The evolution of atrial fibrillation ablation from triggers to substrate.
The surgical approach to treat atrial fibrillation involves compartmentalizing the atrium. By dividing the atrium into discrete segments, the surgeon prevents the arrhythmia's ability to sustain by decreasing the required atrial substrate for propagation of the fibrillatory wavelets. Endocardial catheter ablation techniques used to replicate the surgical procedure were fraught with long procedure times and unacceptably high thromboembolic complications. The realization that the initiation of atrial fibrillation is often caused by triggers within the pulmonary veins has changed the focus from preventing the arrhythmia's ability to maintain itself to preventing the arrhythmia from ever being initiated. Early focal catheter ablation of atrial fibrillation used activation mapping and pace mapping to identify sites of spontaneous firing that led to bursts of atrial fibrillation. Although acute success rates were quite high, recurrences were unacceptably common. When investigators reattempted ablation of these patients, triggers were often found in other areas of the vein initially targeted and/or in remote veins. Because it appeared that either new triggers could arise in nonablated areas of veins or these areas were arrhythmogenic but not realized during initial ablation, the technique of complete isolation of the pulmonary vein was developed. A circular mapping catheter was placed at the funnel-shaped opening of each vein to map electrical exit sites of the vein into the atrium. Early attempts at electrical isolation of the veins occasionally caused pulmonary vein stenosis, on occasion necessitating angioplasty or stenting of the vein. This phenomenon has caused investigators to isolate the veins by using much larger circles with far greater diameters along the posterior left atrium. Many investigators now also have added ablation lines along the roof of the left atrium as well as down to the mitral valve annulus. The technique appears to be more analogous to the surgical model, now isolating triggers as well as preventing arrhythmia propagation.
Verdino
Ralph J
RJ
Division of Cardiovascular Medicine, University of Pennsylvania, Philadelphia, PA, USA. ralph.verdino@uphs.upenn.edu
D000200:Action Potentials; D000818:Animals; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery*; D017115:Catheter Ablation; D018450:Disease Progression; D006329:Heart Conduction System / Q000503:physiopathology* / Q000601:surgery*; D006801:Humans; D008955:Models, Cardiovascular; D016896:Treatment Outcome