Few trials in Cardiology have been so ascertaining of our limited knowledge of cardiac physiology as the Cardiac Arrhythmia Suppression Trial, CAST. That trial made us aware of the complexity of the interaction between antiarrhythmic drugs and factors that control cardiac contractility and rhythm. A balance between structural and ionic components is required for the electromechanical impulse to propagate orderly across the myocardial cells. When structural heart disease or genetic or iatrogenic factors modify this interaction, the result can be the formation of a chaotic electrical activity or fibrillation which can affect either chamber of the heart, atria or ventricles. The atrial chaos or atrial fibrillation (AF) is defined as an erratic activation of the atria, causing an irregular heart rhythm at the ventricular level. AF remains the Achilles′ heel of cardiac rhythmology. Despite the overall advance in the treatment of the cardiac dysrhythmias with the introduction of radio frequency ablation, therapeutic options in AF have remained largely unchanged and aimed at controlling the heart rate and anticoagulation. New surgical and ablation techniques are being developed, while promising they are still extremely laborious and available only to a handful of patients. The limited success in the therapy of AF is in part due to our Poor understanding of its molecular pathophysiology. Advances in genetics and molecular biology will like1y give new insights into the development of the disease. Molecular research of AF has focused on two main fields, identification of the genes that playa role in the initiation of the disease and altered gene expression during the disease state. These studies are aimed at identifying not only the triggering factors in the acute form but also those that perpetuate the arrhythmia and convert it into a chronic form.
KeywordsAtrial Fibrillation Familial Form Radio Frequency Ablation Brugada Syndrome Monogenic Disease
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