Page 16 - ADD-ON ABLATION SURGERY IN PATIENTS WITH ATRIAL FIBRILLATION

Chapter 1
(BNP), whose concentration in LAF is significantly higher than in age- and sex- matched healthy subjects55 and the Apelin, an endogenous peptide hormone that appears to have a physiological role in counter-regulation of the angiotensin and vasopressin systems, whose levels were significantly lower in patients with LAF compared with control subjects with sinus rhythm56. It has been demonstrated that activation of the renin-angiotensin system (RAS) with increase in Angiotensin II levels promotes formation of collagen.Therefore, pharmacological inhibition of this system could represent a novel approach to counteract the development of fibrosis and recurrence of AF57. Finally, it has been suggested that a specific polymorphism of matrix metalloproteinase-2 gene is a risk factor for chronic LAF, while C allele of the interleukin-10 (IL-10) polymorphism represents a protective factor58.
Triggers
There is general agreement that AF requires a trigger usually located in the pulmonary veins and left atrium59-63. Haissaguerre and colleagues64 demonstrated that paroxysmal AF originates from ectopic beats in the pulmonary veins in 94% of cases. This likely relates to the anatomical transition from pulmonary vein endothelium to left atrial endocardium; at this juncture, two types of tissue with different electric properties are juxtaposed, and this may potentiate development of AF64, 65. Catheter ablation of the posterior left atrium, including the antra surrounding the pulmonary veins, has proven effective at ablating both paroxysmal and permanent AF64-67.
Other anatomical structures that may also provide ectopic beats causing LAF are the superior vena cava, the vein of Marshall, the musculature of coronary sinus and the posterior wall of the left atrium (LA). However, for LAF to become sustained the presence of an atrial substrate of sufficient mass capable of maintaining re- entrant circuits is necessary.The LA-PV junction and the posterior wall of the LA are critical structures in this regard68.
Finally, increasing evidence suggests that sustained AF is the result of a combination of PV vein focal discharge and PV-LA re-entrant activity69.
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