither intrinsic sympathomimetic activity, nor membrane stabilising action. Animal and human studies show that Corgard slows the sinus rate and depresses AV conduction. Corgard has low lipophilicity as determined by octanol/water partition coefficient (0.71). The extent to which it crosses the blood-brain barrier is limited compared with the less hydrophilic beta adrenergic blockers and may contribute to a lower incidence of CNS side effects.

The mechanism of the antihypertensive effects of beta-adrenergic receptor blocking agents has not been established. While cardiac output and arterial pressure are reduced by nadolol therapy, renal haemodynamics are stable, with preservation of renal blood flow and glomerular filtration rate.

By blocking catecholamine-induced increases in the heart rate, the velocity and extent of myocardial contraction, and in blood pressure, Corgard® (nadolol) generally reduces the oxygen requirements of the heart at any given level of effort, making it useful for many patients in the long-term management of angina pectoris. On the other hand, nadolol can increase oxygen requirements by increasing left ventricular fibre length and end diastolic pressure, particularly in patients with heart failure.

Although beta-adrenergic receptor blockade is useful in treatment of angina and hypertension, there are situations in which sympathetic stimulation is vital, and beta-adrenergic blocker therapy not appropriate. For example, in patients with severely damaged hearts, adequate ventricular function may depend on sympathetic drive. Beta-adrenergic blockade may worsen AV block by preventing the necessary facilitating effects of sympathetic activity on conduction. Beta2-adrenergic blockade results in passive bronchial constriction in patients subject to bronchospasm, and may interfere with endogenous or exogenous bronchodilators in such patients.

The mechanism of the antimigraine effect of Corgard has not been established.

The Class II antiarrhythmic activity of beta blockers is primarily due to its selectively blocking ß-adrenergic modulation of the atrioventricular node, which increases the effective refractory period of the AV node.

Beta-adrenergic blockade controls symptoms associated with hyperthyroidism, including tremor, anxiety and muscle weakness.

For a complete data sheet on Corgard click this link

Amiodarone (Cordarone)
Actions AMIODARONE is a Class III anti-arrhythmic agent prolonging the action potential duration and hence refractory period of atrial, nodal and ventricular tissues thereby giving a very broad spectrum of activity. An increase in the refractory period of the atrial cells is a major contributing action to the control of atrial tachyarrhythmias.

A reduction in the permeability of A-V node, both anterograde and retrograde, explains the efficacy of the agent in nodal tachycardias caused by re-entry through the A-V node.

Its action on ventricular arrhythmias is explained by a number of mechanisms. The effect on the atrium and A-V node results in a reduction in the frequency of stimuli reaching the ventricles thus giving the ventricular cell mass time to repolarise in cases where there has been desynchronisation of the refractory periods. Furthermore, a lengthening of the refractory period of the His-Purkinje system and ventricular contractile fibres reduces or prevents micro re-entry. AMIODARONE increases coronary blood flow, decreases cardiac oxygen requirements without producing negative inotropic effects and also suppresses `ectopic pacemakers' and this is particularly valuable in arrhythmias associated with ischaemic damage or angina pectoris. AMIODARONE demonstrates non-competitive alpha- and beta-adrenoceptor antagonism.

The site and mode of action of AMIODARONE can be summarised in terms of its effect on myocardial electrophysiology.

Myocardial Electrophysiology: Sinus Node: It decreases sinus automaticity by reducing the slow diastolic depolarisation gradient in the nodal cell. This is a direct effect and is not mediated through the sympathetic or parasympathetic system.

Atrio-Ventricular (A-V) Node: It reduces the speed of conduction and increases the refractory period of the A-V node.

His-Purkinje System: It increases the refractory period but does not modify the speed of conduction of the His-Purkinje system.

Contractile Fibres: It increases the action potential but does not alter the rate of depolarisation of the atrial or ventricular myocardial cells; an effect that is more marked in the atria than the ventricles.

For a complete discussion on Amioderone click this link

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Sotalol hydrochloride uniformly prolongs the action potential duration in cardiac tissues by delaying only the repolarisation phase. Its major effects are prolongation of the atrial, ventricular and accessory pathway effective refractory periods. The Class II and Class III properties may be reflected on the surface electrocardiogram by a lengthening of the PR, QT and QTc (QT corrected for heart rate) intervals with no significant alteration of the QRS duration.

Although significant beta-adrenergic blockade may occur at oral doses as low as 25mg, Class III effects are usually seen at daily doses of greater than 160mg.

Pharmacologically, in addition to its antiarrhythmic properties, sotalol hydrochloride also has antihypertensive and antianginal properties.

Haemodynamics: In humans, APO-SOTALOL produces consistent reductions in heart rate and cardiac output, with no reduction in stroke volume.

In hypertensive patients, APO-SOTALOL produces significant reductions in both systolic and diastolic blood pressures. Although sotalol hydrochloride is usually well tolerated haemodynamically, caution should be exercised in patients with marginal cardiac reserve as deterioration in cardiac performance may occur.

Electrophysiology: In humans, the Class II (beta-blockade) electrophysiological effects of sotalol hydrochloride are manifested by increased sinus cycle length (slowed heart rate), decreased AV nodal conduction and increased AV nodal refractoriness. The Class III electrophysiological effects include prolongation of the atrial and ventricular monophasic action potentials and effective refractory period prolongation of atrial muscle, ventricular muscle and atrioventricular accessory pathways (where present) in both the anterograde and retrograde directions. With oral doses of 160mg to 640 mg per day, the surface ECG shows dose-related mean increases of 40-100msec in QT and 10-40msec in QTc. No significant alteration in QRS interval is observed.

For a complete Data Sheet on Sotalol click this link

Ibutilide prolongs action potential duration in isolated adult cardiac myocytes and increases both atrial and ventricular refractoriness in vivo. Voltage clamp studies indicate that ibutilide, at nanomolar concentrations, delays repolarization by activation of a slow, inward current (predominantly sodium) rather than by blocking outward potassium currents, which is the mechanism by which most other class III antiarrhythmics act.

In humans, the predominant electrophysiologic property of CORVERT Solution for Infusion is demonstrated by prolongation of effective refractory periods in atrial and ventricular muscle.

When ibutilide fumarate solution was given intravenously to animals at doses greater than ten times the human dose, mild, negative inotropic effects were observed (less than 8% decrease in left ventricular contractility).

A study of hemodynamic function in patients stratified for ejection fractions (greater than or equal to 35% and less than 35%) demonstrated no clinically significant effects on cardiac output, mean pulmonary arterial pressure, or capillary wedge pressure at doses up to 0.03mg/kg ibutilide fumarate.

CORVERT produces mild slowing of the sinus rate and atrioventricular conduction. CORVERT produces no clinically significant effect on QRS duration at intravenous doses up to 0.03mg/kg ibutilide fumarate administered over a 10-minute period. Although there is no established relationship of plasma concentration to antiarrhythmic effect, CORVERT produces dose-related prolongation of the QT interval, which is thought to be associated with its antiarrhythmic activity. Maximal concentrations and maximal QT interval prolongations are observed at the end of infusion. The observed maximum effect was a function of the dose and the infusion rate of CORVERT as well as the age of the subject: the magnitude of prolongation was less in older subjects. No difference in QT interval prolongation was observed between males and females.

For a complete data sheet on Corvert click this link

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Verapamil hydrochloride is a calcium antagonist that inhibits influx of calcium into cells. As such it inhibits transmission of the cardiac action potential through the atrioventricular node and causes relaxation of vascular smooth muscle.

Pharmacokinetics

Verapamil is almost completely absorbed from the gastrointestinal tract after oral administration, but it is subject to considerable first-pass metabolism such that systemic bioavailability ranges from 20-35%. Peak plasma concentrations are achieved at approximately 30 minutes after administration of a single tablet dose and range between 50-100ng/mL depending upon the potency given. Slightly higher plasma levels may be achieved at steady state after chronic administration. A non-linear correlation between verapamil dose administered and verapamil plasma levels exists.

After capsule administration, two peaks in the plasma levels are seen, one at approximately one hour and the other at approximately eight hours. This is a reflection of the product formulation in that a small percentage of the verapamil hydrochloride is present in a form allowing immediate release after capsule administration.

The following pharmacokinetic parameters have been measured after administration of a single 80mg verapamil HCl tablet: Cmax 78.8ng/mL, tmax 1.05h and AUC 280.8ngh/mL.

At steady state after continuous administration of 80mg three times a day, the measured parameters were: Cmax 172.8ng/mL, tmax 1.52h and AUC 694.2ngh/mL.

The following pharmacokinetic parameters have been measured after administration of a single dose of the 240mg capsules: Cmax 83.82ng/mL, tmax 7.55h and AUC0-48h 1128.5ngh/mL. At steady state after continuous administration of 240mg once daily as the capsule, the measured parameters were: Cmax 117.6ng/mL, tmax 7.68h and AUC0-48h 1573.0ngh/mL.

Other single dose studies using the tablets give plasma half-lives ranging from 3-7 hours, while at steady state after continuous administration some studies have shown an increase in t1/2 to between 4.5-12 hours. For the capsules the half-life has been measured as 8.9 hours after single dose administration and 9.0 hours after continuous administration. Verapamil hydrochloride is extensively bound to plasma proteins.

Elimination occurs by metabolism in the liver followed by excretion in the urine and faeces. About 70% of a dose will appear as urinary metabolites, 16% as faecal metabolites and 3-4% as unchanged verapamil in the urine within 5 days of administration of the dose. Twelve metabolites have been identified in the plasma, all except norverapamil are present in trace amounts only. Norverapamil exhibits about 20% of the activity of verapamil. Plasma levels can approach those of verapamil. After administration of an 80mg tablet, the following pharmacokinetic parameters have been measured for norverapamil: Cmax 52.7ng/mL and 140.0ng/mL, tmax 1.9h and 1.8h, AUC0-48h 467.0ngh/mL and 888.7ngh/mL, t1/2 7.0h and 10.0h for single dose and continuous administration respectively. After administration of 240mg verapamil hydrochloride as the capsule, the pharmacokinetic parameters for norverapamil were: Cmax 69.6ng/mL and 112.8ng/mL, tmax 9.4h and 9.0h, AUC0-48h 1459.6ngh/mL and 1981.2ngh/mL, t1/2 11.5h and 12.4h, for single dose and continuous administration respectively.

In patients with hepatic insufficiency, metabolism is delayed with prolongation of plasma half-life, increase in volume of distribution and reduction in plasma clearance to about 30% of normal. Therapeutic verapamil plasma concentrations may be obtained with one third of normal oral daily doses.

On continuous administration verapamil and norverapamil can enter cerebrospinal fluid, partition coefficients having been estimated as 0.06 for verapamil and 0.04 for norverapamil.

This data is extracted from the full data sheet available here:

Diltiazem hydrochloride acts as a potent coronary vasodilator and also has a moderate effect on the peripheral circulation. Diltiazem hydrochloride may also prolong AV nodal conduction.

Pharmacokinetics

Diltiazem hydrochloride is almost completely absorbed and reaches peak plasma levels within half an hour. It is metabolised in the liver and excretion is mainly faecal. Its half-life is approximately 4 to 6 hours.

The main active metabolite is desacetyl diltiazem. This is present in the plasma at levels of 10 to 20% of the parent medicine and is 25 to 50% as potent as a coronary vasodilator as diltiazem.

This data is extracted from the full data sheet available here:

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Ablation

Internal Atrial Cardioverter: Cardioverter-defibrillators have been developed for prevention of sudden death by fast irregular heart beats from the lower cardiac chambers (ventricles). This technology has also been applied to paroxysmal atrial fibrillation with the advent of an internal atrial defibrillator. This is permanently implanted with specialized shocking lead systems and a battery source is attached to the leads. If AF is sensed and the device delivers an internal shock in order to convert it to normal rhythm. This is currently in early stages of experimentation. Attempts are being made to determine optimal lead placement in order to be successful at the lowest energy and highest energy. The patient selection is going to be limited due to clinical circumstances.

Just being released for use in electrophysiology labs is a temporary wire to internally cardiovert patients into normal sinus rhythm. It will have applications during electrophysiology studies and for patients who fail external (meaning to deliver a shock energy through the chest wall to the heart) cardioversion. Thus it will be used in a limited number of patients, but will likely be very helpful for difficult cases.

Open HeartSurgery Maze/Corridor: The other rhythm controling treatments are in experimental phases. Open heart operations (Corridor or Maze Procedures) that create, through specific atrial (two top chambers of the heart) incisions, an inability to sustain AF have been successful in select patient populations. In a preliminary sense, these techniques are revolutionary with far reaching implications.

Catheter Maze: They have led to another anatomic and physiologic approach which has used theories similar to the open heart procedures. It is a catheter ablation (cautery) technique without the need for open heart surgery. It attempts to mimic the lines of blockade proven successful by the heart surgery incisions.
Cautery is performed utilizing radiofrequency energy which is directed through a wire tip called a catheter. The size of the tip and contact to the heart muscle causes a temperature rise which then eliminates the electrical properties of the tissue. The cautery procedure (AV nodal ablation) requires that a pacemaker be permanently installed. The pacemaker can be placed before or after the cautery procedure depending on the patients circumstances.

Prognosis

The disorder is usually controllable with treatment. Atrial fibrillation may become a chronic condition. Atrial flutter is usually a short-term problem.
When an underlying cause of atrial fibrillation is identified and treated, the arrhythmia frequently resolves. Achieving a normal heartbeat is less likely for individuals who have long-standing rheumatic heart disease or any condition in which the atria are enlarged.

Principles of Prognosis This site provides an excellent dissertation of the guiding principles in determining a prognosis.