What Causes Atrial Fibrillation and Why We Fail With Ablation
What Causes Atrial Fibrillation and Why We Fail With Ablation
If what we have learned from this informative study is that substrate abnormalities may be progressive and we do not have a uniformly effective method to treat structural arrhythmogenic substrate in patients with AF, can we hope for a true disease-modifying effect with ablation in the future? If AF is simply a symptom of an underlying process related to the components of MS and possibly diastolic dysfunction, how can we address AF in a permanent fashion without changing the underlying process? The paracardiac autonomic nervous system lies in close physical proximity to the pulmonary vein ostia and has been investigated as a potential target for AF ablation. Present approaches pioneered by Scherlag et al. involve atrial ablation to target these epicardial ganglia. However, the enhanced inflammatory response with myocardial ablation along with proarrhythmic macrore-entry may offset gains. Given the decreased incidence of AF in denervated hearts after transplantation, perhaps approaches similar to these need to be developed to render AF less likely to recur regardless of an ongoing provocatory substrate? Knowing that we cannot halt the underlying process, can we make the atria immune to fibrillation?
Is There a Way Out?
If what we have learned from this informative study is that substrate abnormalities may be progressive and we do not have a uniformly effective method to treat structural arrhythmogenic substrate in patients with AF, can we hope for a true disease-modifying effect with ablation in the future? If AF is simply a symptom of an underlying process related to the components of MS and possibly diastolic dysfunction, how can we address AF in a permanent fashion without changing the underlying process? The paracardiac autonomic nervous system lies in close physical proximity to the pulmonary vein ostia and has been investigated as a potential target for AF ablation. Present approaches pioneered by Scherlag et al. involve atrial ablation to target these epicardial ganglia. However, the enhanced inflammatory response with myocardial ablation along with proarrhythmic macrore-entry may offset gains. Given the decreased incidence of AF in denervated hearts after transplantation, perhaps approaches similar to these need to be developed to render AF less likely to recur regardless of an ongoing provocatory substrate? Knowing that we cannot halt the underlying process, can we make the atria immune to fibrillation?
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