Treatment of Atrial fibrillation
Goal of the treatment:
• To prevent formation of blood clots that might lead to blockage of other vessels.
• To control the rate of contraction so that ventricles have enough time to fill up.
• To restore the sinus rhythm so that the atria and ventricles work together in coordination.
• Preventive measures

Blood clot prevention
Drugs such as warfarin, heparin and aspirin are prescribed to reduce the risk of blood clot.
Warfarin and heparin are anticoagulants that act via the coagulation cascade.
Warfarin interrupts the coagulation pathway by causing an antagonising the effect of Vitamin K. The activity of clotting factors II, VII, IX,X are dependent on vitamin K.


Heparin inhibits the pathway by enhancing the effect of antithrombin. Antithrombin inactives the enzyme thrombin, that is responsible for the conversion of fibrinogen into fibrin.


Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets.
Thromboxane A2 has the effect of increasing the number of platelets and also causing platelets to coagulate.
This anticoagulant property makes aspirin useful for reducing the incidence of heart attacks.


Rate control
Doctors prescribe medicines to slow down the rate at which the ventricles are beating so that the ventricles have time to fill up completely.
Beta blockers (for example, metoprolol and atenolol), calcium channel blockers (diltiazem and verapamil) are the drugs used.



Beta-blockers bind to beta-adrenoceptors located in cardiac nodal tissue, the conducting system, and contracting myocytes. The heart has both β1 and β2 adrenoceptors, although the predominant receptor type in number and function is β1. These receptors primarily bind norepinephrine that is released from sympathetic adrenergic nerves. Additionally, they bind norepinephrine and epinephrine that circulate in the blood. Beta-blockers prevent the normal ligand (norepinephrine or epinephrine) from binding to the beta-adrenoceptor by competing for the binding site.
Beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate.

Calcium channel blockers work by blocking voltage-gated calcium channels in cardiac muscle and blood vessels. This decreases intracellular calcium leading to a reduction in muscle contraction. In the heart, a decrease in calcium available for each beat results in a decrease in cardiac contractility.
Cardiac contractility is defined as the ability of cardiac muscles to contract to at a given fiber length.
Calcium channel blockers also tend to decrease the blood pressure and the sympathetic nerve will adjust for this drop in BP by causing increase in heart rate.

Therefore calcium channel blockers are often taken with a beta blocker to avoid the reflexive action.

Rhythm control
The longer you have AF, the less likely it is that an abnormal heart rhythm can be restored to a normal heart rhythm. This is especially true for people who have had AF for 6 months or more.
Medicines used to control the heart rhythm include amiodarone, sotalol, flecainide, propafenone, dofetilide, and ibutilide.
Most of the drugs that control rhythm act on the conduction velocity of electric impulses(Sodium-channel blockers) or the duration of the refractory periods of the muscles(Potassium-channel blockers).
Sodium-channel blockers decrease the conduction velocity by making only a few channels available for passage of ions. In reducing the conduction velocity, the time between atrial and ventricular contractions is increased. This type of drug is used to treat tachyarrhythmias.





Procedures
Cardioversion
Transient delivery of electrical current causes a momentary depolarization of most cardiac cells allowing the sinus node to resume normal pacemaker activity. In the presence of reentrant-induced arrhythmia electrical cardioversion interrupts the self-perpetuating circuit and restores a sinus rhythm.
http://www.youtube.com/watch?v=Ud0m7IrEQf0
To perform synchronized electrical cardioversion two electrode pads are used, each comprising a metallic plate which is faced with a saline based conductive gel.
The pads are placed on the chest of the patient, or one is placed on the chest and one on the back. These are connected by cables to a machine which has the combined functions of an ECG display screen and the electrical function of a defibrillator.
A synchronizing function (either manually operated or automatic) allows the cardioverter to deliver a reversion shock, by way of the pads, of a selected amount of electric current over a predefined number of milliseconds at the optimal moment in the cardiac cycle which corresponds to the R wave of the QRS complex on the ECG. Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period (or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation. If the patient is conscious, various drugs are often used to help sedate the patient and make the procedure more tolerable.
http://www.youtube.com/watch?v=1rcg6Ce7p18&feature=related

Catheter ablation may be used to restore a normal heart rhythm when medicines or electrical cardioversion don't work. During this procedure, a wire is inserted through a vein in the leg or arm and threaded to the heart.

Radio wave energy is sent through the wire to destroy abnormal tissue that may be disrupting the normal flow of electrical signals.

Sometimes catheter ablation is used to destroy the atrioventricular (AV) node. The AV node is where the heart's electrical signals pass from the atria to the ventricles. This procedure requires your doctor to surgically implant a device called a pacemaker to maintain a normal heart rhythm.



Maze surgery
Another procedure to restore a normal heart rhythm is called "maze" surgery. During this procedure, the surgeon makes small cuts or burns in the atria that prevent the spread of disorganized electrical signals.
This procedure requires open-heart surgery, so it's usually done when a person requires heart surgery for other reasons, such as for valve disease


Prognosis
• the risk of stroke for lone atrial fibrillation was 4 times higher
• female sex in patients with AF without rheumatic heart disease is associated with a higher risk of stroke
• underlying heart disease increases the risk of stroke in non-rheumatic atrial fibrillation
• up to 20% of patients with atrial fibrillation and a stroke will have a second stroke within one year
• in a follow-up of the Framingham study, atrial fibrillation was independently associated with a 50-90% increase in the risk of death.
Reference
www.emedicine.com
www.nhlbi.nih.gov
http://www.cvpharmacology.com/