Treating Atrial Fibrillation: What's Next?: Commentary on Looking at the Future Treating Atrial Fibrillation

During the past few years, several approaches have been introduced in an attempt to maintain sinus rhythm in symptomatic patients with atrial fibrillation (AF). New developments are certainly dependent on acquisition of new knowledge and on technological advances. At the present time, two main basic concepts govern our therapeutic approaches. First, triggers proceeding from the pulmonary veins frequently initiate AF. Second, once initiated a critical mass of atrium is required to maintain this arrhythmia. Hence, current ablation strategy in patients with paroxysmal AF is to isolate the triggers by eliminating conduction from the pulmonary veins into the left atrium. Linear atrial lesions are added to pulmonary vein isolation in patients with persistent AF in an attempt to eliminate the critical mass of atrium required to support the arrhythmia. The challenge is to obtain these results effectively and with minimal complications. At the present time, the use of radiofrequency energy is associated with several limitations including unpredictable lesion depth and endothelial damage with thrombus and char formation. Other sources of energy are needed to obtain more consistent results with preservation of endothelial integrity. However, even if technology improves, many questions remain to be answered. For example, where should linear lesions be made to prevent reentry? How do we identify other potential triggers of atrial fibrillation? Can we modulate the effect of the autonomic nervous system on atrial vulnerability? Still, not all patients with AF require invasive procedures. Hence, more effective and specific antiarrhythmic agents are needed to prevent initiation and perpetuation of AF. Drugs that prolong atrial but not ventricular refractoriness are needed to terminate AF without the risk of inducing life-threatening ventricular arrhythmias. An ideal antiarrhythmic for atrial fibrillation should prolong the refractoriness only at atrial sites with abnormally short refractory periods without altering conduction velocity. Anticoagulation with warfarin is effective in reducing the risk of embolic complications, but remains a challenge due to drug and food interactions. A direct thrombin inhibitor that does not require anticoagulation monitoring and has no interactions is now been evaluated and may soon replace warfarin. The pathophysiology of AF is not fully understood, and therefore, treatment is only palliative. Why do patients with otherwise normal hearts develop this arrhythmia? Do they have structural, embryologic, or electrophysiologic abnormalities that we can not detect with present techniques? As we improve our understanding of this fascinating arrhythmia, we will be able to tailor therapeutic interventions to each individual patient, instead of using the same treatment for all patients.