Atrial Fibrillation - Essay Example

Possible causes that give rise to AF include comorbidities like hypertension, coronary ischemia, heart failure, and obstructive sleep apnoea. The characteristic features of electrical remodeling are alterations in atrial refractoriness, atrial conduction, and sinus node function. This happens very quickly and is considered possible to reverse. Loss of contractility results from the contractile remodeling that happens in AF and like electrical remodelling happens very quickly. Reduction in the release of systolic calcium ions is believed to contribute to this change.

Myolysis or the loss of sarcomeres is also a likely candidate for this change. The consequences of contractile remodeling are thrombus formation and atrial dilation. The advance of AF may be caused by contractile remodeling through the coexistence of multiple wavelets. Reversing contractility changes takes longer than in the case of reversing electrical remodeling changes possible because of the time involved in the replacement of lost sarcomeres. Persistent AF has been associated with the structural changes within the atria.

Many of these changes are considered to be irreversible. Evidence from animal studies suggests that these changes occur more slowly than the changes that occur from electrical and contractile remodeling and primarily reflect dedifferentiation. The striking changes seen in animal models are increased cell size, myolysis, and the collection of glycogen around the nucleus of the cell. From the limited data from humans, there is an indication that degenerative changes may occur (Cohen & Naccarelli, 2008).

Treatment The treatment is based on the of AF into first detected episode duration know and more than or equal to 48hrs or of unknown duration, recurrent AF and recurrent atrial flutter. Management of AF is a three-pronged strategy. The first is of the prongs is anticoagulation. The use of anticoagulation is guided by the CHAD scoring system set forth by the American College of Cardiology, American Heart Association, and the European Society of cardiology. When the AF patient has any one of these risk factors the score is one and the use of anticoagulation is at the discretion of the attending physician.

When the patient has more than one of these risk factors present the score goes to two or more and anticoagulation is no longer at the discretion of the attending physician, but a must. Warfarin is the suggested anticoagulation agent in such cases. The second prong in the treatment of AF is rhythm control and the third prong is rate control. To establish normal rhythm the choices of intervention are cardioversion with or with the use of drugs or the use of ablation (Strickberger, 2007). The recommended guideline for the treatment of an acute episode of AF is treatment with warfarin unless the immediate risk of bleeding outweighs the risk of thromboembolic prior to cardioversion and anticoagulation.

In the case of chronic AF, the recommended guideline is the estimation of the risk of thrombo-embolism using CHADS 2 estimation of risk of bleeding for chronic anticoagulation. Use of warfarin or aspirin unless the long term risk of bleeding outweighs the risk of thromboembolism.